Peripheral vascular adrenergic depression during hypotension induced by E coli endotoxin.

Previous studies support the concept that most vascular beds exhibit some degree of blood flow autoregulation (ie, vasodilation) in response to a fall in local perfusion pressure. However, when systemic pressure is reduced by acute hemorrhage, this vasodilation is converted to vasoconstriction. This response is due to extrinsic influences (ie, elevated adrenergic activity) which overwhelm the intrinsic autoregulatory response. The objective of the present investigation was to compare the regional vascular behavior in selected tissues (ie, skeletal muscle, skin, mesenteric and renal) during local hypotension and systemic hypotension induced by stepwise hemorrhage and endotoxin. Previously published data on local hypotension accomplished by gradual occlusion of the arterial inflow, and systemic hypotension induced by stepwise hemorrhage were compared to systemic hypotension induced by IV administration of 2 mg/kg E coli endotoxin. The pressure/vascular conductance data suggest the following: 1) Skeletal muscle, mesenteric, and renal vasculature respond to local hypotension by autoregulating while skin exhibits passive vasoconstriction; 2) all four vascular beds respond to hemorrhage by intense vasoconstriction; and 3) all four vascular beds respond to endotoxin by vasodilating. The data are compatible with the concept that endotoxin inhibits the extrinsic compensatory vasoconstrictor response to systemic hypotension in all of these vascular beds.