Mechanism of Congestive Heart Failure Following Aorta Constriction in Rabbits

Abstract

Severe constriction of the abdominal aorta in rabbits caused congestive heart failure and death in 4 to 7 days. Expansion of total plasma volume suggested that aortic narrowing increases the vascular bed distal to the stricture. Reduction of total body fluids did not prevent total plasma volume expansion, unless it caused severe dehydration. A large percentage of dietary sodium was retained. Expansion of extraccilular volume occurred even when sodium intake was reduced. The early, gradual post-operative rise in arterial pressure probably depends, in part, on development of an effective circulating plasma volume. A tentative answer is given to the question of what factors determine the exact time that heart failure will occur.

The Thrombotic Activity of Activation Product*

“…The clear demonstration of the thrombotic potential of activation product has implications of importance for human thrombotic disease. The injection of the activation product from only 6 ml of human plasma can trigger thrombosis in a 2 kg rabbit with an estimated plasma volume of 70 to 110 ml (28). Thus, the injected activity must be the equivalent of only a small fraction of the animal's own activation product potential.…”

Peripheral Circulation

“…Alexander (287) in studying the development of congestive heart failure in rabbits following aortic constriction has shown that the effective circulat ing plasma volume increases early after the constriction and that this is associated with sodium retention by the kidneys and expansion of extracel lular fluid volume. Further, constriction of the aorta in steps rather than sudden severe constriction prevents the congestive phase of failure in these animals (288).…”