Control of Skeletal Muscle Blood Flow during Postural Changes in Acute Myocardial Infarction

Abstract

Central and local regulation of skeletal muscle blood flow in the leg was studied in the acute phase of myocardial infarction. Blood flow was measured by the local 133Xe washout technique in the anterior tibial muscle. The vasoconstrictor response to increase in venous transmural pressure was not present on day 1 after coronary occlusion but gradually returned during days 2, 3 and 7. A normal response to decrease in arterial perfusion pressure was observed, suggesting that intrinsic vascular reactions responsible for autoregulation of blood flow were not affected in the acute phase of myocardial infarction. Passive head-up tilt (30 degrees) induced vasoconstriction in skeletal muscle tissue. There were no differences in this response at any time during the course of acute myocardial infarction. The abolition of the vasoconstrictor response to increase in venous transmural pressure on day 1 is most likely due to centrally elicited increase in sympathetic activity as a normal vasoconstrictor response was obtained the following days. Decrease in baroreceptor activity induced by head-up tilt enabled a marked neurogenically mediated vasoconstriction in skeletal muscle tissue which was almost unaffected during the course of myocardial infarction.

Lack of effect of moderate hypoxaemia on human postural reflexes to skeletal muscle

“…Also, effects of norepinephrine released endogenously could differ from those accompanying exogenous infusion (Elsner & Gooden 1983). Another possibility is that moderate hypoxaemia increases the background level of sympathetic discharge to skeletal muscle (Skagen & Henriksen 1983) which is not reflected in an increase in plasma norepinephrine level (Goldring et al 1962, Richardson et al 1967, Rowell & Blackmon 1985).…”