Differential release of endothelin in myocutaneous island flaps in response to gradually insetting venous stasis or arterial ischemia

Abstract

Endothelin (ET) provokes strong and sustained contraction in preparations of isolated vascular smooth muscle, and the production of ET is thought to increase secondary to increased wall shear stress and hypoxia. The release of ET and blood flow distribution between arteriovenous shunts and capillaries were studied in autoperfused myocutaneous pig island flaps during graded arterial or venous blood flow reduction (N = 12). A group comprising four flaps was not exposed to blood flow reduction and served as controls. Total flap blood flow (venous outflow [VO]) was reduced in 1-hour periods to 50%, 25%, and 0%. Downregulation of VO caused a lower capillary blood flow (CBF) at 25% ( P < .05) and at 50% ( P < .05) in flaps exposed to venous stasis as compared with flaps with arterial ischemia. The reduction in blood flow was paralleled by decreasing oxygen consumption, although flaps with venous stasis had lower oxygen consumption than flaps exposed to arterial ischemia ( P < .05). ET was found to be released from these island flaps before blood flow was reduced. Gradual arterial clamping caused a statistically significant ( P < .05) decrease in the release of ET from 8.7 ± 1.3 fmol/min before ischemia to 4.1 ± 1.7 at 50% blood flow and 4.1 ± 1.0 at 25% blood flow. In contrast, the release of ET with venous stasis remained unchanged at a level of 7.5 ± 1.6 fmol/min before blood flow reduction, 7.3 ± 0.7 at 50% blood flow, and 8.5 ± 1.6 at 25% blood flow. These data suggest a relationship between CBF, intravascular pressure, and ET production. Determining whether intravascular pressure or hypoxia are the reasons for maintained ET release in response to venous stasis or whether a persistently high ET release during venous stasis causes reductions in CBF requires further study.