Vascular Responses (vascular + response)

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Vascular Responses

  • forearm vascular response

  • Selected Abstracts

    Cutaneous Vascular Response to Local Warming: A Response to Letter from Cracowski and Roustit

    MICROCIRCULATION, Issue 2 2010
    No abstract is available for this article. [source]

    Vascular response to laser photothermolysis as a function of pulse duration, vessel type, and diameter: Implications for port wine stain laser therapy

    Sol Kimel PhD
    Abstract Background and Objective Treatment of port wine stains (PWS) by photothermolysis can be improved by optimizing laser parameters on an individual patient basis. We have studied the critical role of pulse duration (tp) on the treatment efficacy. Study Design/Materials and Methods The V-beam laser (Candela) allowed changing tp over user-specified discrete values between 1.5 and 40 milliseconds by delivering a series of 100 microsecond spikes. For the 1.5 and 3 millisecond pulses, three spikes were observed at intervals tp/2 and for tp,,,6 milliseconds, four spikes separated by tp/3. The ScleroPlus laser (Candela) has a smooth output over its fixed 1.5 milliseconds duration. Blood vessels in the chick chorioallantoic membrane (CAM) were irradiated at fixed wavelength (595 nm), spot size (7 mm), radiant exposure (15 Jcm,2), and at variable tp. The CAM contains an extensive microvascular network ranging from capillaries with diameter D,<,30 ,m to blood vessels of D,,,120 ,m. The CAM assay allows real-time video documentation, and observation of blood flow in pre-capillary arterioles (A) and post-capillary venules (V). Vessel injury was graded from recorded videotapes. Mathematical modeling was developed to interpret results of vessel injury when varying tp and D. A modified thermal relaxation time was introduced to calculate vessel wall temperature following laser exposure. Results Arterioles. For increasing tp, overall damage was found to decrease. For fixed tp, damage decreased with vessel size. Venules. For all D, damage was smaller than for corresponding arterioles. There was no dependence of damage on tp. For given tp, no variation of damage with D was observed. Photothermolysis due to spiked (V-beam) vs. smooth (Scleroplus) delivery of laser energy at fixed tp (1.5 milliseconds), showed similar vessel injuries for al values of D (P>0.05). Conclusions The difference between initial arteriole and venule damage could be explained by the threefold higher absorption coefficient at 595 nm in (oxygen-poor!) arterioles. In human patients, PWS consist of ectatic venules (characterized by higher absorption), so that these considerations favor the use of 595-nm irradiation for laser photothermolysis. For optimal treatment of PWS it is proposed that tp be between 0.1 and 1.5 milliseconds. This is based on a modified relaxation time ,d,, defined as the time required for heat conduction into the full thickness of the vessel wall, which is assumed to have a thickness ,D ,,0.1D. The corresponding ,d, will be a factor of about six smaller than given in the literature. For vessels with D between 30 and 300 ,m, ,d, ranges from 0.1 to 1.5 milliseconds. Lasers Surg. Med. 30:160,169, 2002. © 2002 Wiley-Liss, Inc. [source]

    Enhanced vascular responses to hypocapnia in neurally mediated syncope

    ANNALS OF NEUROLOGY, Issue 3 2008
    Lucy Jane Norcliffe-Kaufmann PhD
    Objective The susceptibility to suffer neurally mediated syncope and loss of consciousness varies markedly. In addition to vasodilatation and bradycardia, hyperventilation precedes loss of consciousness. The resultant hypocapnia causes cerebral vasoconstriction and peripheral vasodilatation. We postulate that more pronounced cerebral and peripheral vascular responses to reductions in arterial CO2 levels underlie greater susceptibility to neurally mediated syncope. Methods We compared vascular responses to CO2 among 31 patients with histories of recurrent neurally mediated syncope and low orthostatic tolerance and 14 age- and sex-matched control subjects with no history of syncope and normal orthostatic tolerance. Vascular responses to CO2 were calculated after all subjects had fully recovered and their blood pressures and heart rates were stable. We measured blood flow velocity in the middle cerebral artery (transcranial Doppler) and in the left brachial artery (brachial Doppler), and end-tidal CO2 during voluntary hyperventilation and hypoventilation (end-tidal CO2 from 21,45mm Hg), and determined the slopes of the relations. Results Hypocapnia produced a significantly greater reduction in cerebral blood flow velocity and in forearm vascular resistance in patients with neurally mediated syncope than in control subjects. Opposite changes occurred in response to hypercapnia. In all subjects, the changes in cerebral blood flow velocity and forearm vasodilatation were inversely related with orthostatic tolerance. Interpretation Susceptibility to neurally mediated syncope can be explained, at least in part, by enhanced cerebral vasoconstriction and peripheral vasodilatation in response to hypocapnia. This may have therapeutic implications. Ann Neurol 2007 [source]

    Vascular responses to ,-adrenoceptor subtype-selective agonists with and without endothelium in rat common carotid arteries

    S. Chiba
    1 Using the cannula inserting method, vasodilator responses to ,-adrenoceptor agonists (isoprenaline, denopamine and procaterol) were investigated in isolated and perfused rat common carotid arteries. 2 Each ,-adrenoceptor agonist induced a vasodilation in preparations preconstricted by phenylephrine in a dose-related manner. The potencies were in the order of isoprenaline > procaterol >> denopamine. 3 Denopamine-induced dilations were significantly inhibited by 1 nmol betaxolol (a selective ,1 -adrenoceptor antagonist), but it was not influenced by 1 nmol ICI 118,551 (a selective ,2 -adrenoceptor antagonist). On the other hand, procaterol-induced vasodilations were significantly inhibited by 1 nmol ICI 118,551 but not modified by 10 nmol betaxolol. 4 ACh-induced vasodilations disappeared after intraluminal saponin injection to remove endothelium, but procaterol- and denopamine-induced dilations were not modified by removal of the endothelium. 5 Pretreatment with L -NG -nitroarginine methyl ester (L -NAME) readily inhibited ACh-induced vasodilations. However, neither procaterol- or denopamine-induced vasodilation was modified by L -NAME treatment. 6 From these results, it is concluded that in the rat common carotid arteries (1) there are abundant ,2 - and a few ,1 -adrenoceptors, and (2) there is no participation of the endothelium-dependent mechanism in ,-adrenoceptor mediated vasodilations. [source]

