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Effects of Perindopril on Left Ventricular Remodeling and Aortic Regurgitation in Rats Assessed by EchocardiographySecond Department of Internal Medicine, Kagawa Medical University, Kagawa, Japan.
Second Department of Internal Medicine, Kagawa Medical University, Kagawa, Japan.
Second Department of Internal Medicine, Kagawa Medical University, Kagawa, Japan.
Department of Pharmacology, Kagawa Medical University, Kagawa, Japan.
Department of Pharmacology, Kagawa Medical University, Kagawa, Japan.
Second Department of Internal Medicine, Kagawa Medical University, Kagawa, Japan. This study investigated the effect of the angiotensin-converting enzyme (ACE) inhibitor perindopril on left ventricular (LV) remodeling and cardiac function in rats with aortic regurgitation (AR). Twenty male Sprague-Dawley rats in which AR was produced by closed-chest aortic valve puncture were divided into untreated and perindopril-treated (5 mg/kg/day) rats. Ten control rats were sham-operated. Blood pressure, body weight, and echocardiographic recordings were followed every 2 weeks for a period of 12 weeks. LV dimension (LVD) and fractional shortening (FS) were calculated. The heart was finally excised for weight, hydroxyproline measurements, and histopathology. At 12 weeks, end- diastolic LVD increased in untreated rats (10.8 ±0.2 mm) but did not dilate in treated rats (9.6 ± 0.3 mm, p < 0.01 vs untreated rats). FS decreased from 6 weeks in untreated rats (27.3 ±0.9% at 12 weeks), but did not change in treated rats (33.8 ±0.5%, p < 0.001). The ratio of LV weight to body weight in untreated rats (2.62 ±0.11 mg/g, p < 0.05) was higher than in sham-operated rats (1.52 ±0.02 mg/g) and than in treated rats (1.95 ±0.07 mg/g). Interstitial collagen accumulation histopathologically increased in untreated rats and was inhibited in treated rats. LV collagen of untreated rats (1.46 ±0.08 mg/100 mg, p = 0.03) was higher than those of treated (1.08 ±0.09 mg/100 mg) and sham-operated rats (1.06 ±0.14 mg/100 mg). Perindopril inhibited LV remodeling induced by volume overload and preserved LV function in AR rats.
Angiology, Vol. 51, No. 11,
943-952 (2000) |
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