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目的:研究血管紧张素Ⅱ受体拮抗剂缬沙坦和新型血管紧张素转化酶抑制剂福辛普利对心肌肥厚的影响.方法:SD大鼠ip去甲肾上腺素1.5 mg·kg~(-1)·d~(-1)×15 d,造成心肌肥厚模型.缬沙坦ig 15 mg· kg~(-1)·d~(-1)×15 d,福辛普利ig 30 mg·kg~(-1)·d~(-1)×15 d.测量心重指数,心肌胶原含量,肌球蛋白ATP酶及细胞膜和线粒体Na~+,K~+-ATP酶,Ca~(2+)-ATP酶的活性,并检测此模型中心肌细胞的凋亡水平.结果:缬沙坦和福辛普利均能阻止心肌肥厚的发生,减少胶原合成,提高肌球蛋白ATP酶及细胞膜和线粒体Na~+,K~+-ATP酶、Ca~(2+)-ATP酶的活力,抑制心肌细胞的凋亡.结论:缬沙坦和福辛普利可防止儿茶酚胺诱导的心肌重塑,心肌细胞凋亡可能在儿茶酚胺诱导的心肌重塑中起重要作用.
Objective: To investigate the effects of valsartan, an angiotensin Ⅱ receptor antagonist, and fosinopril, a novel angiotensin converting enzyme inhibitor, on cardiac hypertrophy.Methods: ip norepinephrine 1.5 mg · kg ~ (-1) 1) · d ~ (-1) × 15 d, resulting in the model of myocardial hypertrophy.Valsartan ig 15 mg · kg -1 · d -1 × 15 d, fosinopril ig 30 mg · kg -1 · d -1, kg ~ (-1) · d ~ (-1) × 15d, the cardiac index, myocardial collagen content, myosin ATPase, Na +, K + -ATPase, Ca 2+ ) -ATPase activity and the level of apoptosis of cardiomyocytes in this model.Results Valsartan and fosinopril could prevent cardiac hypertrophy, reduce collagen synthesis, increase myosin ATPase and cell membrane and Mitochondrial Na ~ +, K ~ + -ATPase, Ca ~ (2 +) - ATPase activity, inhibit cardiomyocyte apoptosis.Conclusion: Valsartan and fosinopril can prevent catecholamine-induced myocardial remodeling, Cardiomyocyte apoptosis may play an important role in catecholamine-induced myocardial remodeling.