    Inspiration-induced vasoconstrictive responses in dominant versus non-dominant hands

    Harvey N. Mayrovitz
    Summary Single rapid and deep inspirations (inspiratory gasps, IG) result in arteriolar vasoconstriction with concomitant transient decreases in skin blood flow that are most prominent in fingers and toes. Vascular responses (inspiratory gasp responses, IGR) are determined as the maximum percentage reduction in blood flow and have been used to assess sympathetic neurovascular function in several conditions. Previous studies have described various features of the response but there has been no reported systematic investigation of the degree of similarity between IGR obtained on dominant and non-dominant hands. This aspect is important in procedures that may use IGR to evaluate suspected unilateral sympathetic dysfunction of a limb-pair or to test the effectiveness of physiological interventions imposed on a single limb of a pair. Thus, the goal of our study was to compare IGR magnitudes that were simultaneously determined in paired-fingers of dominant and non-dominant hands. In 30 healthy seated subjects, skin blood perfusion via laser-Doppler (SBF) was measured on the dorsum of the middle finger of both hands while subjects performed three sequential IG at 3-min intervals. Analysis of variance for repeated measures revealed no significant difference in IGR between dominant (79·3 ± 11·2%) and non-dominant hands (81·9 ± 11·6%, P = 0·965) with an overall IGR of 80·6 ± 11·4%. These results indicate that hand-dominance is not a factor that is likely to significantly effect IGR differentials determined in paired-limbs. [source]

    The role of the ,-adrenergic receptor in the leg vasoconstrictor response to orthostatic stress

    ACTA PHYSIOLOGICA, Issue 3 2009
    M. Kooijman
    Abstract Aim:, The prompt increase in peripheral vascular resistance, mediated by sympathetic ,-adrenergic stimulation, is believed to be the key event in blood pressure control during postural stress. However, despite the absence of central sympathetic control of the leg vasculature, postural leg vasoconstriction is preserved in spinal cord-injured individuals (SCI). This study aimed at assessing the contribution of both central and local sympathetically induced ,-adrenergic leg vasoconstriction to head-up tilt (HUT) by including healthy individuals and SCI, who lack central sympathetic baroreflex control over the leg vascular bed. Methods:, In 10 controls and nine SCI the femoral artery was cannulated for drug infusion. Upper leg blood flow (LBF) was measured bilaterally using venous occlusion strain gauge plethysmography before and during 30° HUT throughout intra-arterial infusion of saline or the non-selective ,-adrenergic receptor antagonist phentolamine respectively. Additionally, in six controls the leg vascular response to the cold pressor test was assessed during continued infusion of phentolamine, in order to confirm complete ,-adrenergic blockade by phentolamine. Results:, During infusion of phentolamine HUT still caused vasoconstriction in both groups: leg vascular resistance (mean arterial pressure/LBF) increased by 10 ± 2 AU (compared with 12 ± 2 AU during saline infusion), and 13 ± 3 AU (compared with 7 ± 3 AU during saline infusion) in controls and SCI respectively. Conclusion:, Effective ,-adrenergic blockade did not reduce HUT-induced vasoconstriction, regardless of intact baroreflex control of the leg vasculature. Apparently, redundant mechanisms compensate for the absence of sympathetic ,-adrenoceptor leg vasoconstriction in response to postural stress. [source]

    The Neurogenic Vasodilator Response to Endothelin-1: A Study in Human Skin In Vivo

    Ruwani Katugampola
    We have investigated the mediators and mechanisms underlying the vasodilator effects of the potent vasoactive peptide, endothelin-1 (ET-1) and its isomers ET-2 and ET-3 in human skin, in vivo, using cutaneous microdialysis to quantify the release of mediators within the dermal response and scanning laser Doppler imaging to measure changes in blood flux. The effects of local anaesthesia, inhibition of nitric oxide synthase (NOS) by L-NAME and ET receptor blockade on the ET-induced vascular response were also investigated. ET-1, -2 and -3 all caused a dose-dependent area of pallor surrounded by a long-lasting flare which was accompanied by a short-lived burning pruritus. The concentration of nitric oxide (NO) in dialysate collected within the pallor response to 5 ,M ET-1 (1.43 ± 0.64 ,M, n = 5) was not significantly different from baseline levels collected prior to injection (0.86 ± 0.38 ,M) whilst that in the flare increased to reach a peak value of 2.28 ± 0.61 ,M at between 4 and 10 min after intradermal injection (P < 0.004). Pretreatment with local anaesthetic slowed the development of the flare and significantly reduced its size by up to 52% at 20 min after injection (P < 0.05) but had no significant effect on the central pallor. L-NAME, delivered by dialysis also caused a significant reduction in the ET-1-induced flare (P < 0.005). Bosentan, the non-selective ETA/ETB antagonist, when given by dialysis at the site of injection, reduced the area of both the ET-1-induced pallor and surrounding flare by 41 and 26%, respectively. No significant increase in tissue histamine was measured within either the pallor or flare response to ET-1, -2 or -3. Together these data confirm that the vasodilator response to endothelin-1 in human skin is neurogenic in origin and that it is in part mediated by the local release of nitric oxide. There appears to be little evidence for the involvement of mast cell-derived histamine in the initiation or modulation of ET-induced vasodilatation, in vivo. [source]

    Targeted gene analysis in Ulmus americana and U. pumila tissues

    FOREST PATHOLOGY, Issue 2 2008
    C. Nasmith
    Summary Steady-state gene expression was compared between Dutch elm disease (DED)-susceptible Ulmus americana and DED-resistant U. pumila callus, leaf midrib, root and inner bark tissues. Stress-related cDNAs including phenylalanine ammonia-lyase (PAL), chitinase (CHT) and polygalacturonase-inhibiting protein (PGIP) were isolated and compared following RT-PCR of elm tissues. Complete CHT and partial PAL and PGIP cDNA transcripts were identified, each displaying sequence variation between elm species. These transcripts were Dig-labelled and subsequently used for northern analyses of the elm tissues. Midrib and root tissue displayed highest steady-state gene expression compared with inner bark and callus tissues. A modified nucleic acid isolation technique was necessary for downstream RNA analyses. Lithium chloride and polyvinylpyrrolidone were critical for efficient removal of polysaccharides and phenolics associated with some of the elm tissues. Steady-state gene expression is discussed in relation to the tissues investigated. The use of tissues other than in vitro callus culture more closely represents the tissues associated with the elm's vascular response to DED. [source]

