SUMMARY Severe constriction of the suprarenal abdominal aorta of 3-kg rabbits to 3.7 ± 0.2 mm 2 and maintenance of a daily sodium intake of 10 mEq by infusion of 0.9% sodium chloride resulted in a progressive increase in central ear arterial pressure to 106 ± 3 (SEM) mm Hg (control = 79 ± 1). This was accompanied by a progressive increase in left ventricular end-diastolic pressure to 22 ± 2 mm Hg (control = 3 ± I), plasma renin activity to 21 ± 5 ng of angiotensin/hour per ml (control = 5 ± 1), plasma aldosterone concentration to 99 ± 23 pg/ml (control = 14 ± 4), and plasma sodium concentration to 142 ± 1 mEq/liter (control = 136 ± 1). Urinary excretion of sodium decreased to 3.9 ± 0.7 mEq/day and marked fluid retention occurred. We also found that these changes were accompanied by a decrease in hematocrit to 24 ± 2% (control = 40 ± 1), the formation of 36 ± 9 ml of fluid in the thoracic cavity, 33 ± 9 ml of ascites, pulmonary congestion and edema, hepatic congestion, and enlargement and hypertrophy of both the left and right ventricles. All rabbits died of ventricular failure at a time that was partly related to the degree of aortic constriction and that ranged from 2 to 12 days. The model we have established is chronic, highly reproducible, easy to produce, and inexpensive, and resembles the clinical syndrome of right and left congestive heart failure in man. Furthermore, the studies provide evidence for an important role of the renin-angiotensin-aldosterone system in the fluid retention that leads to pulmonary and systemic venous congestion after suprarenal aortic constriction.STUDIES of the mechanisms for experimental congestive heart failure require an animal model that is chronic, highly reproducible, inexpensive, and comparable to the clinical syndrome in man. Models resembling right 1 ' 2 and left 3 ' 4 congestive heart failure have been produced previously in this laboratory in the dog by constriction of the thoracic inferior vena cava,' pulmonary artery stenosis, 2 or an aortic left atrial shunt and aortic constriction.
-4 Constriction of the abdominal aorta of the rabbit has been reported to lead to congestive heart failure; 5 " 7 however, little attention was given to the mechanisms for fluid retention that lead to pulmonary edema and heart failure. Therefore, in the present study the mechanisms of fluid retention in congestive heart failure were evaluated in the rabbit after constriction of the abdominal aorta and during maintenance of daily sodium intake by infusion of 0.9% sodium chloride. In attempting to define more completely the pathophysiology of the model, one of the primary aims of this study was to determine the role of the reninangiotensin-aldosterone system, which has been found to be an important cause of fluid retention in experimental congestive heart failure.
"4 A secondary outcome of these studies was the establishment of a method for the consistent, reproducible production of experimental congestive heart failure that satisfies the criteria stated above; the present model might pro...