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Skin Blood Flow Response (skin + blood_flow_response)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Does aerobic fitness influence microvascular function in healthy adults at risk of developing Type 2 diabetes?

DIABETIC MEDICINE, Issue 4 2005
A. R. Middlebrooke
Abstract Aim To investigate whether aerobic fitness is associated with skin microvascular function in healthy adults with an increased risk of developing Type 2 diabetes. Methods Twenty-seven healthy normal glucose-tolerant humans with either a previous diagnosis of gestational diabetes or having two parents with Type 2 diabetes and 27 healthy adults who had no history of diabetes were recruited. Maximal oxygen uptake was assessed using an incremental exercise test to exhaustion. Skin microvascular function was assessed using laser Doppler techniques as the maximum skin hyperaemic response to a thermal stimulus (maximum hyperaemia) and the forearm skin blood flow response to the iontophoretic application of acetylcholine (ACh) and sodium nitroprusside. Results Maximal oxygen uptake was not significantly different in the ,at-risk' group compared with healthy controls. Maximum hyperaemia was reduced in those ,at risk' (1.29 ± 0.30 vs. 1.46 ± 0.33 V, P = 0.047); however, the peak response to acetylcholine or sodium nitroprusside did not differ in the two groups. A significant positive correlation was demonstrated between maximal oxygen uptake and maximum hyperaemia (r = 0.52, P = 0.006 l/min and r = 0.60, P = 0.001 ml/kg/min) and peak ACh response (r = 0.40, P = 0.04 l/min and r = 0.47, P = 0.013 ml/kg/min) in the ,at-risk' group when expressed in absolute (l/min) or body mass-related (ml/kg/min) terms. No significant correlations were found in the control group. Conclusions In this ,at-risk' group with skin microvascular dysfunction maximal oxygen uptake was not reduced compared with healthy controls. However, in the ,at-risk' group alone, individuals with higher levels of aerobic fitness also had better microvascular and endothelial responsiveness. [source]

Acetylcholine-Induced Vasodilation and Reactive Hyperemia Are Not Affected by Acute Cyclo-Oxygenase Inhibition in Human Skin

MICROCIRCULATION, Issue 4 2004
Anne Dalle-Ave
Objective: To examine whether prostaglandins are involved in endothelium-dependent vasodilatory responses of the skin microcirculation. Methods: Twenty-three young male volunteers were studied on 2 different days 1,3 weeks apart. On each experimental day the forearm skin blood flow response to iontophoretically applied acetylcholine (Ach, an endothelium-dependent vasodilator) was determined with laser Doppler imaging following the intravenous administration of either the cyclo-oxygenase inhibitor lysine acetylsalicylate (L-AS), 900 mg, or the oral intake of indomethacin, 75 mg. Acetylcholine was iontophoresed both in presence and in absence of surface anesthesia. In some subjects, the effects of L-AS on skin reactive hyperemia were also assessed. Results: Acute cyclo-oxygenase inhibition with either drug influenced neither the skin blood flow response to 4 different doses of Ach (0.28, 1.4, 7, and 14 mC/cm2) nor reactive hyperemia. The peak vasodilatory response to Ach was significantly increased by skin anesthesia, regardless of whether the subjects received the cyclo-oxygenase inhibitor or not. For example, the mean response (± SD) to the largest dose of Ach (tested in 6 subjects, expressed in perfusion units) were as follows: in absence of anesthesia: L-AS 339 ± 105, placebo 344 ± 68; with anesthesia: L-AS 453 ± 76, placebo 452 ± 65 (p < .01 for effect of anesthesia). Conclusions: These data give no support for a contribution of prostaglandins to acetylcholine-induced vasodilation or to reactive hyperemia in the skin microcirculation. In this vascular bed, local anesthesia seems to amplify acetylcholine-induced vasodilation via a prostaglandin-independent mechanism. [source]

Heel skin hyperaemia: direct compression versus vascular occlusion

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2003
Harvey N. Mayrovitz
Summary Vulnerability of the heel to ulceration in bed-bound persons is related to direct pressure-induced blood flow decreases. Periodic pressure reduction is a clinical strategy to help prevent ulcers by allowing flow-repayment hyperaemia that has a magnitude and duration thought to be related to the duration of the prior interval of ischaemia. However, there are reasons to question whether effects of flow stoppages caused by direct tissue loading are similar to those because of ischaemia without superimposed direct pressure. This question was investigated by comparing posterior heel skin blood flow responses via laser-Doppler perfusion monitoring of 27 supine-lying subjects in whom blood flow was reduced by 5-min of direct heel loading on a support surface and by 5-min of ankle-cuff compression. Results showed that blood flow reductions were the same for both methods but the hyperaemia was significantly greater when flow reduction was produced by direct heel loading. This was true for ratio of peak hyperaemic flow to baseline (8·20 ± 1·32 s versus 4·68 ± 0·80 s, P,0·001), hyperaemic to baseline 3-min flow-time area ratios (4·70 ± 0·65 s versus 1·95 ± 0·29 s, P,0·001) and for total hyperaemia durations (352 ± 39 s versus 181 ± 14 s, P<0·001). These findings raise new questions regarding the precise physiological effects of heel and tissue loading in general, the factors that contribute to the hyperaemic response and their clinical impact and interpretation. Possible sources of the observed greater post-loading hyperaemia responses are discussed. [source]