[Right ventricular hypertrophy in rats: effect of ACE inhibitors]

Models of right ventricular hypertrophy in rats have been created and characterized: Daily injections of triiodothyronine, irradiation of the lung in Brown-Norway rats, chronic myocardial infarction, and pulmonary artery stenosis. A new Millar ultraminature catheter pressure transducer designed for right heart catheterization allowed the measurement of right ventricular function. All models were characterized by an increase in right ventricular systolic pressure, by an elevation in the RNA/DNA ratio in the right ventricle, and by an increase in the right ventricular weight/body weight ratio. Myocytes isolated from the right ventricle 4 weeks after coronary artery ligation had a greater volume and cross sectional area. Similar results were obtained 14 days after pulmonary artery stenosis. In this model, the effect of angiotensin converting enzyme inhibition with ramipril (1 mg/kg, daily) was examined. The increase in right ventricular systolic pressure from 35 +/- 2 mm Hg to 61 +/- 4 mm Hg (without ramipril) was not influenced by ramipril (63 +/- 4 mm Hg), neither was the elevation of right ventricular weight. However, the increase in cell volume and cross-sectional area of myocytes isolated from the right ventricle was less pronounced in the ramipril-treated group (+27% compared to +58% in untreated animals). Thus, angiotensin converting enzyme inhibition with ramipril altered the hypertrophic response at the cellular level.