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Perfusion Pressure (perfusion + pressure)
Kinds of Perfusion Pressure Selected AbstractsCharacterization of agonist-induced endothelium-dependent vasodilatory responses in the vascular bed of the equine digitJOURNAL OF VETERINARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2008Y. BERHANE The role of endothelium-derived relaxing factors was studied in the regulation of vascular responses in the Krebs perfused equine isolated digit. Perfusion pressure was recorded in response to bolus doses of 5-hydroxytryptamine (6 nmol) alone or co-administered with carbachol (CCh; 0.2 ,mol), bradykinin (BK; 0.2 nmol), substance P (SP; 0.2 nmol) or sodium nitroprusside (SNP; 0.2 ,mol). N, -Nitro- l -Arginine methyl ester hydrochloride (l -NAME; 300 ,m) caused partial but significant inhibition of CCh-induced vasodilatory response, whereas BK and SP-induced responses were resistant to l -NAME. High potassium (K+, 30 mm) and the cytochrome P - 450 (CYP) epoxygenase inhibitor, clotrimazole (10 ,m) plus l -NAME (100 ,m), completely abolished the CCh, BK and SP-induced vasodilatory responses, whereas the response to SNP was unaffected. In contrast, the l -NAME-resistant proportion of CCh, BK and SP-induced vasodilatory response was not inhibited by the highly selective CYP2C9 inhibitor, sulphaphenazole (10 ,m). The cyclo-oxygenase inhibitor, ibuprofen (10 ,m) did not affect the CCh, BK and SP-induced responses. These data demonstrate that CCh, BK and SP-induced relaxation in the equine digit involve a combination of the NO and endothelium-derived hyperpolarizing factor (EDHF) pathways. These results do not support the evidence for the involvement of CYP-derived epoxyeicosatrienoic acids and the exact nature of EDHF in the equine digit remains to be established. [source] Does limb angular motion raise limb arterial pressure?ACTA PHYSIOLOGICA, Issue 3 2009D. D. Sheriff Abstract Aim:, Mechanical factors such as the muscle pump have been proposed to augment flow by several mechanisms. The potential for limb angular motion to augment local perfusion pressure (pressure = ˝,r2,2, where , is the fluid density, r the radius and , the angular velocity) has been overlooked. We sought to test the hypothesis that limb angular motion augments limb arterial pressure. Methods:, Nine human subjects performed horizontal shoulder flexion (,±90° at 0.75 Hz for 30 s). We measured finger arterial pressure (photoplethysmography) in the moving (Trial 1) and non-moving arm (Trial 2) in separate trials along with the pressure (strain gauge) generated at the fingers within a length of water-filled tubing mounted on the moving arm in both trials. Results:, Arm swinging raised (P < 0.05) the mean pressure measured in the tubing by 11 ± 2 and 14 ± 2 mmHg (Trials 1 and 2 respectively). In response to exercise, the rise in mean finger arterial pressure in the swinging limb (18 ± 3 mmHg, Trial 1) exceeded (P < 0.05) the rise in the resting limb (8 ± 2 mmHg, Trial 2) by an amount similar to the 11 mmHg rise in pressure generated in the tubing in Trial 1. Conclusions:, We conclude that the swinging of a limb creates centrifugal force (a biomechanical centrifuge) which imparts additional pressure to the arteries, but not the veins owing to the venous valves, which further widens the arterial,venous pressure difference. [source] Nitric oxide, superoxide and renal blood flow autoregulation in SHR after perinatal L -arginine and antioxidantsACTA PHYSIOLOGICA, Issue 4 2007M. P. Koeners Abstract Aim:, Nitric oxide (NO) and superoxide are considered to be regulatory in renal blood flow (RBF) autoregulation, and hence may contribute to development of hypertension. To extend our previous observations that dynamic NO release is impaired in the spontaneously hypertensive rat (SHR) we investigated, firstly, if superoxide dependency of RBF autoregulation is increased in SHR and, secondly, if the beneficial effect of perinatal supplementation in SHR is partly as a result of early correction of RBF autoregulation. We hypothesized that perinatal supplementation by restoring dynamic NO release and/or decreasing superoxide dependency and would improve life-long blood pressure regulation. Methods:, Autoregulation was studied using stepwise reductions in renal perfusion pressure in anaesthetized male SHR, SHR perinatally supplemented with arginine and antioxidants (SHRsuppl) and Wistar-Kyoto (WKY), prior to and during i.v. N, -nitro- l -arginine (NO synthase inhibitor) or tempol (superoxide dismutase mimetic). Results:, Spontaneously hypertensive rat displayed a wider operating range of RBF autoregulation as compared with WKY (59 ± 4 vs. 33 ± 2 mmHg, respectively; P < 0.01). Perinatal supplementation in SHR decreased mean arterial pressure, renal vascular resistance and the operating range of RBF autoregulation (43 ± 3 mmHg; P < 0.01). In addition autoregulation efficiency decreased. RBF autoregulation characteristics shifted towards those of normotensive WKY. However, dynamic NO release was still impaired and no clear differences in superoxide dependency in RBF autoregulation between groups was observed. Conclusion:, Perinatal supplements shifted RBF autoregulation characteristics of SHR towards WKY, although capacity of the SHRsuppl kidney to modulate NO production to shear stress still seems impaired. The less strictly controlled RBF as observed in perinatally supplemented SHR could result in an improved long-term blood pressure control. This might partly underlie the beneficial effects of perinatal supplementation. [source] TBI or not TBI: that is the question.DIABETIC MEDICINE, Issue 7 2001Is it better to measure toe pressure than ankle pressure in diabetic patients? Abstract Aims Measurement of ankle blood pressure is a simple method of assessing lower limb arterial blood supply. However, its use in diabetes has been questioned due to the presence of medial artery calcification. Measurement of toe blood pressure has been advocated as an alternative but it is technically more difficult. The aim of this study was to obtain information to guide clinicians as to when pressure measurements should be taken at the toe. Methods Ankle brachial index (ABI) and toe brachial index (TBI) were measured by Doppler ultrasound, or photoplethysmography on 174 subjects with diabetes and 53 control subjects. The Bland and Altman method, and the Cohen's method of measuring agreement between two tests were used to compare ABI with TBI. Results The mean differences between ABI and TBI in control and diabetic subjects are 0.40 ± 0.13 and 0.37 ± 0.15, respectively. Nearly all diabetic patients with an ABI <,1.3 have an ABI,TBI gradient falling within the normal range established from the non-diabetic cohort. In contrast, the majority of diabetic subjects with an ABI ,,1.3 have ABI,TBI differences outside this range. When patients are categorized according to ABI and TBI, there is also good agreement between the tests when ABI is low or normal (84% and 78% agreement, respectively), but not when ABI is elevated. Conclusion In the majority of patients with diabetes, assessment of TBI conveys no advantage over ABI in determining perfusion pressure of the lower limbs. Only in those patients with overt calcification, which gives an ABI ,,1.3, are toe pressure measurements superior. This guideline should simplify assessment and treatment of diabetic patients with disease of the lower limbs. Diabet. Med. 18, 528,532 (2001) [source] Noninvasive Assessment of Coronary Flow Reserve in the Left Anterior Descending Artery by Transthoracic Echocardiography before and after StentingECHOCARDIOGRAPHY, Issue 8 2007Elie Chammas M.D., F.E.S.C. Background: Noninvasive assessment of coronary flow reserve in the left anterior descending artery (LAD) by transthoracic Doppler echocardiography (TTDE) has been already validated as a new method for determining the degree of stenosis over the proximal flow. Objectives: The aim of the study is to determine, by TTDE, the feasibility and the value of the coronary flow reserve (CFR) (defined as the maximal increase in coronary blood flow above its basal pressure for a given perfusion pressure when coronary circulation is maximally dilated) in the mid-to-distal LAD before and after percutaneous angioplasty and to demonstrate the early recovery of microvascular tone immediately after stenting. Methods: The study population consisted of 36 patients with significant isolated LAD stenosis (70,90%) identified by coronary angiography. CFR was recorded in the mid-to-distal LAD at rest and during hyperemia obtained after adenosine intravenous infusion before and after stenting. Results: Adequate visualization of the LAD was obtained in 25 out of 36 patients (70%). At rest the mean CFR was 1.5132 ± 0.33 (1.1,2.58). However, after stenting the mean CFR was significantly higher: 2.18 ± 0.55 (1.3,3.8), with P <0.01. Conclusions: CFR can be easily determined by TTE in approximately 70% of patients. Noninvasive Doppler echocardiography shows impaired CFR in patients with LAD disease. After stenting CFR is restored, demonstrating early recovery of microvascular tone. These results are comparable to those published in the same conditions. Larger series with a long-term follow-up may allow identifying patients at high risk for restenosis after stenting. [source] Role of GABAergic neurones in the nucleus tractus solitarii in modulation of cardiovascular activityEXPERIMENTAL PHYSIOLOGY, Issue 9 2010Jasenka Zubcevic GABAergic neurones are interspersed throughout the nucleus tractus solitarii (NTS), and their tonic activity is crucial to the maintenance of cardiorespiratory homeostasis. However, the mechanisms that regulate the magnitiude of GABAergic inhibition in the NTS remain unknown. We hypothesized that the level of GABAergic inhibition is proportionally regulated by the level of excitatory synaptic input to the NTS from baroreceptors. Using the in situ working heart,brainstem preparation in normotensive and spontaneously hypertensive rats, we blocked GABAA receptor-mediated neurotransmission in the NTS with gabazine (a specific GABAA receptor antagonist) at two levels of perfusion pressure (low PP, 60,70 mmHg; and high PP, 105,125 mmHg) while monitoring the immediate changes in cardiorespiratory variables. In normotensive rats, gabazine produced an immediate bradycardia consistent with disinhibition of NTS circuit neurones that regulate heart rate (HR) which was proportional to the level of arterial pressure (,HR at low PP, ,57 ± 9 beats min,1; at high PP, ,177 ± 9 beats min,1; P < 0.001), suggesting that GABAergic circuitry in the NTS modulating heart rate was arterial pressure dependent. In contrast, there was no significant difference in the magnitude of gabazine-induced bradycardia in spontaneously hypertensive rats at low or high PP (,HR at low PP, ,45 ± 10 beats min,1; at high PP, ,58 ± 7 beats min,1). With regard to thoracic sympathetic nerve activity (tSNA), at high PP there was a significant reduction in tSNA during the inspiratory (I) phase of the respiratory cycle, but only in the normotensive rat (,,tSNA =,18.7 ± 10%). At low PP, gabazine caused an elevation of the postinspiration phase of tSNA in both normotensive (,,tSNA = 23.7 ± 2.9%) and hypertensive rats (,,tSNA = 44.2 ± 14%). At low PP, gabazine produced no change in tSNA during the mid-expiration phase in either rat strain, but at high PP we observed a significant reduction in the mid-expiration phase tSNA, but only in the spontaneously hypertensive rat (,,tSNA =,25.2 ± 8%). Gabazine at both low and high PP produced a reduction in the late expiration phase of tSNA in the hypertensive rat (low PP, ,,tSNA =,29.4 ± 4.4%; high PP, ,tSNA =,22.8 ± 3%), whereas in the normotensive rat this was only significant at high PP (,,tSNA =,42.5 ± 6.1%). Therefore, in the spontaneously hypertensive rat, contrary to the GABAA receptor-mediated control of HR, it appears that GABAA receptor-mediated control of tSNA in the NTS is arterial pressure dependent. This study provides new insight into the origin of GABAergic inhibition in NTS circuitry affecting heart rate and sympathetic activity. [source] Regulation of cerebral blood flow in mammals during chronic hypoxia: a matter of balanceEXPERIMENTAL PHYSIOLOGY, Issue 2 2010Philip N. Ainslie Respiratory-induced changes in the partial pressures of arterial carbon dioxide and oxygen play a major role