    Disparity between prostate tumor interior versus peripheral vasculature in response to verteporfin-mediated vascular-targeting therapy

    Bin Chen
    Abstract Photodynamic therapy (PDT) is a light-based cancer treatment modality. Here we employed both in vivo and ex vivo fluorescence imaging to visualize vascular response and tumor cell survival after verteporfin-mediated PDT designed to target tumor vasculature. EGFP-MatLyLu prostate tumor cells, transduced with EGFP using lentivirus vectors, were implanted in athymic nude mice. Immediately after PDT with different doses of verteporfin, tumor-bearing animals were injected with a fluorochrome-labeled albumin. The extravasation of fluorescent albumin along with tumor EGFP fluorescence was monitored noninvasively with a whole-body fluorescence imaging system. Ex vivo fluorescence microscopy was performed on frozen sections of tumor tissues taken at different times after treatment. Both in vivo and ex vivo imaging demonstrated that vascular-targeting PDT with verteporfin significantly increased the extravasation of fluorochrome-labeled albumin in the tumor tissue, especially in the tumor periphery. Although PDT induced substantial vascular shutdown in interior blood vessels, some peripheral tumor vessels were able to maintain perfusion function up to 24 hr after treatment. As a result, viable tumor cells were typically detected in the tumor periphery in spite of extensive tumor cell death. Our results demonstrate that vascular-targeting PDT with verteporfin causes a dose- and time-dependent increase in vascular permeability and decrease in blood perfusion. However, compared to the interior blood vessels, peripheral tumor blood vessels were found less sensitive to PDT-induced vascular shutdown, which was associated with subsequent tumor recurrence in the tumor periphery. © 2008 Wiley-Liss, Inc. [source]

    Regional cerebral blood flow responses to hyperventilation during sevoflurane anaesthesia studied with PET

    Background: Arterial carbon dioxide tension (PaCO2) is an important factor controlling cerebral blood flow (CBF) in neurosurgical patients. It is still unclear whether the hypocapnia-induced decrease in CBF is a general effect on the brain or rather linked to specific brain regions. We evaluated the effects of hyperventilation on regional cerebral blood flow (rCBF) in healthy volunteers during sevoflurane anaesthesia measured with positron emission tomography (PET). Methods: Eight human volunteers were anaesthetized with sevoflurane 1 MAC, while exposed to hyperventilation. During 1 MAC sevoflurane at normocapnia and 1 MAC sevoflurane at hypocapnia, one H215O scan was performed. Statistical parametric maps and conventional regions of interest analysis were used for estimating rCBF differences. Results: Cardiovascular parameters were maintained constant over time. During hyperventilation, the mean PaCO2 was decreased from 5.5 ± 0.7 to 3.8 ± 0.9 kPa. Total CBF decreased during the hypocapnic state by 44%. PET revealed wide variations in CBF between regions. The greatest values of vascular responses during hypocapnia were observed in the thalamus, medial occipitotemporal gyrus, cerebellum, precuneus, putamen and insula regions. The lowest values were observed in the superior parietal lobe, middle and inferior frontal gyrus, middle and inferior temporal gyrus and precentral gyrus. No increases in rCBF were observed. Conclusions: This study reports highly localized and specific changes in rCBF during hyperventilation in sevoflurane anaesthesia, with the most pronounced decreases in the sub cortical grey matter. Such regional heterogeneity of the cerebral vascular response should be considered in the assessment of cerebral perfusion reserve during hypocapnia. [source]

    Role of Endothelium/Nitric Oxide and Cyclic AMP in Isoproterenol Potentiation of 17ß-Estradiol-Mediated Vasorelaxation

    HY Chan
    Estrogen exerts vasorelaxation and cardiac protection via multiple cellular mechanisms. Estrogen modifies vasodilatation induced by certain relaxants such as ß-adrenoceptor agonists. However, little is known whether low concentrations of ß-adrenoceptor agonists would also influence the acute relaxant response to estrogen. The present study was designed to investigate the synergistic interaction between isoproterenol and 17ß-estradiol, and to study the role of endothelium and cyclic AMP-dependent pathway in this interaction. Changes in vessel tone of the isolated rat mesenteric artery rings were measured by force-displacement Grass transducer. In 9,11-dideoxy-11,, 9,-epoxy-methanoprostaglandin F2, - preconstricted endothelium-intact rings, 17ß-estradiol induced concentration-dependent relaxation with pD2 of 5.074 ± 0.043. Pretreatment of endothelium-intact rings with isoproterenol (1-3 × 10 -9 M, 1-h incubation time) significantly enhanced 17,-estradiol-induced relaxation. Longer incubation (2.5 h) did not produce further amplifying effect. This effect was inhibited by Rp-cGMPS triethylamine (3 × 10 -6 M), and disappeared in the presence of 3 × 10 -5 M NG -nitro-L-arginine methyl ester or in the endothelium-denuded rings. The effect of isoproterenol was partially antagonized by propranolol (3 × 10 -6 M), ICI 118,551 (3 × 10 -6 M) but not by atenolol (10 -5 M). None of three ,-adrenoceptor antagonists affected 17ß-estradiol-induced relaxation in the absence of isoproterenol. Rp-cAMPS triethylamine (3 × 10 -6 M) abolished the effect of isoproterenol. Besides, exposure to 3 × 10 -9 M forskolin for 1 h also potentiated the relaxant response to 17,-estradiol. In summary, this isoproterenol enhancement was dependent on the presence of endothelium and abolished by L-NAME via a ,2 -adrenoceptor-mediated cyclic AMP-dependent mechanism. These data also indicate the possible existence of cyclic AMP-dependent nitric oxide-producing pathway in the regulation of the vascular response to vasodilators. (supported by UPGC Direct Grant) [source]

    Thrombin and PAR-1 stimulate differentiation of bone marrow-derived endothelial progenitor cells

