The effect of vasoactive agents on post-pressure hyperemia.

The cutaneous hyperemic response following the release of direct pressure occlusion lasts much longer than the short-term hyperemia that occurs after proximal arterial occlusion. Post-pressure hyperemia may be an important mechanism to prevent pressure induced injury to the skin. The role of vasoactive mediators in modulating post-pressure hyperemia is unknown. In an effort to better understand this phenomenon, we performed an initial study using microdialysis infusion to measure the effect of several known mediators of vascular response on post-pressure hyperemia. A vise clamp was used to apply direct occlusive pressure to a laser Doppler sensor on the skin surface overlying the microdialysis fiber. Skin blood flow was measured continuously pre, during and post-occlusion while infusing the vasoactive substance or control phosphate buffer. Angiotensin II, Calcitonin gene related peptide and histamine had minimal effect on post pressure blood flow. Conversely, prostaglandin E1, prostaglandin E2, and L-NAME diminished the early phase of the post-occlusion hyperemic response. Perhaps the most profound effect we observed was the decrease in post-occlusive blood flow due to administration of epinephrine, dopamine and prostaglandin F2alpha. In contrast, adenosine and caffeine augmented blood flow post occlusion. In this initial survey study, we have demonstrated differential effects of various vascular mediators on the post-pressure hyperemic phenomenon. Our findings may lead to the development of agents to prevent pressure sores by augmenting the skin blood flow response to locally applied pressure.

Skin blood flow abnormalities in diabetic dermopathy.

BACKGROUND: Diabetic dermopathy is the most common specific cutaneous finding in diabetes. OBJECTIVE: Using laser Doppler technology, we tested the hypothesis that diabetic dermopathy arises from abnormal local skin blood flow. METHODS: We measured cutaneous blood flow in patients with type 1 diabetes without dermopathy and compared values with those in a control group of patients with type 1 diabetes without diabetic dermopathy and in a nondiabetic group. We measured at 3 separate sites on the pretibial area on the legs of each participant, at dermopathy lesions, and at a number of standard sites on the upper and lower extremities. RESULTS: We studied 25 patients with diabetes and diabetic dermopathy, average age 51 ± 2 years, mean duration of diabetes 28 ± 3 years. In all, 58 patients with type 1 diabetes without diabetic dermopathy served as control patients, average age 41 ± 2 years, mean duration of diabetes 23 ± 2 years. There were 67 nondiabetic control subjects, average age 47 ± 3 years. The patients with diabetic dermopathy showed a marked reduction in skin blood flow at 35°C at normal-appearing skin areas on the pretibial surface of the legs (1.1 ± 0.1 mL/min/100 g) compared with 1.7 ± 0.1 mL/min/100 g (P = .01) in the type 1 diabetic control group and 2.1 ± 0.3 mL/min/100 g (P < .01) in the nondiabetic group. The dermopathy lesions themselves showed markedly higher blood flow: 2.5 ± 0.3 mL/min/100 g. LIMITATIONS: Our diabetic dermopathy patients were somewhat older than the control type 1 diabetes subjects, but were of comparable age to the nondiabetic subjects. CONCLUSIONS: These results suggest that patients susceptible to diabetic dermopathy have a functional abnormality in blood flow leading to this scarring process.