Abstract
To establish an experimental model of chronic heart failure, we assessed the morphologic, hemodynamic and neurohumoral effects of a single large dose for isoproterenol (ISO: 150 mg/kg BW s.c.). Two weeks after ISO-application 45 ISO- and 30 control-rats were examined. In addition, we investigated the effects of chronic treatment with ramipril (RAM: 10 mg/KG/d, n = 20). Echocardiography of ISO- and control-rats was performed in anesthetized rats to measure left ventricular (LV) mass and LV-enddiastolic dimension. An increase of LV-mass (LV diastolic posterior wall thickness: 2.8 ± 0.2 vs. 1.9 ± 0.3 mm, LV systolic posterior wall thickness: 4.3 ± 0.4 vs. 3.6 ± 0.3 mm; p < 0.01) and LV enddiastolic dimension (6.9 ± 0.6 vs. 4.9 ± 0.3 mm p < 0.01) was displayed. RAM-treated animals showed a highly significant decrease of LV mass and LV-enddiastolic dimension (p < 0.001). Heart rate was increased in the ISO-group (p < 0.005) compared to RAM- and control-rats (p < 0.005). Central venous pressure was significantly increased in the ISO-group (5.8 ± 2.3; vs 2.3 ± 0.6 mmHG; p < 0.01) and decreased to normal ranges in RAMrats. Mean arterial pressure was decreased in ISO- (121.3 ± 14.8 mmHg) and RAM-rats, (95 ± 3 mmHG) vs controls (132.4 ± 19.5 mmHG)(p < 0.05). Mean renal blood flow between ISO-treated and control group was not significantly different, in contrast the mean blood flow in the abdominal aorta was decreased in the ISO-group (p < 0.05). Cardiac ACE-activity (p < 0.01), circulating atrial natriuretic peptide, renin- and aldosterone-levels were significantly higher in the ISO-treated group as compared tothe control group (p < 0.05). ISO-treated hearts displayed morphological alterations such as myocyte necrosis, cellular reaction and fibrosis. RAM-treated hearts revealed the same infarct-like lesions but at a lower grade. In summary, a highly reproducible model of chronic heart failure was established. Hemodynamic measurements displayed a typical characteristic for advanced heart failure in the ISO-group. Blockade of the renin-angiotensinsystem (RAS) attenuated the observed changes indicating that the RAS may be involved in the development of catecholamine-induced congestive heart failure.
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