    Summary., Endothelial progenitor cells (EPCs) from the bone marrow play an important role in vascular response to injury and ischemia. The mediators involved in the mobilization, recruitment, proliferation and differentiation of EPCs are not fully understood. In this study, the role of coagulation factor thrombin and protease-activated receptor-1 (PAR-1) on bone marrow-derived cell proliferation and differentiation was investigated. Bone marrow cells (BMCs) were isolated from C57/BL6 mice and plated on fibronectin-coated flasks. Cell characteristics, proliferation and the expression of endothelial cell markers were determined using immunohistochemistry, thymidine uptake and fluorescence activated-cell sorting (FACS), respectively. The results show that thrombin stimulated enrichment of bone marrow cells with endothelial morphology, exhibiting acetylated-low-density lipoprotein (LDL) uptake and isolectin staining. Thrombin or PAR-1-activating peptide produced a 2- to 3-fold increase in the total number of cells as well as an increase in vascular endothelial (VE)-cadherin-positive cells. Thrombin treatment of VE-cadherin-negative cells prepared after cell sorting resulted in the generation of 3- to 4-fold higher VE-cadherin-positive cells than the untreated cultures. Increase in VE-cadherin-positive cells was inhibited by hirudin and efegatran. These results provide first evidence for a novel activity of thrombin and PAR-1 on bone marrow progenitor cell proliferation and EPC differentiation, and suggest their potential role in vascular regeneration and recanalization of thrombus. [source]

    A comparison of manual and automated methods of measuring conjunctival vessel widths from photographic and digital images

    Christopher G. Owen
    Abstract We investigated the application of a fully automated computer algorithm for identifying vessels of the conjunctiva from their scleral surround, and compared measures of vessel width with established methods. Vessel widths at 101 locations (ranging from 20 to 140 ,m), from 12 patients, were measured from film and digital images, using a variety of methods, and compared. Widths were measured manually, by semi-automated methods using grey level (densitometric) profiles taken from digital images, and by automated techniques set at different operating levels. Good intra-session repeatibility was obtained using the automated method with an operating sigma value of 3 pixels (16 ,m) (mean difference 0.5 ,m, 95% CI ,8.5 to 9.4 ,m) and manual calliper measurements from digitally created photographic slides (mean difference 0.4 ,m, ,9.3 to 10.1 ,m). For comparison with other measures of width, the latter was used as the gold standard. Widths measured from film were slightly larger than those measured directly from digital images, although this effect was small (5 ,m) for most vessels. Overall widths measured using the automated method, with a sigma value of 3 pixels, agreed best with the gold standard (inter-method repeatibility; mean difference 1.4 ,m, ,32.5 to 35.2 ,m) although the automated method overestimated small widths (<40 ,m) and underestimated larger vessel widths (>40 ,m). Automated detection of vessels of the conjunctiva from digital images avoids manual and operator involved measures which are time consuming, and which preclude large patient studies. The resulting data may help in monitoring the vascular response of the conjunctiva to surgical or pharmacological intervention, and in describing vascular changes in response to ocular or systemic disease. The application of this algorithm to the study of retinal vessels is yet to be realised. [source]

    Does halothane or isoflurane affect hypoxic and post-hypoxic vascular response in rabbit aorta?

    E. Haddad
    Background: Halothane and isoflurane affect differently endothelium-dependent and -independent vasorelaxation at 95% O2. In addition, hypoxic vascular response might involve endothelium-dependent and -independent mechanisms. Therefore, we investigated, in rabbit aortic rings, 1) the influence of halothane and isoflurane on vasodilation at 95% O2 and on hypoxic-induced vasorelaxation at 0% O2 and 2) the influence of halothane and isoflurane on endothelium-dependent and -independent post-hypoxic vascular response. Methods: Endothelium-intact and endothelium-denuded rabbit aortic rings were used. Phenylephrine precontracted rings were exposed, at 95% O2, to acetylcholine (ACh, 10,9 to 10,4 M) or sodium nitroprusside (SNP, 10,9 to 10,4 M) in the presence or absence of anaesthetic at 1 or 2 MAC. Precontracted rings were also exposed to an acute reduction in O2 from 95% to 0% followed by an acute reoxygenation with 95% O2 in the absence or presence of anaesthetic at 1 or 2 MAC. Results: At 95% O2, halothane decreased endothelium-dependent relaxation to ACh, while endothelium-independent relaxation to SNP was decreased only at 2 MAC. Isoflurane did not modify ACh- or SNP-induced relaxation. At 0% O2, neither halothane nor isoflurane altered the hypoxic vascular relaxation. Post-hypoxic response was not changed either. Conclusion: Our results indicate that halothane and isoflurane do not alter vascular hypoxic response in conductance arteries. [source]

    Central command and the cutaneous vascular response to isometric exercise in heated humans

    Manabu Shibasaki
    Cutaneous vascular conductance (CVC) decreases during isometric handgrip exercise in heat stressed individuals, and we hypothesized that central command is involved in this response. Seven subjects performed 2 min of isometric handgrip exercise (35% of maximal voluntary contraction) followed by postexercise ischaemia in normothermia and during heat stress (increase in internal temperature ,1°C). To augment the contribution of central command independent of force generation, on a separate day the protocol was repeated following partial neuromuscular blockade (PNB; i.v. cisatracurium). Forearm skin blood flow was measured by laser-Doppler flowmetry, and CVC was the ratio of skin blood flow to mean arterial pressure. The PNB attenuated force production despite encouragement to attain the same workload. During the heat stress trials, isometric exercise decreased CVC by ,12% for both conditions, but did not change CVC in either of the normothermic trials. During isometric exercise in the heat, the increase in mean arterial pressure (MAP) was greater during the control trial relative to the PNB trial (31.0 ± 9.8 versus 18.6 ± 6.4 mmHg, P < 0.01), while the elevation of heart rate tended to be lower (19.4 ± 10.4 versus 27.4 ± 8.1 b.p.m., P= 0.15). During postexercise ischaemia, CVC and MAP returned to pre-exercise levels in the PNB trial but remained reduced in the control trial. These findings suggest that central command, as well as muscle metabo-sensitive afferent stimulation, contributes to forearm cutaneous vascular responses in heat stressed humans. [source]

    Vascular endothelial growth factor and angiopoietin are required for prostate regeneration