in cerebral blood flow (CBF) regulation. Elevations in (hypercapnia) lead to vasodilatation and increases in CBF, whereas reductions in (hypocapnia) lead to vasoconstriction and decreases in CBF. A fall in (hypoxia) below a certain threshold (<40,45 mmHg) also produces cerebral vasodilatation. Upon initial exposure to hypoxia, CBF is elevated via a greater relative degree of hypoxia compared with hypocapnia. At this point, hypoxia-induced elevations in blood pressure and loss of cerebral autoregulation, stimulation of neuronal pathways, angiogenesis, release of adenosine, endothelium-derived NO and a variety of autocoids and cytokines are additional factors acting to increase CBF. Following 2,3 days, however, the process of ventilatory acclimatization results in a progressive rise in ventilation, which increases and reduces , collectively acting to attenuate the initial rise in CBF. Other factors acting to lower CBF include elevations in haematocrit, sympathetic nerve activity and local and endothelium-derived vasoconstrictors. Hypoxia-induced alterations of cerebrovascular reactivity, autoregulation and pulmonary vascular tone may also affect CBF. Thus, the extent of change in CBF during exposure to hypoxia is dependent on the balance between the myriad of vasodilators and constrictors derived from the endothelium, neuronal innervations and perfusion pressure. This review examines the extent and mechanisms by which hypoxia regulates CBF. Particular focus will be given to the marked influence of hypoxia associated with exposure to high altitude and chronic lung disease. The associated implications of these hypoxia-induced integrative alterations for the regulation of CBF are discussed, and future avenues for research are proposed. [source] The renal effects of alginates isolated from brown seaweed Sargassum vulgareJOURNAL OF APPLIED TOXICOLOGY, Issue 3 2008Alessandra de Paula Alves Sousa Abstract Alginates isolated from Sargassum vulgare, present a strong antitumor activity, associated with kidney reversible damage, as analysed by histopathology of treated animals. In the present study, the renal alteration mechanisms of S. vulgare alginates were investigated using the isolated perfused rat kidney and the isolated perfused rat mesenteric blood vessel methods. The results showed that the effects of Sargassum vulgare low viscosity (SVLV) alginate were more potent than those of Sargassum vulgare high viscosity (SVHV) alginate in the isolated rat kidney. The SVLV alginate caused considerable changes in renal physiology, as shown by an increase in parameters such as perfusion pressure, renal vascular resistance, glomerular filtration rate, urinary flow and sodium, potassium and chloride excretion and by reduction of chloride tubular transport. The effects of SVHV were weaker than those of SVLV. The effects of SVLV on kidney could be related to direct vascular action as demonstrated with SVLV alginate on mesenteric blood vessels. In conclusion, the Sargassum vulgare alginate altered the renal function parameters evaluated. S. vulgare low viscosity alginate renal effects were more potent than S. vulgare high viscosity alginate. It is suggested that physicochemical differences between SVHV and SVLV could explain the differences found in the results. Copyright © 2007 John Wiley & Sons, Ltd. [source] Vasomotion dynamics following calcium spiking depend on both cell signalling and limited constriction velocity in rat mesenteric small arteriesJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 3 2008Ed VanBavel Abstract Vascular smooth muscle cell contraction depends on intracellular calcium. However, calcium-contraction coupling involves a complex array of intracellular processes. Quantitating the dynamical relation between calcium perturbations and resulting changes in tone may help identifying these processes. We hypothesized that in small arteries accurate quantitation can be achieved during rhythmic vasomotion, and questioned whether these dynamics depend on intracellular signalling or physical vasoconstriction. We studied calcium-constriction dynamics in cannulated and pressurized rat mesenteric small arteries (,300 ,m in diameter). Combined application of tetra-ethyl ammonium (TEA) and BayK8644 induced rhythmicity, consisting of regular and irregular calcium spiking and superposition of spikes. Calcium spikes induced delayed vasomotion cycles. Their dynamic relation could be fitted by a linear second-order model. The dirac impulse response of this model had an amplitude that was strongly reduced with increasing perfusion pressure between 17 and 98 mmHg, while time to peak and relaxation time were the largest at an intermediate pressure (57 mmHg: respectively 0.9 and 2.3 sec). To address to what extent these dynamics reside in intracellular signalling or vasoconstriction, we applied rhythmic increases in pressure counteracting the vasoconstriction. This revealed that calcium-activation coupling became faster when vasoconstriction was counteracted. During such compensation, a calcium impulse response remained that lasted 0.5 sec to peak activation, followed by a 1.0 sec relaxation time, attributable to signalling dynamics. In conclusion, this study demonstrates the feasibility of quantitating calcium-activation dynamics in vasomoting small arteries. These dynamics relate to both intracellular sig-nalling and actual vasoconstriction. Performing such analyses during pharmacological intervention and in genetic models provides a tool for unravelling calcium-contraction coupling in small arteries. [source] Improved myocardial perfusion in chronic diabetic mice by the up-regulation of pLKB1 and AMPK signalingJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 5 2010Claudia Kusmic Abstract Previous studies related impaired myocardial microcirculation in diabetes to oxidative stress and endothelial dysfunction. Thus, this study was aimed to determine the effect of up-regulating pAMPK-pAKT signaling on coronary microvascular reactivity in the isolated heart of diabetic mice. We measured coronary resistance in wild-type and streptozotocin (STZ)-treated mice, during perfusion pressure changes. Glucose, insulin, and adiponectin levels in plasma