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首页> 外文期刊>Life sciences >Amlodipine decreases fibrosis and cardiac hypertrophy in spontaneously hypertensive rats: persistent effects after withdrawal.
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Amlodipine decreases fibrosis and cardiac hypertrophy in spontaneously hypertensive rats: persistent effects after withdrawal.

机译：氨氯地平减少自发性高血压大鼠的纤维化和心脏肥大：停药后的持续作用。

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Our objective was to examine the effect of chronic treatment with amlodipine on blood pressure, left ventricular hypertrophy, and fibrosis in spontaneously hypertensive rats and the persistence of such an effect after drug withdrawal. We investigated the effects of treatment with 2, 8 and 20 mg/kg/day of amlodipine given orally for six months and at three months after drug withdrawal. Systolic blood pressure was measured using the tail-cuff method. At the end of the study period, the heart was excised, the left ventricle was isolated, and the left ventricle weight/body weight ratio was calculated as a left ventricular hypertrophy index. Fibrosis, expressed as collagen volume fraction, was evaluated using an automated image-analysis system on sections stained with Sirius red. Age-matched untreated Wistar-Kyoto and SHR were used as normotensive and hypertensive controls, respectively. Systolic blood pressure was reduced in the treated SHR in a dose-dependent way and after amlodipine withdrawal it increased progressively, without reaching the values of the hypertensive controls. Cardiac hypertrophy was reduced by 8 and 20 mg/kg/day amlodipine, but when treatment was withdrawn only the group treated with 8 mg/kg/day maintained significant differences versus the hypertensive controls. All three doses of amlodipine reduced cardiac fibrosis and this regression persisted with the two highest doses after three months without treatment. We concluded that antihypertensive treatment with amlodipine is accompanied by a reduction in left ventricular hypertrophy and regression in collagen deposition. Treatment was more effective in preventing fibrosis than in preventing ventricular hypertrophy after drug withdrawal.
机译：我们的目的是检查氨氯地平对慢性高血压大鼠自发性高血压大鼠血压，左心室肥大和纤维化的长期治疗效果以及停药后这种作用的持久性。我们调查了口服，分别在停药后六个月和三个月内口服2、8和20 mg / kg /天的氨氯地平治疗的效果。使用尾袖法测量收缩压。在研究期结束时，切除心脏，分离左心室，并计算左心室重量/体重比作为左心室肥大指数。使用自动图像分析系统对天狼星红染色的切片进行纤维化，以胶原蛋白的体积分数表示。年龄匹配的未经治疗的Wistar-Kyoto和SHR分别用作血压正常和高血压对照。在治疗的SHR中，收缩压以剂量依赖性方式降低，氨氯地平停药后其逐渐升高，但未达到高血压对照的值。氨氯地平可将心脏肥大降低8和20 mg / kg /天，但是当撤回治疗时，只有8 mg / kg /天的治疗组与高血压对照组相比有显着差异。所有三个剂量的氨氯地平均降低了心脏纤维化，并且在三个月未治疗的情况下，最大的两个剂量持续了这种消退。我们得出的结论是，氨氯地平的降压治疗伴随着左心室肥大的减少和胶原蛋白沉积的降低。停药后，治疗预防纤维化比预防室性肥大更有效。

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