The role of cardiac receptor and arterial baroreceptor reflexes in control of the circulation during acute change of blood volume in the conscious rabbit.

Author:

Ludbrook J,Graham W F

Abstract

We have studied overall reflex control of the circulation by the arterial baroreceptors and cardiac receptors during acute change of blood volume in seven conscious rabbits. A factorial experimental design allowed analysis of the direction, magnitude, and significance of the reflex effects of independent input from each set of receptors, and the reflex interactions when the inputs were combined. Right atrial pressure, arterial pressure, systemic vascular resistance, cardiac output, and heart rate were measured during acute, graded, isohemic change of blood volume over the range +/- 27%. This was done with both reflexes present, only the arterial baroreceptor reflex present (intrapericardial 2% procaine), only the cardiac receptor reflex present (surgical baroreceptor denervation), and with both reflexes absent. As blood volume was depleted, the arterial baroreceptor reflex independently increased systemic vascular resistance and sustained arterial pressure, but the cardiac receptor reflex had no significant independent or interactive effects. As blood volume was expanded, each reflex had an independent effect in decreasing systemic vascular resistance and preventing arterial pressure from rising, the cardiac receptor reflex being the more powerful. Their effect in combination on systemic vascular resistance and arterial pressure was only two-fifths of the sum of their independent effects, so that they interacted negatively. In combination, the reflexes supported right atrial pressure during blood loss, despite their negative interaction, but did not significantly affect the relation of cardiac output to blood volume change in either direction. Thus both reflexes have important actions in moderating the overall effects of acute blood volume changes in conscious rabbits, but these are markedly diminished by their interactions.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Physiology

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