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Capillary Blood Flow (capillary + blood_flow)
Selected AbstractsEpilepsy Patients Treated with Antiepileptic Drug Therapy Exhibit Compromised Ocular Perfusion CharacteristicsEPILEPSIA, Issue 11 2002Emma J. Roff Hilton Summary: ,Purpose: Reduced cerebral blood flow and decreased cerebral glucose metabolism have been identified in patients with epilepsy treated with antiepileptic drug (AED) therapy. The purpose of this study was to determine whether ocular haemodynamics are similarly reduced in patients with epilepsy treated with AEDs. Methods: Scanning laser Doppler flowmetry was used to measure retinal capillary microvascular flow, volume, and velocity in the temporal neuroretinal rim of 14 patients diagnosed with epilepsy (mean age, 42.0 ± 0.9 years). These values were compared with those of an age- and gender-matched normal subject group (n = 14; mean age, 41.7 ± 0.3 years). Student's unpaired two-tailed t tests were used to compare ocular blood-flow parameters between the epilepsy and normal subject groups (p < 0.05; Bonferroni corrected). Results: A significant reduction in retinal blood volume (p = 0.001), flow (p = 0.003), and velocity (p = 0.001) was observed in the epilepsy group (13.52 ± 3.75 AU, 219.14 ± 76.61 AU, and 0.77 ± 0.269 AU, respectively) compared with the normal subject group (19.02 ± 5.11 AU, 344.03 ± 93.03 AU, and 1.17 ± 0.301 AU, respectively). Overall, the percentage mean difference between the epilepsy and normal groups was 36.31% for flow, 28.92% for volume, and 34.19% for velocity. Conclusions: Patients with epilepsy exhibit reduced neuroretinal capillary blood flow, volume, and velocity compared with normal subjects. A reduction in ocular perfusion may have implications for visual function in people with epilepsy. [source] Critical role of the vascular endothelial cell in health and disease: a review articleJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 2 2004Todd C. Duffy DVM Abstract Objective: To review the human and veterinary literature on the role of the vascular endothelial cell in health, as well as during hypoxic and inflammatory disease states. Data sources: Data from human and veterinary literature were reviewed through a Pubmed search and a manual search of the references listed in articles covering some aspect of vascular endothelial cell function. Human data synthesis: The development of techniques that allow the maintenance and growth of endothelial cells in culture has produced an explosion of new research in the area of endothelial cell physiology. This plethora of data has revealed the critical role that vascular endothelial cells play in both health and disease states. Interspecies variations can occur with respect to the vascular endothelial cell physiology and its response to pathologic conditions. Veterinary data synthesis: There is a paucity of information regarding the role of the vascular endothelial cell in health or disease of small animals. Many human studies use species cared for by veterinarians, providing information that may be applied to small animals and that may be used to construct future studies. Conclusion: An organ system itself, the vascular endothelium is an essential component of all organs in the body. The endothelial cell lining functions to maintain selective permeability between the blood and the tissue it supplies, regulate vascular tone, sustain blood fluidity through regulation of coagulation, and modulate interaction of leukocytes with the interstitium and inflammatory reactions. During disease states, the endothelial cell functions locally to limit the boundaries of the disease process. If these functions are not controlled, they can become a part of the pathogenic process, contributing to blood stasis and thrombosis, potentiation of local inflammation and interstitial edema formation, subsequent tissue hypoxia, and multiple organ dysfunction. Pharmacological investigations targeting the modulation of endothelial function during disease states have not yet advanced treatment protocols. Since all critically ill animals are at risk for some degree of endothelial cell dysfunction, treatment regimens should focus on promoting capillary blood flow and tissue oxygen delivery. [source] An In-Vivo Analysis of Capillary Stasis and Endothelial Apoptosis in a Model of HypertensionMICROCIRCULATION, Issue 8 2007Edward D. Tran ABSTRACT Objective: Recent evidence suggests endothelial apoptosis may be a mechanism for capillary rarefaction in hypertensives. The objective of this study was to examine the early phase of endothelial apoptosis and capillary blood flow in the spontaneously hypertensive rat (SHR) and the normotensive Wistar-Kyoto (WKY) rat. Methods: Since hypertension in SHR is dependent on glucocorticoids, the animals were treated with dexamethasone (DEX), by intraperitoneal injection and then by superfusion on exposed mesentery. Selected capillaries were continuously observed. Annexin V and propidium iodide were used to detect apoptosis. Results: Without central pressure reduction, permanent capillary stasis was initiated by the entrapment of leukocytes at the location of an endothelial cell that had platelets attached to it. Apoptosis of the endothelial cell was followed by apoptosis in other endothelial cells of the obstructed capillary. The incidence of stasis and total cell death in WKY+DEX were higher than WKY, whereas there were no differences between