Influences on central hemodynamics in hemorrhage of β2-adrenergic vascular control mechanisms

Abstract

Central hemodynamic responses evoked by standardized hemorrhage (exsanguination of 20 ml .times. kg body wt-1) were followed during 2 h in cats with intact and blocked vascular .beta.2-adrenoceptors using the selective .beta.2-blocker, ICI 118551 [erythro-DL-1-(7-methylindan-4-yloxy)-3-isopropylamino-butan-2-ol]. In the first 10 min after bleeding blood pressure and cardiac output (CO) decreased and total peripheral resistance (TPR) increased by the same amount in the intact and .beta.2-blocked animals. Whereas blood pressure later on reached approximately the same hypotension level in both groups, other hemodynamic variables were distinctly different. In the intact animals there was a gradual, partial recovery of stroke volume (SV) and CO in the face of a restoration to control of TPR. In the .beta.2-blocked animals TPR continued to increase in the face of a maintained low CO and declining SV. The lower SV in the latter group was ascribed to abolition of .beta.2-adrenergic restoration of plasma volume via absorption of tissue fluid into the circulation. The gradual decline of TPR in the intact animals was attributed to .beta.2-adrenergic dilator interaction with constrictor influences on the resistance vessels. .beta.-adrenergic vascular control mechanisms may help to improve nutritional tissue blood flow during hemorrhage by increasing plasma volume, hence venous return and CO, and by decreasing TPR. These reflex .beta.2-adrenergic circulatory events are similar to those aimed at in current shock therapy by transfusion and vasodilator treatment.