Intrinsic versus extrinsic regional vascular control during hemorrhagic hypotension and shock.

An analysis of both intrinsic (eg, autoregulatory) and extrinsic adrenoreceptor regulation of the vascular smooth muscle within skeletal muscle (SM), cutaneous (C), and mesenteric (M) tissues obtained during local tissue hypotension (LH), hemorrhagic hypotension (HH), and shock (S) is presented. A series of pressure/conductance curves show that the intrinsic regulation of vascular tone remains down to LH values of 40 mm Hg in M to 60 mm Hg in SM and does not occur in C; all three vascular beds respond to HH by exhibiting strong extrinsic vasoconstriction, the elevated tone persists throughout HH in C but lasts only a few minutes in M while SM vasoconstriction may last up to 45 min; and during the terminal phase of S, vascular tone was best maintained in C. In vitro studies suggest that the prehemorrhage alpha 1 adrenoreceptor control is greatest in M and least in SM. During compensatory and early decompensatory HH, alpha 1 receptors are depressed in SM. M vessels show this alpha 1 receptor hyposensitivity only during compensatory HH. All vessels show strong responsiveness to NE during all stages of HH and S, yet M vessels demonstrate a progressive increase in the NE concentrations required to elicit and ED50, suggesting some degree of adrenoreceptor desensitization or down regulation. This is in contrast to the adrenoreceptor hypersensitivity noted in SM during both compensatory and decompensatory stages. C vessels show this pattern in all stages except S. These data verify that each vascular bed has its own unique set of vascular control mechanisms that can act independently during HH and S.