Role of adrenergic-neural regulation in failing heart due to aortic regurgitation in rabbits

The purpose of this study was to determine the characteristics of the role of adrenergic-neural regulation in the pathophysiology of heart failure, produced by aortic regurgitation (AR), especially in relation to the compensatory process. AR was produced by perforation of the aortic valves in 25 rabbits. Another 6 normal rabbits served as controls. Myocardial beta-adrenoceptors and catecholamines were measured in 17 rabbits with AR after various periods: 1 day (n = 5), 1 week (n = 6), and 4 weeks after production of AR (n = 6). Serial blood samples were taken without anesthesia through a catheter placed in the jugular vein for determination of the serum catecholamine level in 8 rabbits with AR. Left ventricular free wall weight increased 1 week and 4 weeks after AR. Wall thickness didn't increase until 4 weeks had passed. Maximal binding sites of myocardial beta-adrenoceptors were reduced from 67.8 +/- 16.7 fmol/mg. protein in the controls to 37.6 +/- 9.21 day after AR (p less than 0.01). Down regulation persisted for 1 week (37.3 +/- 5.5). This change was reversed in the 4-week group (55.5 +/- 13.9). Myocardial norepinephrine content was preserved at 1 day, but depleted at 1 week after AR. In the 4-week group it was restored. Serum norepinephrine level increased 1 day after AR. However, it returned toward the normal range thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)