and superoxide formation, NOx levels and heme oxygenase (HO) activity in myocardial tissue were determined. In addition, the expression of HO-1, 3-nitrotyrosine, pLKB1, pAMPK, pAKT, and peNOS proteins in control and diabetic hearts were measured. Coronary response to changes in perfusion pressure diverged from control in a time-dependent manner following STZ administration. The responses observed at 28 weeks of diabetes (the maximum time examined) were mimicked by L-NAME administration to control animals and were associated with a decrease in serum adiponectin and myocardial pLKB1, pAMPK, pAKT, and pGSK-3 expression. Cobalt protoporphyrin treatment to induce HO-1 expression reversed the microvascular reactivity seen in diabetes towards that of controls. Up-regulation of HO-1 was associated with an increase in adiponectin, pLKB1, pAKT, pAMPK, pGSK-3, and peNOS levels and a decrease in myocardial superoxide and 3-nitrotyrosine levels. In the present study we describe the time course of microvascular functional changes during the development of diabetes and the existence of a unique relationship between the levels of serum adiponectin, pLKB1, pAKT, and pAMPK activation in diabetic hearts. The restoration of microvascular function suggests a new therapeutic approach to even advanced cardiac microvascular derangement in diabetes. J. Cell. Biochem. 109: 1033,1044, 2010. © 2010 Wiley-Liss, Inc. [source] Simvastatin effects on portal-systemic collaterals of portal hypertensive ratsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 8 2010Hui-Chun Huang Abstract Background and Aim:, Portal-systemic collateral vascular resistance and vasoconstrictor responsiveness are crucial in portal hypertension and variceal bleeding control. Statins enhance vasodilators production, but their influence on collaterals is unknown. This study aimed to survey the effect of simvastatin on collaterals. Methods:, Partially portal vein-ligated rats received oral simvastatin (20 mg/kg/day) or distilled water from ,2 to +7 day of ligation. After hemodynamic measurements on the eighth postoperative day, baseline perfusion pressure (i.e. an index of collateral vascular resistance) and arginine vasopressin (AVP, 0.1 nM,0.1 µM) responsiveness were evaluated with an in situ perfusion model for collateral vascular beds. RT-PCR of endothelial NO synthase (eNOS), inducible NOS (iNOS), cyclooxygenase-1 (COX-1), COX-2, thromboxane A2 synthase (TXA2 -S) and prostacyclin synthase genes was performed in parallel groups for splenorenal shunt (SRS), the most prominent intra-abdominal collateral vessel. To determine the acute effects of simvastatin, collateral AVP response was assessed with vehicle or simvastatin. SRS RT-PCR of eNOS, iNOS, COX-1, COX-2 and TXA2 -S, and measurements of perfusate nitrite/nitrate, 6-keto-PGF1, and TXB2 levels were performed in parallel groups without AVP. Results:, Acute simvastatin administration enhanced SRS eNOS expression and elevated perfusate nitrite/nitrate and 6-keto-PGF1, concentrations. Chronic simvastatin treatment reduced baseline collateral vascular resistance and portal pressure and enhanced SRS eNOS, COX-2 and TXA2 -S mRNA expression. Neither acute nor chronic simvastatin administration influenced collateral AVP responsiveness. Conclusion:, Simvastatin reduces portal-systemic collateral vascular resistance and portal pressure in portal hypertensive rats. This may be related to the enhanced portal-systemic collateral vascular NO and prostacyclin activities. [source] Portal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B2 -type receptorsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 1 2001MaurÍcio R Loureiro-Silva Abstract Background: We have shown that the portal hypertensive response to bradykinin in normal rats is mediated by B2 receptors. Methods: By using isolated and exsanguinated rat liver perfusion, we studied the portal hypertensive response to bradykinin or des-Arg9 -bradykinin (B1 agonist) in inflamed or cirrhotic rat livers. Livers were perfused with bovine serum albumin Krebs,Henseleit buffer (pH 7.4; 37°C) at a constant flow rate, in the absence or presence of des-Arg9[Leu8]-bradykinin or HOE 140 (B1 and B2 receptor antagonists, respectively). Bradykinin (140 nmol) or des-Arg9 -bradykinin was injected as a bolus via the afferent route to the liver. Results: Basal perfusion pressure in liver-cirrhotic rats was higher than in normal rats. In normal, inflamed, or liver-cirrhotic rats, the presence of the B1 antagonist did not change the portal hypertensive response to bradykinin, while the B2 antagonist abolished this response. A 140-nmol dose of des-Arg9 -bradykinin did not change the perfusion pressure; 700 nmol of this B1 agonist produced an insignificant perfusion pressure increase. The perfusion pressure increase induced by bradykinin in cirrhotic livers was lower than in normal livers. Conclusions: The portal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B2 receptors, but not B1 receptors, and there is a contracting hyporeactivity to bradykinin in cirrhotic rat livers. [source] Morphine, opioids, and the feline pulmonary vascular bedACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2008A. 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] Remifentanil and the brainACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2008V. FODALE Background and aim: Remifentanil is an ultra-short-acting opioid, increasingly used today in neuroanesthesia and neurointensive care. Its characteristics make remifentanil a potentially ideal agent, but previous data have cast a shadow on this opioid, supporting potentially toxic effects on the ischemic brain. The aim of the present concise review is to survey available up-to-date information on the effects of remifentanil on the central nervous system. Method: A MEDLINE search within the past seven years for available up-to-date information on remifentanil and brain was performed. Results: Concise up-to-date information on the effects of remifentanil on the central nervous system was reported, with a particular emphasis on the following topics: cerebral metabolism, electroencephalogram, electrocorticography, motor-evoked potentials, regional cerebral blood flow, cerebral