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Peripheral Vasculature (peripheral + vasculature)
Selected AbstractsThe vasodilatory actions of insulin on resistance and terminal arterioles and their impact on muscle glucose uptakeDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 1 2004Lucy H. Clerk Abstract Whether a discrete vascular action of insulin in skeletal muscle integrally participates in insulin-mediated glucose disposal has been extensively examined but remains a contentious issue. Here, we review some of the data both supporting and questioning the role of insulin-mediated increases in limb blood flow in glucose metabolism. We advance the hypothesis that controversy has arisen, at least in part, from a failure to recognize that insulin exerts at least three separate actions on the peripheral vasculature, each with its own characteristic dose and time responsiveness. We summarize how, viewed in this manner, certain points of contention can be resolved. We also advance the hypothesis that an action on the precapillary arteriole may play the dominant role in mediating perfusion-dependent effects of insulin on glucose metabolism in muscle. Copyright © 2003 John Wiley & Sons, Ltd. [source] Disparity between prostate tumor interior versus peripheral vasculature in response to verteporfin-mediated vascular-targeting therapyINTERNATIONAL JOURNAL OF CANCER, Issue 3 2008Bin 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] Highly accelerated first-pass contrast-enhanced magnetic resonance angiography of the peripheral vasculature: Comparison of gadofosveset trisodium with gadopentetate dimeglumine contrast agentsJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 5 2009Jeffrey H. Maki MD Abstract Purpose: To investigate the blood pool agent gadofosveset trisodium for first-pass, dynamic peripheral contrast-enhanced magnetic resonance angiography (pMRA), and compare the results with a conventional gadolinium contrast agent. Materials and Methods: A total of 16 patients were imaged at 1.5T using a prototype peripheral vascular coil with high SENSE acceleration. Five received gadopentetate dimeglumine (,0.25 mmol/kg), and 11 received gadofosveset trisodium (five standard-dose 0.03 mmol/kg, six high-dose 0.05 mmol/kg). Quantitative contrast-enhancement and qualitative image quality evaluation was compared between agents and doses. Results: High-quality diagnostic images were uniformly obtained. The contrast ratio did not significantly differ between gadopentetate dimeglumine and high-dose gadofosveset trisodium, both of which were greater than standard-dose gadofosveset trisodium. High-dose gadofosveset trisodium was equivalent to gadopentetate dimeglumine in image quality and subjective vessel-to-background ratio, but significantly better for depicting small muscular arteries. Standard-dose gadofosveset trisodium showed equivalent image quality and small artery depiction with a slight but significant decrease in vessel-to-background ratio as compared to gadopentatate dimeglumine. Both gadofosveset trisodium doses trended toward more venous enhancement, but this was not a diagnostic problem. Conclusion: First-pass peripheral CE-MRA using gadofosveset trisodium is feasible, yielding image quality comparable to double to triple-dose gadopentetate dimeglumine. Increasing the gadofosveset trisodium dose to 0.05 mmol/kg yields further improvements. J. Magn. Reson. Imaging 2009;30:1085,1092. © 2009 Wiley-Liss, Inc. [source] Microvascular Structure and Function in Salt-Sensitive HypertensionMICROCIRCULATION, Issue 4 2002Dr. Matthew A. Boegehold In many individuals with essential hypertension, dietary salt can further increase blood pressure by augmentation of an already elevated total peripheral resistance. There is little information on the microvascular changes that contribute to salt-sensitive hypertension in humans, but studies in the Dahl salt-sensitive rat have provided some knowledge of the microcirculation in this form of hypertension. These studies, most of which have used intravital microscopy or isolated vessel technology, are the focus of this review. The salt-induced exacerbation of hypertension in Dahl rats is due to a uniform increase in hemodynamic resistance throughout most of the peripheral vasculature. In the spinotrapezius muscle, this resistance increase is largely due to the intense constriction of proximal arterioles. The mechanisms responsible for this increased arteriolar tone include increased responsiveness to oxygen and a loss of tonic nitric oxide (NO) availability caused by reduced endothelial NO production and/or accelerated NO degradation by reactive oxygen species. Within the last decade, it has become increasingly clear that high salt intake can also lead to changes in microvascular structure and function in the absence of increased arterial pressure. This effect must also be considered when evaluating microvascular changes and their functional consequences in salt-sensitive hypertension. [source] 2424: Pulsatile haemodynamics: potential for end-organ damage?ACTA OPHTHALMOLOGICA, Issue 2010C HUDSON Purpose Increases in velocity pulse wave amplitude, or max:min velocity ratio, represent