2008Journal of Sun Yat-sen UniversityRequires access

Effects of ACE Inhibitor Ramipril on Apoptosis of Cardiac Myocytes and Ventricular Remodeling in Rats with Myocardial Infarction

Cai An-ping, Sun Yat-sen

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Abstract

【Objective】 To investigate the effects of short-term treatment of Ramipril on the apoptosis of cardiomyocyte and ventricular remodeling; and to explore the modifying effects of Ramipril on the expression of Fas-L mRNA. 【Methods】 Acute myocardial infartion models were produced by ligating left coronary arteries in male Wister rats. The rats with AMI were divided into the group treating with Ramipril and control randomly. Ramipril was given to treatment group at the dose of 2.5 mg / kg each day by gavage. Sham-operated control was performed by opening thorax without ligating left coronary arteries. After 2 weeks, the hemodynamic parameters were measured and plasma angiotensin Ⅱ, heart mass indexes, the apoptotic index of cardiac myocytes and the expression of mRNA level of Fas-L were detected. 【Results】 After treatment with Ramipril for 2 weeks. The LVPmax and ±dp / dt in Ramipril treatment group were higher than that of placebo group (P 0.05) and LVEDP was lower than that of it (P 0.05). The plasma AngⅡ in placebo group was higher than that of sham-operation group (P 0.05). The plasma AngII in Ramipril treatment and sham-operation group was not significantly different (P 0.05). The expression of Fas-L mRNA in placebo group was higher than that of sham-operation group (P 0.05),which was down regatated by Ramipril(P 0.05). The apoptosis index of cardiac myocytes in sham-operated, and Ramipril treatment group were 1.15%, 72.52%, and 34.75%, respectively, indicated the apoptosis was suppressed by Ramipril(P 0.05). 【Conclusion】 After acute myocardial infartion, short-term treatment of Ramipril can inhibit the apoptosis of cardiac myocytes and ventricular remodeling, improve the cardiac function. The mechanism may be partly due to its effects on the expression of Fas-L.

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【Objective】 To investigate the effects of short-term treatment of Ramipril on the apoptosis of cardiomyocyte and ventricular remodeling; and to explore the modifying effects of Ramipril on the expression of Fas-L mRNA. 【Methods】 Acute myocardial infartion models were produced by ligating left coronary arteries in male Wister rats. The rats with AMI were divided into the group treating with Ramipril and control randomly. Ramipril was given to treatment group at the dose of 2.5 mg / kg each day by gavage. Sham-operated control was performed by opening thorax without ligating left coronary arteries. After 2 weeks, the hemodynamic parameters were measured and plasma angiotensin Ⅱ, heart mass indexes, the apoptotic index of cardiac myocytes and the expression of mRNA level of Fas-L were detected. 【Results】 After treatment with Ramipril for 2 weeks. The LVPmax and ±dp / dt in Ramipril treatment group were higher than that of placebo group (P 0.05) and LVEDP was lower than that of it (P 0.05). The plasma AngⅡ in placebo group was higher than that of sham-operation group (P 0.05). The plasma AngII in Ramipril treatment and sham-operation group was not significantly different (P 0.05). The expression of Fas-L mRNA in placebo group was higher than that of sham-operation group (P 0.05),which was down regatated by Ramipril(P 0.05). The apoptosis index of cardiac myocytes in sham-operated, and Ramipril treatment group were 1.15%, 72.52%, and 34.75%, respectively, indicated the apoptosis was suppressed by Ramipril(P 0.05). 【Conclusion】 After acute myocardial infartion, short-term treatment of Ramipril can inhibit the apoptosis of cardiac myocytes and ventricular remodeling, improve the cardiac function. The mechanism may be partly due to its effects on the expression of Fas-L.

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Available abstract

【Objective】 To investigate the effects of short-term treatment of Ramipril on the apoptosis of cardiomyocyte and ventricular remodeling; and to explore the modifying effects of Ramipril on the expression of Fas-L mRNA. 【Methods】 Acute myocardial infartion models were produced by ligating left coronary arteries in male Wister rats. The rats with AMI were divided into the group treating with Ramipril and control randomly. Ramipril was given to treatment group at the dose of 2.5 mg / kg each day by gavage. Sham-operated control was performed by opening thorax without ligating left coronary arteries. After 2 weeks, the hemodynamic parameters were measured and plasma angiotensin Ⅱ, heart mass indexes, the apoptotic index of cardiac myocytes and the expression of mRNA level of Fas-L were detected. 【Results】 After treatment with Ramipril for 2 weeks. The LVPmax and ±dp / dt in Ramipril treatment group were higher than that of placebo group (P 0.05) and LVEDP was lower than that of it (P 0.05). The plasma AngⅡ in placebo group was higher than that of sham-operation group (P 0.05). The plasma AngII in Ramipril treatment and sham-operation group was not significantly different (P 0.05). The expression of Fas-L mRNA in placebo group was higher than that of sham-operation group (P 0.05),which was down regatated by Ramipril(P 0.05). The apoptosis index of cardiac myocytes in sham-operated, and Ramipril treatment group were 1.15%, 72.52%, and 34.75%, respectively, indicated the apoptosis was suppressed by Ramipril(P 0.05). 【Conclusion】 After acute myocardial infartion, short-term treatment of Ramipril can inhibit the apoptosis of cardiac myocytes and ventricular remodeling, improve the cardiac function. The mechanism may be partly due to its effects on the expression of Fas-L.

Key concepts: Ramipril, Medicine, Internal medicine, Preload, Myocardial infarction, Cardiology, Apoptosis, Placebo

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Effects of ACE Inhibitor Ramipril on Apoptosis of Cardiac Myocytes and Ventricular Remodeling in Rats with Myocardial Infarction — Research Paper | ScholarLens