blood flow velocity, arterial hypotension and hypertension, intracranial pressure, cerebral perfusion pressure, cerebral autoregulation, cerebrovascular CO2 reactivity, cerebrospinal fluid, painful stimulation, analgesia and hyperalgesia, neuroprotection, neurotoxicity and hypothermia. Conclusion: The knowledge of the influence of remifentanil on brain functions is crucial before routine use in neuroanesthesia to improve anesthesia performance and patient safety as well as outcome. [source] Brain damage following severe acute normovolemic hemodilution in combination with controlled hypotension in ratsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2007Y. L. Ge Background and aim:, The reduced oxygen content and perfusion pressure during acute normovolemic hemodilution (ANH) and controlled hypotension (CH) raise concerns about hypoperfusion and ischemic injury to the brain. In this study on rats, we examined the brain damage following four different degrees of ANH combined with CH. Methods:, Forty rats were randomly assigned to receive a sham operation or CH and ANH [with a hematocrit (Hct) of 30, 25, 20 or 15%]. ANH was performed after baseline physiological parameters had been monitored for 20 min; 30 min later, CH was induced using sodium nitroprusside, and the mean arterial blood pressure was maintained at 50,60 mmHg for 1 h. Rats were killed 3.5 h after hemodilution. Ultrastructural alterations in the CA1 region of the rat hippocampus were observed, and serum concentrations of S100B and neuron-specific enolase (NSE) were measured before and after ANH. Results:, The serum S100B concentration increased significantly in the Hct 20% + CH and Hct 15% + CH groups. However, there were no significant differences in the serum levels of NSE between the groups. In the CA1 region of the rat hippocampus, marked ultrastructural alterations, such as mitochondrial denaturalization and nucleus distortion, were observed in the Hct 20% + CH and Hct 15% + CH groups. Conclusion:, Severe ANH (Hct , 20%) combined with CH may induce cerebral damage, as confirmed by marked ultrastructural alterations in the CA1 region of the rat hippocampus and significantly increased serum levels of S100B, and should be avoided. [source] Application of intensive care medicine principles in the management of the acute liver failure patientLIVER TRANSPLANTATION, Issue S2 2008David J. Kramer Key Points 1Acute liver failure is a paradigm for multiple system organ failure that develops as a consequence of sepsis. 2In the United States, systemic inflammatory response, sepsis, and septic shock are common reasons for intensive care unit admission. Intensive care management of these patients serves as a template for the management of patients with acute liver failure. 3Acute liver failure is attended by high mortality. Although intensive care results in improved survival, the key treatment is liver transplantation. Intensive care unit intervention may open a "window of opportunity" and enable successful liver transplantation in patients who are too ill at presentation. 4Intracranial hypertension complicates the course for many patients with acute liver failure. Initially, intracranial hypertension results from hyperemia, which is cerebral edema that reduces cerebral blood flow and eventuates in herniation. The precepts of neurocritical care,monitoring cerebral perfusion pressure, cerebral blood flow, and cortical activity,with rapid response to hemodynamic abnormalities, maintenance of normoxia, euglycemia, control of seizures, therapeutic hypothermia, osmotic therapy, and judicious hyperventilation are key to reducing mortality attributable to neurologic failure. Liver Transpl 14:S85,S89, 2008. © 2008 AASLD. [source] Fluid resuscitation from severe hemorrhagic shock using diaspirin cross-linked hemoglobin fails to improve pancreatic and renal perfusionACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2004A. Pape Background:, Fluid resuscitation from hemorrhagic shock is intended to abolish microcirculatory disorders and to restore adequate tissue oxygenation. Diaspirin cross-linked hemoglobin (DCLHb) is a hemoglobin-based oxygen carrier (HBOC) with vasoconstrictive properties. Therefore, fluid resuscitation from severe hemorrhagic shock using DCLHb was expected to improve perfusion pressure and tissue perfusion of kidneys and pancreas. Methods:, In 20 anesthetized domestic pigs with an experimentally induced coronary stenosis, shock (mean arterial pressure 45 mmHg) was induced by controlled withdrawal of blood and maintained for 60 min. Fluid resuscitation (replacement of the plasma volume withdrawn during hemorrhage) was performed with either 10% DCLHb (DCLHb group, n = 10) or 8% human serum albumin (HSA) oncotically matched to DCLHb (HSA group, n = 10). Completion of resuscitation was followed by a 60-min observation period. Regional blood flow to the kidneys and the pancreas was measured by use of the radioactive microspheres method at baseline, after shock and 60 min after fluid resuscitation. Results:, All animals (10/10) resuscitated with DCLHb survived the 60-min observation period, while 5/10 control animals died within 20 min due to persisting subendocardial ischemia. In contrast to HSA survivors, pancreas and kidneys of DCLHb-treated animals revealed lower total and regional organ perfusion and regional oxygen delivery. Renal and pancreatic blood flow heterogeneity was higher in the DCLHb group. Conclusion:, DCLHb-induced vasoconstriction afforded superior myocardial perfusion, but impaired regional perfusion of the kidneys and the pancreas. [source] Ephedrine in the cat lung vasculatureACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2003A. M. Fields Background:, Ephedrine is one of the most commonly used non-catecholamine sympathomimetic agents. It is used in operating rooms and critical care settings worldwide. While it has many side effects, its ability to rapidly raise blood pressure makes it an ideal agent to maintain homeostasis as well as in emergency situations. While its effects are known to be mediated by an ,-mediated mechanism, the exact , subtype is unknown. In addition, no studies using ephedrine have been performed in the pulmonary vascular bed of the cat. Methods:, The effects of phentolamine, a non-selective ,-receptor blocker, and prazosin, an ,1 -selective antagonist, were investigated on pulmonary arterial responses to ephedrine, phenylepherine, norepinephrine, and U-46619. Lobar arterial perfusion pressure was continuously monitored, electronically averaged, and recorded with constant flow in the isolated left lower lobe vascular bed of the cat. Results:, Phentolamine and prazosin significantly reduced vasoconstrictor pulmonary perfusion pressure increases induced by ephedrine. Conclusion:, Ephedrine has significant vasopressor activity in the pulmonary vascular bed of the cat meditated predominantly by ,1 adrenergic receptor activation. [source] Does dopexamine influence regional vascular tone and oxygenation during intestinal hypotension?ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2002S. Lehtipalo Background: Local effects of dopexamine on intestinal vascular tone and oxygenation were investigated during intestinal hypotension. To this end, we employed an experimental model, in which the superior mesenteric arterial pressure (PSMA) was controlled by an adjustable perivascular clamp. This approach enabled us to keep the intestinal perfusion pressure (IPP) constant in the face of any systemic circulatory alterations. Methods: In 11 barbiturate-anesthetized pigs, we instrumented the superior mesenteric circulation for assessments of vascular resistance (RMES), IPP, jejunal mucosal perfusion (Laser Doppler) and intestinal tissue oxygenation (microoximetry). Measurements were carried out before and during dopexamine infusions (0.5 and 1.0 µg·kg,1·min,1) at a freely variable PSMA (i.e. the perivascular clamp fully open) and at a PSMA of 50 mmHg and 30 mmHg. Results: At a constant PSMA of 50 mmHg, dopexamine had no significant intestinal vascular effects. However, at a constant PSMA of 30 mmHg, both doses of dopexamine were associated with decreases in RMES. Effects of dopexamine on intestinal oxygen delivery and extraction were minimal during these procedures, while a minor decrease in intestinal tissue oxygen tension was observed during dopexamine administration at the lowest IPP level. Conclusion: At very low intestinal perfusion pressures (approximately 30 mmHg) dopexamine produces intestinal vasodilation in excess of what is produced by intrinsic autoregulation. This suggests that there is a vasodilatory reserve in the intestine under such conditions and that a pharmacological vasodilator like dopexamine may improve intestinal circulation during regional severe hypotension. [source] Neurological outcome after experimental cardiopulmonary resuscitation: a result of delayed and potentially treatable neuronal injury?ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2002X. L. Liu Background: In experimental cardiopulmonary resuscitation (CPR) aortic balloon occlusion, vasopressin, and hypertonic saline dextran administration improve cerebral blood flow. Free radical scavenger ,-phenyl-N-tert-butyl-nitrone (PBN) and cyclosporine-A (CsA) alleviate neuronal damage after global ischemia. Combining these treatments, we investigated neurological outcome after experimental cardiac arrest. Methods: Thirty anesthetized piglets, randomly allocated into three groups, were subjected to 8 min of ventricular fibrillation followed by 5 min of closed-chest CPR. The combined treatment (CT) group received all the above-mentioned modalities; group B was treated with balloon occlusion and epinephrine; and group C had sham balloon occlusion with epinephrine. Indicators of oxidative stress (8-iso-PGF2,), inflammation (15-keto-dihydro-PGF2,), energy crisis (hypoxanthine and xanthine), and anoxia/hypoxia (lactate) were monitored in jugular bulb venous blood. Neurological outcome was evaluated 24 h after CPR. Results: Restoration of spontaneous circulation (ROSC) was more rapidly achieved and neurological outcome was significantly better in the CT group, although there was no difference in coronary perfusion pressure between groups. The jugular venous PCO2 and cerebral oxygen extraction ratio were lower in the CT group at 5,15 min after ROSC. Jugular venous 8-iso-PGF2, and hypoxanthine after ROSC were correlated to 24 h neurological outcome Conclusions: A combination of cerebral blood flow promoting measures and administration of ,-phenyl-N-tert-butyl-nitrone and cyclosporine-A improved 24 h neurological outcome after 8 min of experimental normothermic cardiac arrest, indicating an ongoing neuronal injury in the reperfusion phase. [source] Renal impairment in deoxycorticosterone acetate-salt hypertensive ratsNEPHROLOGY, Issue 4 2000Catherine Dallemagne Summary: This study has compared renal function in deoxycorticosterone (DOCA)-salt hypertensive Wistar rats (uninephrectomy followed by administration of DOCA 25 mg subcutaneously every fourth day and 1% NaCl in the drinking water) with various control rats using the isolated perfused kidney preparation. The systolic blood pressure of DOCA-salt hypertensive rats was 180 ± 10 mmHg (uninephrectomy controls: 136 ± 9 mmHg) while normalization of calcium intake (DOCA-Ca rats, 1% CaCl2 in water) attenuated this increase (systolic blood pressure, 146 ± 5 mmHg). Renal mass corrected for body weight increased by 25% after uninephrectomy, 55% in uninephrectomized rats given NaCl, 152% in DOCA-salt rats and 147% in DOCA-Ca rats. At a renal perfusion pressure of 135 mmHg, isolated perfused kidneys from DOCA-salt rats showed decreases of 48% in glomerular filtration rate and 69% in sodium excretion with an increase of 44% in renal vascular resistance compared with uninephrectomized rats. There were no significant differences in renal function between DOCA-salt and DOCA-Ca rats. Histological assessment of renal pathology showed proximal tubular hypertrophy and hyperplasia, marked focal distal tubular atrophy, interstitial fibrosis and glomerular hypercellularity in DOCA rats compared with UNX rats. Lesions were less obvious in UNX-salt or DOCA-Ca rats. The lack of direct correlation between alterations in function and pathology may be explained by the compensatory effect of remaining healthy or hypertrophied nephrons. Thus, the DOCA-salt