    THE PROSTATE, Issue 5 2007
    Gui-min Wang
    Abstract BACKGROUND The regulation of the prostate size by androgens may be partly the result of androgen effects on the prostatic vasculature. We examined the effect of changes in androgen levels on the expression of a variety of angiogenic factors in the mouse prostate and determined if vascular endothelial growth factor (VEGF)-A and the angiopoietins are involved in the vascular response to androgens. METHODS Expression of angiogenic factors in prostate was quantitated using real-time PCR at different times after castration and after administration of testosterone to castrated mice. Angiopoietins were localized in prostate by immunohistochemistry and in situ hybridization. The roles of VEGF and the angiopoietins in regeneration of the prostate were examined in mice inoculated with cells expressing soluble VEGF receptor-2 or soluble Tie-2. RESULTS Castration resulted in a decrease in VEGF-A, VEGF-B, VEGF-C, placenta growth factor, FGF-2, and FGF-8 expression after 1 day. In contrast, VEGF-D mRNA levels increased. No changes in angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), hepatocyte growth factor, VEGF receptor-1, VEGF receptor-2, or tie-2 mRNA levels were observed. Administration of testosterone to castrated mice had the opposite effect on expression of these angiogenic factors. Ang-2 was expressed predominately in prostate epithelial cells whereas Ang-1 was expressed in epithelium and smooth muscle. Inoculation of mice with cells expressing soluble VEGF receptor-2 or Tie-2 blocked the increase in vascular density normally observed after administration of testosterone to castrated mice. The soluble receptors also blocked the increase in prostate weight and proliferation of prostatic epithelial cells. CONCLUSION VEGF-A and angiopoietins are required for the vascular response to androgens and for the ability of the prostate to regenerate in response to androgens. Prostate 67: 485,499, 2007. © 2007 Wiley-Liss, Inc. [source]

    Effect of Hemodiafiltration on Pulmonary Hemodynamics in Endotoxic Shock

    ARTIFICIAL ORGANS, Issue 12 2003
    B. Lambermont
    Abstract:, Hemofiltration can improve pulmonary hemodynamics during septic shock. The main objective of the study was to determine whether hemodiafiltration (HDF) would also have beneficial effects on pulmonary hemodynamics during septic shock. In the Endo group, six anesthetized pigs received a 0.5 mg/kg endotoxin infusion over 30 min. In the HDF group (n = 6), HDF was started 30 min after the end of the endotoxin infusion, while in the Control group (n = 4) they received HDF but no endotoxin infusion. Pulmonary hemodynamics were analyzed in detail with a four-element windkessel model. Although in the Control group, HDF did not alter pulmonary hemodynamic parameters, in the HDF group, it was responsible for an amplification of the deleterious pulmonary vascular response to endotoxin insult. Our results show that HDF must be used cautiously in septic shock since it can precipitate right heart failure by increasing pulmonary vascular resistance. [source]

    A comparison of the International Index of Erectile Function and erectile dysfunction studies

    BJU INTERNATIONAL, Issue 7 2003
    W. Kassouf
    OBJECTIVE To evaluate the ability of the five-item version of the International Index of Erectile Function (IIEF-5) to diagnose the vascular aetiology and severity of erectile dysfunction (ED), and to compare it with pharmacological testing and duplex Doppler ultrasonography, as such questionnaires are widely used by the pharmaceutical industry to categorize the severity of ED and to assess the efficacy of drug therapy. PATIENTS AND METHODS In all, 80 patients (mean age 45.2 years, sd 14.0; mean duration of ED 3.5 years) were reviewed by an examiner unaware of their IIEF scores during testing. Penile blood flow was assessed in each patient after an intracavernosal injection with prostaglandin-E1 (10 µg), with self-stimulation in privacy. The peak systolic velocity, end diastolic velocity and resistive index were measured for the vascular diagnosis. Visual ratings of erectile responses were also used for analysis. RESULTS Of the 80 patients, 30 had a normal vascular response, 38 arterial insufficiency and 12 were diagnosed with venous leakage. There was no significant difference in the IIEF scores among patients with a normal vascular response, arterial insufficiency or venous leakage. Analysis of visual ratings of erections showed no difference in IIEF scores among the different groups of patients. CONCLUSION The IIEF was designed and developed specifically for assessing and evaluating sexual function in clinical trials. However, as shown here, the IIEF cannot and should not be used as a tool to diagnose or compare specific vascular causes of ED. [source]

    Abnormal peripheral vascular response to occlusion provocation in normal tension glaucoma patients

    Purpose: To assess peripheral vascular reactive hyperemia in response to occlusion provocation test, using two-channels laser Doppler probe in patients with normal tension glaucoma (NTG) and normal subjects. Methods: 15 patients with NTG (12 women and 4 men), mean aged 58,9 and 15 control subjects (13 women and 2 men), mean aged 60,6 were subjected to an occlusion test. The experiment comprised following steps: 1/ a 5-minute baseline-period 2/ a 2-minute occlusion of the left hand using a 15 cm wide cuff located directly over the elbow (the pressure in the cuff was 50 mmHg higher than the systolic pressure measured on the arm 3/ a 15- minute final recovery period after occlusion. Finger hyperemia was assessed by two-channels laser-Doppler flowmeter MBF-3d, Moor Instruments, Ltd., continuously during the experiment. For measurements of hyperemia two surface probes were attached to the pulp of the second finger (mean probe) and third finger (basic probe) of the left hand. The following hyperemia parameters were measured: RF (rest flow), BZ (biological zero), TM (time to peak flow), TH (half-time of hyperemia), MAX (maximum of hyperemia) and hyperemia amplitude (MAX-RF)/RF 100% was calculated. Kruskal-Wallis test analysis was used to test the differences between the group of patients and normal subjects for TM1,MXF1 (basic probe) and TM2, MXF2 (mean probe) parameters. Results: In NTG patients, TM1 was significantly higher comparing with healthy subjects whereas MAX was significantly lower as compared to the control group. Conclusions: Occlusion provocation test elicits a different systemic hyperemia response in patients with NTG compared with healthy subjects. [source]


