A review of the skin and muscle hemodynamics during hemorrhagic hypotension and shock.

Abstract

The primary objective of this study was to compare the hemodynamic responses in a vascular bed known to exhibit decompensation (ie, skeletal muscle) with a nondecompensating bed such as the cutaneous vascular bed during systemic and local reductions in perfusion pressure induced by hemorrhage and sequential inflow arterial occlusion. The secondary objective was to examine the mechanisms which may be responsible for skeletal muscle vascular decompensation. Systemic hypotension was produced by a stepwise hemorrhage of 5 ml/kg body weight with 5-minute intervals between bleedings. The carotid sinus impact was examined during bilateral carotid artery occlusion. The intrinsic effects were evaluated during reductions in local perfusion pressure. The data show that skeletal muscle vasculature exhibits autoregulation but skin vasculature does not. Both vascular beds respond to acute hemorrhage by vasoconstriction; however, the vasoconstriction in the skin occurs as a result of increased plasma levels of catecholamines acting on alpha receptors with no neural component, whereas the vasoconstriction in skeletal muscle occurs as a result of both neural and humoral hyperactivity. The data presented also suggest that the skeletal muscle vascular decompensation occurring late in shock is the result of prostaglandin inhibition of a hyperactive sympathetic nervous system.