| |||
Blood Flow Regulation (blood + flow_regulation)
Selected AbstractsThe Receptors and Role of Angiotensin II in Knee Joint Blood Flow Regulation and Role of Nitric Oxide in Modulation of Their FunctionMICROCIRCULATION, Issue 5 2003H. NAJAFIPOUR ABSTRACT Objectives: Angiotensin-converting enzyme (ACE) upregulation in the stroma cells of arthritis rheumatoid joints may produce a higher tissue concentration of angiotensin II (angII), which is a vasoconstrictor and mitogen factor that causes local hypoxia and synovial proliferation. No study in the literature has examined the role of angII in joint blood flow (JBF) regulation and the potential effect of ACE inhibitors on JBF. Methods: The study was performed on 20 Dutch white rabbits to examine the JBF response to angII, angII receptor subtypes, and the role of nitric oxide (NO) in angII effects in knee joint blood vessels. Drugs were administered locally through retrograde saphenous artery cannulation. Joint vascular resistance (JVR) was calculated by dividing the arterial blood pressure by the JBF. Results: AngII increased JVR dose dependently. The angII type 1 (AT1) receptor antagonist losartan did not change the basal JVR but completely blocked the effect of angII on JVR. N, -nitro-L-arginin methyl ester (L-NAME) increased JVR by a mean (±SEM) of 25.8 ± 8.7% (p < 0.05) but did not affect the joint vessel response to angII and losartan. Conclusions: AngII receptors are from the AT1 subtype in normal joint blood vessels, but angII plays no significant role in JBF regulation. The basal release of NO plays a role in resting JBF regulation, but NO does not affect the AT1 receptor-mediated vasoconstriction of joint blood vessels. [source] Negative impact of systemic catecholamine administration on hepatic blood perfusion after porcine liver transplantationLIVER TRANSPLANTATION, Issue 2 2005Arianeb Mehrabi Catecholamines are often administered during and after liver transplantation (LTx) to support systemic perfusion and to increase organ oxygen supply. Some vasoactive agents can compromise visceral organ perfusion. We followed the hypothesis that the vasculature of transplanted livers presents with a higher sensitivity, which leads to an increased vulnerability for flow derangement after application of epinephrine (Epi) or norepinephrine (NorEpi). Hepatic macroperfusion and microperfusion during systemic Epi or NorEpi infusion were measured by Doppler flow and thermodiffusion probes in porcine native, denervated, and transplanted livers (n = 16 in each group). Epi or NorEpi were infused (n = 8 in each subgroup) in predefined dosages (low dose = 5 ,g/kg/minute and high dose = 10 ,g/kg/minute) over 240 minutes. Systemic cardiocirculatory parameters were monitored continuously. Hepatic perfusion data were compared between all groups at comparable time points and dosages. In all native, denervated, and transplanted liver groups, Epi and NorEpi induced an inconsistent rise of mean arterial pressure and heart rate shortly after onset of infusion in both dosages compared with baseline. No significant differences of cardiovascular parameters at comparable time points were observed. In native livers, Epi and NorEpi induced only temporary alterations of hepatic macrocirculation and microcirculation, which returned to baseline 2 hours after onset of infusion. No significant alterations of hepatic blood flow were detected after isolated surgical denervation of the liver. By contrast, transplanted livers showed a progressive decline of hepatic macrocirculation (33,75% reduction) and microcirculation (39,58% reduction) during catecholamine infusions in a dose-dependent fashion. Characteristics of liver blood flow impairment were comparable for both vasoactive agents. In conclusion, pronounced disturbances of hepatic macrocirculation and microcirculation were observed during systemic Epi and NorEpi infusion after LTx compared with native and denervated livers. Microcirculation disturbances after LTx might be explained by impairment of hepatic blood flow regulation caused by an increased sensitivity of hepatic vasculature after ischemia-reperfusion and by lengthening of vasopressor effects caused by reduced hepatocyte metabolism. Clinicians should be aware of this potentially hazardous effect. Therefore, application of catecholamines after clinical LTx should be indicated carefully. (Liver Transpl 2005;11:174,187.) [source] 2422: Ocular blood flow in diabetesACTA OPHTHALMOLOGICA, Issue 2010G GARHOFER Diabetes is among the most prominent reasons for developing blindness in industrialized nations. In the recent years there is cumulating evidence that a dysfunctional ocular microcirculation is involved in the pathogenesis of the disease. Although ocular blood flow in diabetic retinopathy has been thoroughly investigated, the reported results are inconsistent. This may be at least partially be related to the fact that blood flow is dependent on the severity of the disease. In particular, most of the studies, but not all report an increased ocular blood flow in early stages of diabetic retinopathy whereas blood flow seems to be decreased in the proliferative form of the disease. More importantly, it has been shown that beside changes in baseline flow, endothelial dysfunction is present even in very early stages of the disease. Based on this observation it has been hypothesized that endothelial dysfunction may precede other diabetes related complications. In this