    Harald M Stauss
    SUMMARY 1Blood pressure and organ perfusion are controlled by a variety of cardiovascular control systems, such as the baroreceptor reflex and the renin,angiotensin system (RAS), and by local vascular mechanisms, such as shear stress-induced release of nitric oxide (NO) from the endothelium and the myogenic vascular response. Deviations in arterial blood pressure from its set point activate these mechanisms in an attempt to restore blood pressure and/or secure organ perfusion. However, the response times at which different cardiovascular mechanisms operate differ considerably (e.g. blood pressure control by the RAS is slower than blood pressure control via the baroreceptor reflex). 2Owing to these different response times, some cardiovascular control systems affect blood pressure more rapidly and others more slowly. Thus, identifying the frequency components of blood pressure variability (BPV) by power spectral analysis can potentially provide important information on individual blood pressure control mechanisms. 3Evidence is presented that the RAS, catecholamines, endothelial-derived NO and myogenic vascular function affect BPV at very low frequencies (0.02,0.2 Hz) and that low-frequency (LF) BPV (0.2,0.6 Hz) is affected by sympathetic modulation of vascular tone and endothelial-derived NO in rats. In humans, LF BPV (0.075,0.15 Hz) is affected by sympathetic modulation of vascular tone and myogenic vascular function. The impact of the RAS and endothelial-derived NO on BPV in humans requires further investigation. 4In conclusion, power spectral analysis is a powerful diagnostic tool that allows identification of pathophysiological mechanisms contributing to cardiovascular diseases, such as hypertension, heart failure and stroke, because it can separate slow from fast cardiovascular control mechanisms. The limitation that some cardiovascular control mechanisms affect the same frequency components of BPV requires the combination of blood pressure spectral analysis with other techniques. [source]

    Effect of pioglitazone on insulin sensitivity, vascular function and cardiovascular inflammatory markers in insulin-resistant non-diabetic Asian Indians

    DIABETIC MEDICINE, Issue 5 2006
    A. Raji
    Abstract Aims To determine the effects of pioglitazone (30 mg once daily for 16 weeks) on insulin sensitivity, insulin-mediated vasodilation, vascular inflammatory markers, fat distribution and lipids in Asian Indians and Caucasians of European ancestry. Methods Cross-sectional study. Eighteen non-diabetic Asian Indians and 17 Caucasians of comparable age (34 ± 3 vs. 36 ± 3 years) and body mass index (26.0 ± 1.2 vs. 24.7 ± 1.0 kg/m2) had measurements of insulin sensitivity (M, insulin clamp at 6 pmol/kg per min), abdominal fat (computed tomographic scan at L4-L5), endothelial-dependent (reactive hyperaemia, RH) and -independent (0.4 mg sublingual nitroglycerin, TNG) vasodilation using brachial artery ultrasound before and after the 2-h clamp at baseline and after pioglitazone therapy. Results Asian Indians were insulin resistant compared with Causasians during the baseline clamp (M = 25.6 ± 1.7 vs. 41.1 ± 2.2 µmol/kg per min, P < 0.0001) and improved significantly after pioglitazone (to 33.9 ± 1.7 µmol/kg per min, P < 0.001). Vasodilatory responses to RH and TNG were similar in Asian Indians and Caucasians at baseline and did not change. Insulin-mediated vasodilation improved after pioglitazone in Asian Indians, but not in Caucasians, and correlated with the change in insulin sensitivity (r = 0.52, P = 0.03). C-reactive protein (CRP) was higher in Asian Indians vs. Caucasians (1.6 ± 0.4 vs. 0.9 ± 0.2 mg/l) and was negatively correlated with insulin sensitivity (r = ,0.53, P = 0.02). In the Asian Indian group, CRP and plasminogen activator inhibitor-1 decreased and adiponectin increased after pioglitazone, but there were no significant changes in total or visceral fat. Conclusions These results demonstrate that insulin-resistant Asian Indians respond favourably to an insulin sensitizer with improvements in insulin sensitivity, cardiovascular and inflammatory risk markers, and vascular responses to insulin. These agents may have a role in decreasing the risk of diabetes and cardiovascular disease in this high-risk population. [source]

    Circulation in normal and inflamed dental pulp

    ENDODONTIC TOPICS, Issue 1 2007
    In the pulp, arteries branch into a capillary network before they leave the pulp as venules through the apical foramina. The tissue has low compliance, as it is enclosed in dentin, and has a relatively high blood flow and blood volume. The interstitial fluid pressure (IFP) and colloid osmotic pressure are relatively high whereas the net driving blood pressure is low. The high pulsatile IFP is probably the major force for propelling lymph in the dental pulp. Vasodilation in neighboring tissue as well as arteriovenous (AV) shunts in the pulp itself can contribute to a fall in total and coronal pulpal blood flow, respectively. The pulp blood flow is under nervous, humoral, and local control. Inflammatory vascular responses, vasodilation, and increased vessel permeability induce an increase in IFP that can be followed by a temporarily impaired blood flow response. Lipopolysaccharides (LPS) from bacteria may cause endothelial activation in the pulp, leading to vasoconstriction and reduced vascular perfusion. Lymphatic vessels are identified with specific lymphatic markers in the pulp but so far, little is known about their function. Because of the special circulatory conditions in the pulp, there are several clinical implications that need to be considered in dental treatment. Received 13 February 2009; accepted 28 August 2009. [source]

    Effects of endothelin-1 on portal-systemic collaterals of common bile duct-ligated cirrhotic rats

    C.-C. Chan
    Abstract Background/Aims, Endothelin-1 (ET-1) may induce intrahepatic vasoconstriction and consequently increase portal pressure. Endothelin-1 has been shown to exert a direct vasoconstrictive effect on the collateral vessels in partially portal vein-ligated rats with a high degree of portal-systemic shunting. This study investigated the collateral vascular responses to ET-1, the receptors in mediation and the regulation of ET-1 action by nitric oxide and prostaglandin in cirrhotic rats with a relatively low degree of portal-systemic shunting. Methods, The portal-systemic collaterals of common bile duct-ligated (BDL) cirrhotic rats were tested by in situ perfusion. The concentration-response curves of collaterals to graded concentrations of ET-1 (10,10,10,7 m) with or without BQ-123 (ETA receptor antagonist, 2 × 10,6 m), BQ-788 (ETB receptor antagonist, 10,7 m) or both were recorded. In addition, the collateral responses to ET-1 with preincubation of N, -nitro-L-arginine (NNA, 10,4 M), indomethacin (INDO, 10,5 M) or in combination were assessed. Results, Endothelin-1 significantly increased the perfusion pressures of portal-systemic collaterals. The ET-1-induced constrictive effects were inhibited by BQ-123 or BQ-123 plus BQ-788 but not by BQ-788 alone. The inhibitory effect was greater in the combination group. Pretreatment of NNA or NNA plus INDO equivalently enhanced the response of ET-1 while pretreatment of INDO alone exerted no effect. Conclusion, Endothelin-1 has a direct vasoconstrictive effect on the collaterals of BDL cirrhotic rats, mainly mediated by ETA receptor. Endogenous nitric oxide may play an important role in modulating the effects of ET-1 in the portal-systemic collaterals of BDL cirrhotic rats. [source]

