This study elucidates the sequential roles of autonomic mechanisms and neurohumoral factors (AVP, ANG II) in maintaining arterial pressure during progressive hemorrhage in conscious rabbits.
Conscious instrumented rabbits were bled at a constant rate of congruent to 3% of the blood volume (BV) per minute. We determined the BV-response relationships for mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), mesenteric and hindlimb blood flows, and for the corresponding conductances. We studied the responses 1) under normal conditions; 2) after pretreatment with captopril, arginine vasopressin (AVP) antagonist, or both; 3) during total autonomic blockade (TAB); and 4) during neurohumoral blockade (NHB, i.e., TAB + captopril + AVP antagonist). We determined the direct local response component from the responses obtained during NHB. The local chronotropic effects congruent to 0, so that the reflex rise in HR was entirely autonomically mediated. The local vascular response consisted of vasodilatation and provided the base line for assessing the estimated constrictor component from the net response from control, with the former ranging from 2 to 16 times the conventional estimates based on the net responses. In normal rabbits, the phase of good maintenance of MAP was entirely governed by autonomic mechanisms, which minimized the fall in CO and offset the local vasodilator component. During the hypotensive phase immediately after hemorrhage, when congruent to 30-35% BV had been removed, the constrictor effects of AVP and angiotensin II (ANG II) became important, whereas the role of autonomic mechanisms diminished. During TAB, the constrictor effects of AVP and ANG II were prominent even with small BV losses.
Körner et al. (1990) studied this question.