model of hypertension in rats is associated with marked structural kidney damage and severely decreased kidney function. Marked attenuation of systemic hypertension by normalizing calcium intake in DOCA-salt rats did not prevent impairment of kidney function. [source] Management of critically ill children with traumatic brain injuryPEDIATRIC ANESTHESIA, Issue 6 2008GILLES A. ORLIAGUET MD PhD Summary The management of critically ill children with traumatic brain injury (TBI) requires a precise assessment of the brain lesions but also of potentially associated extra-cranial injuries. Children with severe TBI should be treated in a pediatric trauma center, if possible. Initial assessment relies mainly upon clinical examination, trans-cranial Doppler ultrasonography and body CT scan. Neurosurgical operations are rarely necessary in these patients, except in the case of a compressive subdural or epidural hematoma. On the other hand, one of the major goals of resuscitation in these children is aimed at protecting against secondary brain insults (SBI). SBI are mainly because of systemic hypotension, hypoxia, hypercarbia, anemia and hyperglycemia. Cerebral perfusion pressure (CPP = mean arterial blood pressure , intracranial pressure: ICP) should be monitored and optimized as soon as possible, taking into account age-related differences in optimal CPP goals. Different general maneuvers must be applied in these patients early during their treatment (control of fever, avoidance of jugular venous outflow obstruction, maintenance of adequate arterial oxygenation, normocarbia, sedation,analgesia and normovolemia). In the case of increased ICP and/or decreased CPP, first-tier ICP-specific treatments may be implemented, including cerebrospinal fluid drainage, if possible, osmotic therapy and moderate hyperventilation. In the case of refractory intracranial hypertension, second-tier therapy (profound hyperventilation with PaCO2 < 35 mmHg, high-dose barbiturates, moderate hypothermia, decompressive craniectomy) may be introduced, after a new cerebral CT scan. [source] Ex vivo hypothermic recirculatory adenoviral gene transfer to the transplanted pig heartTHE JOURNAL OF GENE MEDICINE, Issue 7 2006Keiji Oi Abstract Background To facilitate the application of adenoviral gene therapy in clinical heart transplantation, we developed an ex vivo hypothermic recirculatory adenoviral gene transfer method to the transplanted pig heart. Methods Experimental animals were assigned into three groups; controls, 1 × 108 plaque-forming units (pfu)/ml group and 1 × 109 pfu/ml group. During the 30 min gene transfer perfusion, 200 ml of University of Wisconsin solution containing the adenoviral vector was recirculated through the coronary vessels. The myocardial temperature was maintained below 4 °C and the perfusion pressure was adjusted at 50 mmHg. Results Cardiac myocyte transduction efficiencies in the 1 × 108 pfu/ml group were 0.04% and 0.07%, whereas transduction efficiencies in the 1 × 109 pfu/ml group were widely distributed from 0.45% to 22.62%. The gene transduction efficiency increased with the virus titer. Additionally, no difference in the transduction efficiency was observed between different segments of the left ventricle. The current gene transfer method at 1 × 109 pfu/ml of adenovirus titer enabled homogeneous gene transduction into the transplanted pig heart up to a maximum of 22.62%. Conclusions This model can be applied to a large isolated heart and will greatly facilitate the investigation of gene therapy in large animal models of heart transplantation. Copyright © 2006 John Wiley & Sons, Ltd. [source] Autoregulation of the cerebral circulation during sleep in newborn lambsTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Daniel A. Grant Autoregulation is a vital protective mechanism that maintains stable cerebral blood flow as cerebral perfusion pressure changes. We contrasted cerebral autoregulation across sleep,wake states, as little is known about its effectiveness during sleep. Newborn lambs (n= 9) were instrumented to measure cerebral blood flow (flow probe on the superior sagittal sinus) and cerebral perfusion pressure, then studied during active sleep (AS), quiet sleep (QS) and quiet wakefulness (QW). We generated cerebral autoregulation curves by inflating an occluder cuff around the brachiocephalic artery thereby lowering cerebral perfusion pressure. Baseline cerebral blood flow was higher (P < 0.05) and cerebral vascular resistance lower (P < 0.05) in AS than in QW (76 ± 8% and 133 ± 15%, respectively, of the AS value, mean ±s.d.) and in QS (66 ± 11% and 158 ± 30%). The autoregulation curve in AS differed from that in QS and QW in three key respects: firstly, the plateau was elevated relative to QS and QW (P < 0.05); secondly, the lower limit of the curve (breakpoint) was higher (P < 0.05) in AS (50 mmHg) than QS (45 mmHg); and thirdly, the slope of the descending limb below the breakpoint was greater (P < 0.05) in AS than QS (56% of AS) or QW (56% of AS). Although autoregulation functions in AS, the higher breakpoint and greater slope of the descending limb may place the brain at risk for vascular compromise should hypotension occur. [source] Pressures within air-filled tracheal cuffs at altitude , an in vivo studyANAESTHESIA, Issue 3 2004J. Henning Summary Aeromedical transport of mechanically ventilated critically ill patients is now a frequent occurrence. However, the performance of the air filled tracheal tube cuff at altitude has not been studied in vivo. We measured the tracheal cuff pressures at ground level and at 3000 ft, in 10 intubated patients. With air providing the seal in the cuff the mean rise in cuff pressure was 23 cmH2O, which took the pressures above the critical perfusion pressure of the tracheal mucosa. This could lead to tracheal injury. [source] Perfusate Lactate Dehydrogenase Level and Intrarenal Resistance Could Not Be Adequate Markers of Perfusion Quality During Isolated Kidney PerfusionARTIFICIAL ORGANS, Issue 11 2000Berta Herrera Abstract: The main goal of this work was to study the influence of perfusion pressure and flow waveform during kidney perfusion, and the relationship between renal vascular resistance (RVR) and lactate dehydrogenase (LDH) concentration in the perfusate. Simultaneous constant pressure kidney perfusions were performed with either pulsatile or continuous flow at either 30 or 80 mm Hg of constant perfusion pressure. Mean flow, pressure, and RVR were displayed online during perfusion. Perfusate samples for LDH, creatine phosphatase kinase (CPK), and alkaline phosphatase (AP) determinations were taken. At the end of the perfusion, 2 ml of Evans blue was injected into the circuit to obtain images of perfusate distribution, and the kidneys were weighed. Also, hematoxylin/eosine studies were performed, showing more Bowman's space and tubular dilation in kidneys perfused with high pressure. We did not find differences in RVR between kidneys perfused at 30 and 80 mm Hg; nevertheless, perfusate distribution was better in the 80 mm Hg perfusions. We did not find any correlation between enzyme release and RVR in kidneys perfused with different mean pressures. These findings suggest that vascular resistance and LDH concentration cannot be independently considered as adequate markers of perfusate distribution. [source] Comparative Study of Bioartificial Liver Support and Plasma Exchange for Treatment of Pigs with Fulminant Hepatic FailureARTIFICIAL ORGANS, Issue 4 2000Yukio Kamohara Abstract: Recently, bioartificial liver (BAL) treatment was reported to provide beneficial effects for patients with fulminant hepatic failure (FHF). Some success in experimental or clinical trials has been reported; however, the evaluation of BAL efficacy remains unclear, especially in comparison with other treatments for FHF. The purpose of this study was to compare the efficacy between BAL and plasma exchange (PE) in experimentally induced FHF in pigs. Pigs undergoing hepatic devascularization (HD) were placed into the following groups: no treatment (control; n = 6), BAL treatment (BAL; n = 5), and plasma exchange (PE; n = 5). Each treatment was initiated 6 h after HD and lasted for 4 h. BAL treatment significantly improved liver functions in FHF pigs. The decrease in cerebral perfusion pressure was also significantly suppressed in the pigs with BAL, and their survival time was prolonged compared with the results in pigs with PE. The effects of BAL outperform those of PE in the treatment of experimental FHF model. [source] ,1A -Adrenoceptors predominate in the control of blood pressure in mouse mesenteric vascular bedAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 3 2007S. G. Martínez-Salas Summary 1,The pressor action of the ,1A -adrenoceptor agonist, A61603 (N -[5-(4,5-dihydro-1H -imidazol-2-yl)-2-hydroxy-5,6,7,8-tetrahydronaphthalen-1-yl] methanesulfonamide) or the ,1 -adrenoceptor agonist phenylephrine, and their blockade by selective ,1 -adrenoceptor antagonists in the mouse isolated mesenteric vascular bed were evaluated. 2,A61603 showed a , 235-fold higher potency in elevating perfusion pressure in mesenteric bed compared to phenylephrine. 3,The ,1A -adrenoceptor selective antagonist RS 100329 (5-methyl-3-[3-[4-[2-(2,2,2,-trifluoroethoxy) phenyl]-1-piperazinyl] propyl]-2,4-(1H)-pyrimidinedione), displaced with high affinity agonist concentration,response curves to the right in a concentration-dependent manner. 4,The ,1D -adrenoceptor selective antagonist BMY 7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5] decane-7,9-dione), did not displace A61603 nor did it block the phenylephrine-induced pressor response. 5,The ,1B/D -adrenoceptor alkylating antagonist chloroethylclonidine (CEC), caused a rightward shift of the phenylephrine concentration,response curve and reduced its maximum response; however, CEC only slightly modified A61603 evoked contraction. 6,The results indicate that the isolated mouse mesenteric vascular bed expresses ,1A -adrenoceptors and suggest a very discrete role for 1B -adrenoceptors. [source] Functional alterations of mesenteric vascular bed, vas deferens and intestinal tracts in a rat hindlimb unloading model of microgravityAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2004G. De Salvatore Summary 1 Prolonged bed rest or exposure to microgravity may cause several alterations in autonomic nervous system response (ANSR). 2 Hindlimb unloading (HU) rats were used as an animal model of simulated microgravity to investigate ANSR changes. The experiments were carried out to investigate the effects of simulated microgravity on the autonomic nervous response of the perfused mesenteric vascular bed (MVB), vas deferens and the colon and duodenum from 2-week HU rats. 3 In MVB preparations of HU rats, the frequency-dependent increases in perfusion pressure with perivascular nerve stimulation (PNS; 8,40 Hz) were inhibited, whereas the noradrenaline (NA) concentration-dependent (1,100 ,m) perfusion pressure increases were potentiated. The latter most probably reflected up-regulation of , -adrenergic receptor function. Relaxant responses of NA-precontracted MVB to PNS (4,30 Hz) or isoprenaline were not different between control and HU preparations, while vasodilation induced by the endothelial agonist ACh was reduced. 4 Transmural stimulation (2,40 Hz) induced frequency-dependent twitches of the vas deferens which were reduced in vas deferens of HU rats, while the sensitivity to NA-induced contraction was significantly increased. 5 In the gastroenteric system of HU rat, direct contractile responses to carbachol or tachykinin as well as relaxant or contractile responses to nervous stimulation appeared unchanged both in the proximal colon rings and in duodenal longitudinal strips. 6 In conclusion, HU treatment affects peripheral tissues in which the main contractile mediators are the adrenergic ones such as resistance vessels and vas deferens, probably by reducing the release of neuromediator. This study validates NA signalling impairment as a widespread process in microgravity, which may most dramatically result in the clinical phenotype of orthostatic intolerance. [source] Re: Association of cerebral perfusion pressure with headache in women with pre-eclampsiaBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 1 2001Karel Mar No abstract is available for this article. [source] | ||||||||||||||||||||||||||||