SHR+DEX and SHR. Blockade of the lectin domain of L-selectin or a platelet membrane adhesion molecule (glycoprotein IIb/IIIa) blocked the development of stasis. Conclusions: Glucocorticoid facilitates cell death and microvessel stasis. Immobilized platelets and leukocytes play a central role in capillary stasis, which leads to progression of endothelial apoptosis. [source] Microvascular Rheology and HemodynamicsMICROCIRCULATION, Issue 1 2005HERBERT H. LIPOWSKY ABSTRACT The goal of elucidating the biophysical and physiological basis of pressure,flow relations in the microcirculation has been a recurring theme since the first observations of capillary blood flow in living tissues. At the birth of the Microcirculatory Society, seminal observations on the heterogeneous distribution of blood cells in the microvasculature and the rheological properties of blood in small bore tubes raised many questions on the viscous properties of blood flow in the microcirculation that captured the attention of the Society's membership. It is now recognized that blood viscosity in small bore tubes may fall dramatically as shear rates are increased, and increase dramatically with elevations in hematocrit. These relationships are strongly affected by blood cell deformability and concentration, red cell aggregation, and white cell interactions with the red cells and endothelium. Increasing strength of red cell aggregation may result in sequestration of clumps of red cells with either reductions or increases in microvascular hematocrit dependent upon network topography. During red cell aggregation, resistance to flow may thus decrease with hematocrit reduction or increase due to redistribution of red cells. Blood cell adhesion to the microvessel wall may initiate flow reductions, as, for example, in the case of red cell adhesion to the endothelium in sickle cell disease, or leukocyte adhesion in inflammation. The endothelial glycocalyx has been shown to result from a balance of the biosynthesis of new glycans, and the enzymatic or shear-dependent alterations in its composition. Flow-dependent reductions in the endothelial surface layer may thus affect the resistance to flow and/or the adhesion of red cells and/or leukocytes to the endothelium. Thus, future studies aimed at the molecular rheology of the endothelial surface layer may provide new insights into determinants of the resistance to flow. [source] Role of villus microcirculation in intestinal absorption of glucose: coupling of epithelial with endothelial transportTHE JOURNAL OF PHYSIOLOGY, Issue 2 2003J. R. Pappenheimer Capillaries in jejunal villi can absorb nutrients at rates several hundred times greater (per gram tissue) than capillaries in other tissues, including contracting skeletal muscle and brain. We here present an integrative hypothesis to account for these exceptionally large trans-endothelial fluxes and their relation to epithelial transport. Equations are developed for estimating concentration gradients of glucose across villus capillary walls, along paracellular channels and across subjunctional lateral membranes of absorptive cells. High concentrations of glucose discharged across lateral membranes to subjunctional intercellular spaces are delivered to abluminal surfaces of villus capillaries by convection-diffusion in intercellular channels without significant loss of concentration. Post-junctional paracellular transport thus provides the series link between epithelial and endothelial transport and makes possible the large trans-endothelial concentration gradients required for absorption to blood. Our analysis demonstrates that increases of villus capillary blood flow and permeability-surface area product (PS) are essential components of absorptive mechanisms: epithelial transport of normal digestive loads could not be sustained without concomitant increases in capillary blood flow and PS. The low rates of intestinal absorption found in anaesthetised animals may be attributed to inhibition of normal villus microvascular responses to epithelial transport. [source] Mechanism of action of vitamin C in sepsis: Ascorbate modulates redox signaling in endotheliumBIOFACTORS, Issue 1 2009John X. Wilson Abstract Circulating levels of vitamin C (ascorbate) are low in patients with sepsis. Parenteral administration of ascorbate raises plasma and tissue concentrations of the vitamin and may decrease morbidity. In animal models of sepsis, intravenous ascorbate injection increases survival and protects several microvascular functions, namely, capillary blood flow, microvascular permeability barrier, and arteriolar responsiveness to vasoconstrictors and vasodilators. The effects of parenteral ascorbate on microvascular function are both rapid and persistent. Ascorbate quickly accumulates in microvascular endothelial cells, scavenges reactive oxygen species, and acts through tetrahydrobiopterin to stimulate nitric oxide production by endothelial nitric oxide synthase. A major reason for the long duration of the improvement in microvascular function is that cells retain high levels of ascorbate, which alter redox-sensitive signaling pathways to diminish septic induction of NADPH oxidase and inducible nitric oxide synthase. These observations are consistent with the hypothesis that microvascular function in sepsis may be improved by parenteral administration of ascorbate as an adjuvant therapy. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] | |||||||||||||