early haemodynamic disturbances associated with diabetic retinopathy (DR) and age-related macular degeneration. This change reflects an increase in vessel wall rigidity that is generally accepted to occur in the central vasculature but the peripheral vasculature is also implicated in this process. This presentation will highlight the implications of these changes in terms of end-organ damage in DR. Methods The sample comprised 4 groups: Group 1: 50 non-diabetic control subjects. Group 2: 56 diabetic patients without clinically visible DR. Group 3: 54 diabetic patients with micro-aneurysms and / or hard exudates within 2 disc diameters of the fovea in the absence of clinically manifest diabetic macular edema (DME). Group 4: 40 patients with clinically manifest DME. The diabetic patients were predominantly type 2. Retinal hemodynamics were assessed in the superior temporal retinal arteriole using the Canon Laser Blood Flowmeter. Intraocular pressure, blood pressure and relevant systemic markers of diabetes control and complications were also assessed. Results The velocity pulse wave amplitude was elevated with increasing risk of DME (p<0.0001). No significant differences were found between the groups with respect to diameter, velocity or flow. Pulse wave amplitude was correlated to age, duration of diabetes, blood pressure, pulse rate, IOP and serum potassium levels. Conclusion The increase in velocity pulse wave amplitude will induce excessive pressure pulsatility in the retinal arterioles and capillaries, changes in vascular function (e.g. loss of vascular regulation) and changes in vessel structure. Commercial interest [source] Renal And Cardiovascular Actions Of 20-Hydroxyeicosatetraenoic Acid And Epoxyeicosatrienoic AcidsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2000Richard J Roman SUMMARY 1. Arachidonic acid (AA) is metabolized by cytochrome P450 (CYP)-dependent pathways to epoxyeicosatrienoic acids (EET) and 20-hydroxyeicosatetraenoic acid (20-HETE) in the kidney and the peripheral vasculature. 2. The present short review summarizes the renal and cardiovascular actions of these important mediators. 3. Epoxyeicosatrienoic acids are vasodilators produced by the endothelium that hyperpolarize vascular smooth muscle (VSM) cells by opening Ca2+ -activated K+ (KCa) channels. 20-Hydroxyeicosatetraenoic acid is a vasoconstrictor that inhibits the opening of KCa channels in VSM cells. Cytochrome P450 4A inhibitors block the myogenic response of small arterioles to elevations in transmural pressure and autoregulation of renal and cerebral blood flow in vivo. Cytochrome P450 4A blockers also attenuate the vasoconstrictor response to elevations in tissue PO2, suggesting that this system may serve as a vascular oxygen sensor. Nitric oxide and carbon monoxide inhibit the formation of 20-HETE and a fall in 20-HETE levels contributes to the activation of KCa channels in VSM cells and the vasodilator response to these gaseous mediators. 20-Hydroxyeicosatetraenoic acid also mediates the inhibitory actions of peptide hormones on sodium transport in the kidney and the mitogenic effects of growth factors in VSM and mesangial cells. A deficiency in the renal production of 20-HETE is associated with the development of hypertension in Dahl salt-sensitive rats. 4. In summary, the available evidence indicates that CYP metabolites of AA play a central role in the regulation of renal, pulmonary and vascular function and that abnormalities in this system may contribute to the pathogenesis of cardiovascular diseases. [source] Homocysteine levels in patients with risk factors for atherosclerosisCLINICAL CARDIOLOGY, Issue 6 2001Arnon Blum M.D. Abstract Background: Abundant epidemiological evidence has demonstrated that the presence of mild to moderate hyperhomocysteinemia is an independent risk factor for atherosclerosis in the coronary, cerebral, and peripheral vasculature, and for vascular disease, including coronary disease. It has been demonstrated that plasma total homocysteine level is a strong predictor of mortality in patients with angiographically confirmed coronary artery disease. Hypothesis: The study was undertaken to determine the extent of homocysteine levels in patients without documented coronary artery disease, but with at least one risk factor for atherosclerosis. Methods: Fasting blood samples were collected prospectively from 160 consecutive patients (50 women and 110 men, mean age 65 ± 7 years) who had at least one risk factor for atherosclerosis, but had no documented coronary artery disease. Homocysteine levels were measured by an immunoassay method. Results: Of the patients studied, 78 (48.75%) with at least one risk factor for atherosclerosis had high homocysteine levels; 62 patients had mild hyperhomocysteinemia (15,30 ,mol/l); and 16 patients had moderate hyperhomocysteinemia (30,100 ,mol/l). Conclusions: Our data suggest that hyperhomocysteinemia is highly prevalent in patients with risk factors for atherosclerosis. Homocysteine level (an independent convertible risk factor to atherosclerosis) should be measured routinely in patients with risk factors for atherosclerosis and treated appropriately. [source] | ||||||||||