    Aerobic exercise acutely improves insulin- and insulin-like growth factor-1-mediated vasorelaxation in hypertensive rats

    Ai-Lun Yang
    Limited information is available concerning the effects of aerobic exercise on vasorelaxation in hypertension. The aim of this study was to investigate the effects of a single bout of aerobic exercise on insulin- and insulin-like growth factor-1 (IGF-1)-induced vasorelaxation in hypertensive rats. Four-month-old spontaneously hypertensive rats were randomly divided into a sedentary group (SHR) and an exercise group (SHR+Ex) subjected to a single bout of aerobic exercise conducted by treadmill running at 21 m min,1 for 1 h. Age-matched Wistar,Kyoto rats were used as a normotensive control group (WKY). Insulin- and IGF-1-induced vasorelaxant responses in the three groups were evaluated by using isolated aortic rings, with or without endothelial denudation, in organ baths. Possible roles of phosphatidylinositol 3-kinase (PI3K) and nitric oxide synthase (NOS) involved in the NO-dependent vasorelaxation were examined by adding selective inhibitors. The role of superoxide was also clarified by adding superoxide dismutase (SOD). In addition, the endothelium-independent vascular responses to sodium nitroprusside (SNP), a NO donor, were examined. The insulin- and IGF-1-induced vasorelaxation was significantly (P < 0.05) decreased in the SHR group compared with the WKY group. This decreased response in SHR was improved by exercise. These vasorelaxant responses among the three groups became similar after endothelial denudation and pretreatment with the PI3K inhibitor, NOS inhibitor or SOD. Also, no difference among groups was found in the SNP-induced vasorelaxation. We concluded that a single bout of aerobic exercise acutely improves insulin- and IGF-1-mediated vasorelaxation in an endothelium-dependent manner in hypertensive rats. [source]

    Forearm vascular responses to combined muscle metaboreceptor activation in the upper and lower limbs in humans

    Ken Tokizawa
    Our previous studies showed that venous occlusion or passive stretch of the lower limb, assuming a mechanical stimulus, attenuates the vasoconstriction in the non-exercised forearm during postexercise muscle ischaemia (PEMI) of the upper limb. In this study, we investigated whether a metabolic stimulus to the lower limb induces a similar response. Eight subjects performed a 2 min static handgrip exercise at 30% maximal voluntary contraction (MVC) followed by 3 min PEMI of the upper limb, concomitant with or without 2 min static ankle dorsiflexion at 30% MVC followed by 2 min PEMI of the lower limb. During PEMI of the upper limb alone, forearm blood flow (FBF) and forearm vascular conductance (FVC) in the non-exercised arm decreased significantly, whereas during combined PEMI of the upper and lower limbs, the decreases in FBF and FVC produced by PEMI of the upper limb was attenuated. Forearm blood flow and FVC were significantly greater during combined PEMI of the upper and lower limbs than during PEMI of the upper limb alone. When PEMI of the lower limb was released after combined PEMI of the upper and lower limbs (only PEMI of the upper limb was maintained continuously), the attenuated decreases in FBF and FVC observed during combined PEMI of the upper and lower limbs was not observed. Thus, forearm vascular responses differ when muscle metaboreceptors are activated in the upper limb and when there is combined activation of muscle metaboreceptors in both the upper and lower limbs. [source]

    Regional cerebral blood flow responses to hyperventilation during sevoflurane anaesthesia studied with PET

    Background: Arterial carbon dioxide tension (PaCO2) is an important factor controlling cerebral blood flow (CBF) in neurosurgical patients. It is still unclear whether the hypocapnia-induced decrease in CBF is a general effect on the brain or rather linked to specific brain regions. We evaluated the effects of hyperventilation on regional cerebral blood flow (rCBF) in healthy volunteers during sevoflurane anaesthesia measured with positron emission tomography (PET). Methods: Eight human volunteers were anaesthetized with sevoflurane 1 MAC, while exposed to hyperventilation. During 1 MAC sevoflurane at normocapnia and 1 MAC sevoflurane at hypocapnia, one H215O scan was performed. Statistical parametric maps and conventional regions of interest analysis were used for estimating rCBF differences. Results: Cardiovascular parameters were maintained constant over time. During hyperventilation, the mean PaCO2 was decreased from 5.5 ± 0.7 to 3.8 ± 0.9 kPa. Total CBF decreased during the hypocapnic state by 44%. PET revealed wide variations in CBF between regions. The greatest values of vascular responses during hypocapnia were observed in the thalamus, medial occipitotemporal gyrus, cerebellum, precuneus, putamen and insula regions. The lowest values were observed in the superior parietal lobe, middle and inferior frontal gyrus, middle and inferior temporal gyrus and precentral gyrus. No increases in rCBF were observed. Conclusions: This study reports highly localized and specific changes in rCBF during hyperventilation in sevoflurane anaesthesia, with the most pronounced decreases in the sub cortical grey matter. Such regional heterogeneity of the cerebral vascular response should be considered in the assessment of cerebral perfusion reserve during hypocapnia. [source]

