Roles of carotid baroreceptor and cardiac afferents in hemodynamic responses to acute central hypovolemia.

Abstract

When central blood volume is progressively reduced, there is a biphasic hemodynamic response. In phase I, sympathetic vasoconstrictor drive and systemic vasoconstriction steadily increase so arterial pressure is well maintained. In phase II, these compensatory mechanisms fail abruptly. The origin of the signal that triggers the onset of phase II is unclear. In this study of conscious rabbits, we have compared the responses of arterial pressure, systemic vascular conductance, the heart rate with acute central hypovolemia produced by gradual constriction of the inferior vena cava with those resulting from graded reduction in carotid sinus pressure, with the input from carotid baroreceptors and cardiac afferents present or absent. We confirm that the compensatory changes in phase I are due to input from arterial baroreceptors with no contribution from cardiac afferents. Input from cardiac afferents played an important role in triggering phase II during acute central hypovolemia, but there was no suggestion of a central switch from sympathoexcitation to sympathoinhibition when input from carotid baroreceptors reached a critically low level during carotid constriction.