Mechanism of volume replacement and vascular constriction following hemorrhage

Abstract

Experiments in the anesthetized dog suggest that fluid moves into the vascular system following hemorrhage because of fall in capillary hydrostatic pressure subsequent to decrease in aortic and right atrial pressure and increase in precapillary resistance. Postcapillary resistance also rises but not sufficiently to prevent the fall in capillary pressure. The increase in precapillary resistance results from active constriction, passive constriction, and, very transiently, increase in blood viscosity. The active constriction of precapillary vessels is due to a baroreceptor-induced sympathico-adrenal discharge and to some nonadrenal, nonrenal circulating vasoconstrictor substance. The active vasoconstriction is not well maintained in forelimb, intestine, or kidney because of local regulation ("autoregulation") and baroreceptor-induced lessening of the sympathico-adrenal discharge subsequent to movement of tissue fluid into the vascular system. This waning constriction together with a rise in perfusion pressure permits partial recovery of flow. The increase in forelimb postcapillary resistance results mainly from passive constriction. Active constriction subsequent to the sympathico-1 adrenal discharge is seen only with large hemorrhage.