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Microvascular Responses (microvascular + response)

Distribution by Scientific Domains

Life Sciences	60%
Medical Sciences	40%

Selected Abstracts

Liver Perfusion in Sepsis, Septic Shock, and Multiorgan Failure

THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 6 2008
Herbert Spapen
Abstract Sepsis causes significant alterations in the hepatic macro- and microcirculation. Diverging views exist on global hepatic blood flow during experimental sepsis because of the large variety in animal and sepsis models. Fluid-resuscitated clinical sepsis is characterized by ongoing liver ischemia due to a defective oxygen extraction despite enhanced perfusion. The effects of vasoactive agents on the hepatosplanchnic circulation are variable, mostly anecdotal, and depend on baseline perfusion, time of drug administration, and use of concomitant medication. Microvascular blood flow disturbances are thought to play a pivotal role in the development of sepsis-induced multiorgan failure. Redistribution of intrahepatic blood flow in concert with a complex interplay between sinusoidal endothelial cells, liver macrophages, and passing leukocytes lead to a decreased perfusion and blood flow velocity in the liver sinusoids. Activation and dysfunction of the endothelial cell barrier with subsequent invasion of neutrophils and formation of microthrombi further enhance liver tissue ischemia and damage. Substances that regulate (micro)vascular tone, such as nitric oxide, endothelin-1, and carbon monoxide, are highly active during sepsis. Possible interactions between these mediators are not well understood, and their therapeutic manipulation produces equivocal or disappointing results. Whether and how standard resuscitation therapy influences the hepatic microvascular response to sepsis is unknown. Indirect evidence supports the concept that improving the microcirculation may prevent or ameliorate sepsis-induced organ failure. Anat Rec, 291:714,720, 2008. © 2008 Wiley-Liss, Inc. [source]

Microcirculatory Responses To Electrical Spinal Cord Stimulation In Painful Diabetic Neuropathy And Other Painful Conditions

JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000
Nd Harris
Electrical spinal cord stimulation (ESCS) has been used to provide pain relief in a number of conditions, including painful diabetic neuropathy (PDN). ESCS has also been shown to increase microvascular blood flow in peripheral vascular disease. If nerve hypoxia contributes to pain in PDN, ESCS may relieve this by increasing nerve blood flow. We have therefore investigated skin and sural nerve microvascular responses to ESCS. We studied subjects implanted with ESCS for pain relief, 4 had PDN and 7 were controls with other painful conditions. Blood flow, before and during stimulation, was assessed using Laser Doppler flowmetry. Only one (PDN) subject showed a statistically significant increase in skin blood flow during stimulation. The three remaining PDN subjects showed significant reductions in skin blood flow, as did 3/7 of controls. Sural nerve blood flow was measured on a separate occasion. During stimulation nerve blood flow increased in 1 (control) subject, decreased in 1 (PDN) subject and did not change in the other 5 tested (3 PDN and 2 control). In summary, ESCS did not produce any consistent increase in skin or nerve microvascular blood flow. ESCS reduces pain in a variety of different conditions, however this does not appear to be mediated by changes in blood flow. Until a thorough understanding of the pathogenic mechanisms causing PDN is achieved, therapy will be limited to providing symptomatic relief. [source]

Exercise prevents age-related decline in nitric-oxide-mediated vasodilator function in cutaneous microvessels

THE JOURNAL OF PHYSIOLOGY, Issue 14 2008
Mark A. Black
Ageing is associated with impaired endothelium-derived nitric oxide (NO) function in human microvessels. We investigated the impact of cardiorespiratory fitness and exercise training on physiological and pharmacological NO-mediated microvascular responses in older subjects. NO-mediated vasodilatation was examined in young, older sedentary and older fit subjects who had two microdialysis fibres embedded into the skin on the ventral aspect of the forearm and laser Doppler probes placed over these sites. Both sites were then heated to 42°C, with Ringer solution infused in one probe and N -nitro- l -arginine methyl ester (l -NAME) through the second. In another study, three doses of ACh were infused in the presence or absence of l -NAME in similar subjects. The older sedentary subjects then undertook exercise training, with repeat studies at 12 and 24 weeks. The NO component of the heat-induced rise in cutaneous vascular conductance (CVC) was diminished in the older sedentary subjects after 30 min of prolonged heating at 42°C (26.9 ± 3.9%CVCmax), compared to older fit (46.2 ± 7.0%CVCmax, P < 0.05) and young subjects (41.2 ± 5.2%CVCmax, P < 0.05), whereas exercise training in the older sedentary group enhanced NO-vasodilator function in response to incremental heating (P < 0.05). Similarly, the NO contribution to ACh responses was impaired in the older sedentary versus older fit subjects (low dose 3.2 ± 1.3 versus 6.6 ± 1.3%CVCmax; mid dose 11.4 ± 2.4 versus 21.6 ± 4.5%CVCmax; high dose 35.2 ± 6.0 versus 52.6 ± 7.9%CVCmax, P < 0.05) and training reversed this (12 weeks: 13.7 ± 3.6, 28.9 ± 5.3, 56.1 ± 3.9%CVCmax, P < 0.05). These findings indicate that maintaining a high level of fitness, or undertaking exercise training, prevents age-related decline in indices of physiological and pharmacological microvascular NO-mediated vasodilator function. Since higher levels of NO confer anti-atherogenic benefit, this study has potential implications for the prevention of microvascular dysfunction in humans. [source]

Role of villus microcirculation in intestinal absorption of glucose: coupling of epithelial with endothelial transport

THE JOURNAL OF PHYSIOLOGY, Issue 2 2003
J. 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]

Increased asymmetric dimethylarginine and endothelin 1 levels in secondary Raynaud's phenomenon: Implications for vascular dysfunction and progression of disease

ARTHRITIS & RHEUMATISM, Issue 7 2003
Sanjay Rajagopalan
Objective To compare microvascular and macrovascular functions in a cohort of patients with primary and secondary Raynaud's phenomenon (RP) who were matched for demographic, risk factor, and severity profiles. Methods Forty patients with primary or secondary RP matched for vascular risk factors and severity scores underwent testing of endothelial function and cold pressor responsiveness of the brachial artery. Microvascular perfusion of the digital vasculature was assessed using laser Doppler fluxmetry in response to reactive hyperemia. Plasma was assayed for endothelin 1 (ET-1), asymmetric dimethylarginine (ADMA), intercellular adhesion molecule 1, vascular cell adhesion molecule 1 (VCAM-1), and monocyte chemoattractant protein 1 (MCP-1). Results Patients with RP had abnormal vasoconstrictor responses to cold pressor tests (CPT) that were similar in primary and secondary RP. There were no differences in median flow-mediated and nitroglycerin-mediated dilation or CPT of the brachial artery in the 2 populations. Patients with secondary RP were characterized by abnormalities in microvascular responses to reactive hyperemia, with a reduction in area under the curve adjusted for baseline perfusion, but not in time to peak response or peak perfusion ratio. Plasma ET-1, ADMA, VCAM-1, and MCP-1 levels were significantly elevated in secondary RP compared with primary RP. There was a significant negative correlation between ET-1 and ADMA values and measures of microvascular perfusion but not macrovascular endothelial function. Conclusion Secondary RP is characterized by elevations in plasma ET-1 and ADMA levels that may contribute to alterations in cutaneous microvascular function. [source]