    Vascular alterations in the rabbit patellar tendon after surgical incision

    JOURNAL OF ANATOMY, Issue 5 2001
    Open incision of the patellar tendon (PT) is thought to promote acute vascular responses which ultimately result in an enhanced degree of tendon repair. Such a clinical procedure is commonly applied to patients with refractory tendinitis. The objective of this study was to quantify the vascular adaptations (both anatomical and physiological) to longitudinal incision of the PT, and the resultant effects on tendon organisation. Fifty-four New Zealand White rabbits were separated into 3 experimental groups and 2 control groups. Experimental groups underwent surgical incision of the right PT, and were assessed 3 d, 10 d and 42 d following injury; normal unoperated controls were evaluated at time zero, and sham-operated controls were evaluated at 3 d to control for the effects of incising the overlying skin. Quantitative measures of PT blood supply (blood flow, microvascular volume) and geometric properties of PT substance were obtained for each PT. Histomorphology was assessed to evaluate vascular remodelling and matrix organisation in the healing PT. Longitudinal open incision surgery of the PT led to rapid increases in both blood flow and vascular volume. The incision of overlying tissues alone (sham-operated) contributed to this measurable increase, and accounted for 36% and 42% of the elevated blood flow and vascular volume respectively at the 3 d interval. In the incised PT, blood flow significantly increased by 3 d compared with both time zero and sham-operated controls, and remained significantly elevated at the 10 d interval. Similarly, vascular volume of the incised PT increased at 3 d compared both with time zero and sham-operated controls. At the 10 d interval, the increase in vascular volume was greatest in the central PT substance. By 42 d both blood flow and vascular volume of the incised tendon had diminished, with only blood flow remaining significantly different from controls. In the contralateral limb, a significant neurogenically mediated vasodilation was measured in the contralateral PTs at both early time intervals, but was not seen by the later 42 d interval. With respect to PT geometric properties in the experimental animals, a larger PT results as the tendon matrix and blood vessels remodel. PT cross-sectional area increased rapidly by 3 d to 1·3 times control values, and remained significantly elevated at 42 d postinjury. Morphological assessments demonstrated the disruption of matrix organisation by vascular and soft tissue components associated with the longitudinal incisions. Substantial changes in matrix organisation persisted at 42 d after surgery. These findings suggest that open longitudinal incision of the PT increases the vascular supply to deep tendon early after injury. These changes probably arise through both vasomotor and angiogenic activity in the tissue. Since PT blood flow and vascular volume return towards control levels after 6 wk but structural features remain disorganised, we propose that vascular remodelling is more rapid and complete than matrix remodelling after surgical incision of the PT. [source]

    Radiation-induced morphologic changes in the rhesus monkey (Macaca mulatta) brain

    Roger E. Price
    The right cerebral hemisphere of 24 rhesus monkeys scheduled for necropsy at the completion of another project were studied histopathologically 1,30 days after a single dose of 60Co-irradiation. Histopathologically, inflammation and gliosis consistently occurred at specific time points but varied in severity between individuals. Multifocal hemorrhage, edema, and an acute neutrophilic inflammatory response were observed initially whereas perivascular accumulations of lymphocytes were observed in specimens at the end of the study. Microglia/macrophages were most prominent during the first week after irradiation, whereas astrocytes were reactive throughout the observation period. The early clinical manifestations of the central nervous system (CNS), because of brain irradiation in humans, correspond temporally with acute vascular responses, acute and subacute inflammatory cell responses, and subacute demyelination and reactive astrocytic and microglial responses observed in the rhesus monkey. Initial responses of the CNS to gamma-irradiation may have potential implications for the development of radiation-induced late injury of the CNS. [source]

    Morphine, opioids, and the feline pulmonary vascular bed

    A. D. KAYE
    Background: Opioid-induced vasodepressor responses have been reported in a variety of species and laboratory models. The aim of this study was to ascertain the relative potencies of different clinically relevant opioids compared with traditional vasodepressor agents in the feline pulmonary vascular bed. A second aim was to study the effects of morphine and to identify the receptors involved in the mediation or the modulation of these effects. Methods: This was a prospective vehicle-controlled study involving an intact chest preparation of adult mongrel cats. The effects of various opioids, morphine, fentanyl, remifentanil, sufentanil, and meperidine were compared with other vasodepressor agents. Additionally, the effects of l - N5 -(1-iminoethyl) ornithine hydrochloride (l -NIO) (nitric oxide synthase inhibitor), nimesulide [selective cyclooxygenase (COX)-2 inhibitor], glibenclamide (ATP-sensitive K+ channel blocker), naloxone (non-selective opioid receptor antagonist), and diphenhydramine (histamine H1 -receptor antagonist) were investigated on pulmonary arterial responses to morphine and other selected agonists in the feline pulmonary vascular bed. The systemic pressure and lobar arterial perfusion pressure were continuously monitored, electronically averaged, and recorded. Results: In the cat pulmonary vascular bed of the isolated left lower lobe, morphine, remifentanil, fentanyl, sufentanil, and meperidine induced a dose-dependent moderate vasodepressor response and it appeared that sufentanil was the most potent on a nanomolar basis. The effects of morphine were not significantly altered after administration of l -NIO, nimesulide, and glibenclamide. However, the vascular responses to morphine were significantly attenuated following administration of naloxone and diphenhydramine. Conclusion: The results of the present study suggest that sufentanil appears to have slightly more potency and morphine the least of the five opioid agonists studied on a nanomolar basis. Morphine-induced vasodilatory responses appeared to be mediated or modulated by both opioid receptor and histamine-receptor-sensitive pathways. [source]

    Melatonin interactions with blood pressure and vascular function during l -NAME-induced hypertension

    Ludovit Paulis
    Abstract:, The mechanisms responsible for the antihypertensive effect of melatonin are not completely understood. To elucidate the possible role of the nitric oxide (NO) pathway in the hemodynamic actions of melatonin, the effects of this indolamine on vascular function during hypertension induced by the NO-synthase (NOS) inhibitor, N, -nitro- l -arginine-methyl ester (l -NAME) were investigated. Four groups of male adult Wistar rats were employed: control, L-NAME (40 mg/kg), melatonin (10 mg/kg) and l -NAME + melatonin for 5 wks. Systolic and diastolic blood pressure were measured invasively in the carotid artery. Conjugated dienes concentration (an oxidative load marker), NOS RNA expression and its activity and RNA expression of cyclooxygenase-(COX)-1 and COX-2 were determined in the aorta. Acetylcholine-induced responses and their NO-mediated component were evaluated in femoral and mesenteric artery. Moreover, endothelium-derived constricting factor (EDCF)-dependent vasoconstriction and inner diameter were determined in the femoral artery. Chronic l -NAME treatment induced hypertension, elevated the oxidative load and inhibited NOS activity. Moreover, impaired NO-dependent relaxation, augmented EDCF-constriction, increased COX-2 expression and reduced arterial inner diameter were observed. Melatonin added to l -NAME treatment completely prevented elevation of the oxidative load in the aorta. However, melatonin was not able to prevent NOS activity decline, elevation of COX-2 expression or the impairment of vascular responses (except moderate improvement in relaxation of small mesenteric arteries) and it exerted only slight antihypertensive effect. In conclusion, in addition to the reduction of the oxidative load, the restoration of the NO pathway seems to play an important role in the antihypertensive effect of melatonin. [source]