talk our current knowledge about blood flow regulation in patients with diabetes will be summarized. [source] 3123: Non-invasive measurement of retinal oxygenation: principles and expectationsACTA OPHTHALMOLOGICA, Issue 2010M HAMMER Purpose To determine oxygen saturation (SO2) of blood inside retinal vessels which is an essential measure for the estimation of oxygen supply to the tissue as well as its oxygen consumption. Methods Two-, four-, and multiple - wavelength approaches to the non-invasive measurement of SO2 will be discussed. The dual wavelength technique, imaging the fundus at 548 and 610 nm, showed to be most appropriate for clinical routine investigations. The SO2 of the hemoglobin in retinal arterioles and venules is calculated from the ratio of the optical densities of the vessels at both wavelengths. Results From a healthy control population, mean arterial and venous SO2 were measured to be 98±10.1% and 65±11.7% with reproducibility of 2.52% and 3.25% respectively. In a cohort of 41 patients (mean age: 65±12.3 years) with diabetic retinopathy (DR), we found an increase of the venous SO2 with the severity of DR: Mild non-proliferative DR 69±7%, moderate non-proliferative DR 70±5%, severe non-proliferative DR, 75±5%, and proliferative DR 75±8%. Measurements of SO2 in accordance with vessel diameters revealed a correlation of the venous SO2 with arterial as well as venous diameters in 159 diabetic patients (mean age: 55.8±13.9 years) with no or non , proliferative DR. Increased venous SO2 is an indicator of insufficient oxygen supply to the retinal tissue. The correlation of the vessel diameters with venous SO2 may point to compensatory mechanisms of retinal blood flow regulation. Conclusion Accurate retinal vessel oximetry is possible by non , invasive optical methods. Combined with measurements characterising the retinal blood flow, it is a powerful tool for the estimation of retinal oxygen supply and consumption. Commercial interest [source] 2323: Role of nitric oxide in optic nerve head blood flow regulation during isometric exercise in healthy humansACTA OPHTHALMOLOGICA, Issue 2010D SCHMIDL Purpose Nitric oxide (NO) is an important regulator of optic nerve head (ONH) blood flow in humans. We have previously shown that NO is also involved in choroidal blood flow regulation during isometric exercise. Inhibition of NO synthase (NOS) has been reported to shift choroidal pressure,flow curves during squatting to the right. The hypothesis for the present study was that inhibition of NOS may also influence ONH blood flow during isometric exercise. Methods To test this hypothesis, a randomized, double-masked, placebo-controlled, three-way crossover study was performed in 18 healthy volunteers. Subjects received on different study days intravenous infusions of NG-monomethyl- L-arginine (L-NMMA), phenylephrine, or placebo. During these infusion periods, subjects were asked to squat for 6 minutes. ONH blood flow was assessed with laser Doppler flowmetry, and ocular perfusion pressure (OPP) was calculated from mean arterial pressure and intraocular pressure. Results L-NMMA and phenylephrine increased resting OPP (p < 0.001 versus baseline), but only L-NMMA reduced resting ONH blood flow (p = 0.02 versus baseline). The relative increase in OPP during isometric exercise was comparable with all drugs administered (p = 0.69). In addition, the change of ONH blood flow was comparable with all administered drugs (p = 0.43). Conclusion These data indicate that NO plays an important role in the regulation of ONH blood flow at baseline, but does not change the response of ONH blood flow during isometric exercise. [source] Role of NO in retinal vascular diseaseACTA OPHTHALMOLOGICA, Issue 2009L SCHMETTERER Purpose Nitric oxide (NO) is a key regulator of vascular tone in all vascular beds including the eye. Hence, inhibition of NO synthase with L-arginine analogues leads to a reduction of blood flow to all ocular tissues. This enables the investigation of the role of NO in the physiology of blood flow regulation, but also abnormalities of the vascular L-arginine/NO system in ocular vascular disease. Methods A variety of studies investigating the role of NO in healthy humans but also in patients with vascular disease is summarized. Results Inhibition of NO synthase reduces retinal, choroidal and optic nerve head blood. A variety of studies also indicate that NO plays a role in the ocular vasodilator effects of numerous agonists including acetylcholine, bradykinin, carbon dioxide, histamine and insulin. In addition, NO appears to modulate the autoregulatory behavior of ocular vascular beds and is involved in retinal neurovascular coupling. In several ocular diseases such as diabetic retinopathy or open angle glaucoma abnormalities in the NO system can be observed. Conclusion NO is a major regulator of ocular blood flow in humans. The existence of different NO synthase isoforms makes it, however, difficult to therapeutically intervent via the L-arginine/NO pathway. Further studies are required to characterize the role of the NO synthase isoforms in the control of ocular blood flow in more detail and to allow for therapeutic interventions in ischemic ocular eye disease via this attractive pathway. [source] Choroidal blood flow regulation and possible implications to glaucomaCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 2 2008Ehud Rechtman MD No abstract is available for this article. [source] |