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[Long-term effects of TCV116 on cardiac function changes after myocardial infarction].

Ze‐Wei Tao, Yuanwei Wang, Yao Wang

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Abstract

OBJECTIVE: To investigate the long-term effects of TCV116 (candesartan cilexetil) on cardiac function changes after myocardial infarction. METHODS: Myocardial infarction (MI) was induced by ligation of the left anterior descending coronary artery in rats. One week after the surgical performance,the surviving rats were randomly assigned to the following treatment groups: (1) MI rats with no therapy; (2) MI rats treated with TCV116 2 mg/kg per day; (3) Sham-operated control and (4) Sham-operated rats treated with TCV116 2 mg/kg per day. At 22 weeks, left ventricular function and cardiac histomorphometric parameters were measured, mRNA expression of cardiac genes such as beta myosin heavy chain, B-type natriuretic peptide, transforming growth factor beta1, collagen I and III quantified, and survival rates calculated. RESULTS: Treatment with TCV116 significantly improved LV function, suppressed mRNA expression of cardiac genes,and extended the survival period compared with MI rats with no therapy (P<0.05). CONCLUSION: Treatment with long-term angiotensin II type 1 receptor blocker may improve LV function and prolong the survival of rats after MI.

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OBJECTIVE: To investigate the long-term effects of TCV116 (candesartan cilexetil) on cardiac function changes after myocardial infarction. METHODS: Myocardial infarction (MI) was induced by ligation of the left anterior descending coronary artery in rats. One week after the surgical performance,the surviving rats were randomly assigned to the following treatment groups: (1) MI rats with no therapy; (2) MI rats treated with TCV116 2 mg/kg per day; (3) Sham-operated control and (4) Sham-operated rats treated with TCV116 2 mg/kg per day. At 22 weeks, left ventricular function and cardiac histomorphometric parameters were measured, mRNA expression of cardiac genes such as beta myosin heavy chain, B-type natriuretic peptide, transforming growth factor beta1, collagen I and III quantified, and survival rates calculated. RESULTS: Treatment with TCV116 significantly improved LV function, suppressed mRNA expression of cardiac genes,and extended the survival period compared with MI rats with no therapy (P<0.05). CONCLUSION: Treatment with long-term angiotensin II type 1 receptor blocker may improve LV function and prolong the survival of rats after MI.

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Available abstract

OBJECTIVE: To investigate the long-term effects of TCV116 (candesartan cilexetil) on cardiac function changes after myocardial infarction. METHODS: Myocardial infarction (MI) was induced by ligation of the left anterior descending coronary artery in rats. One week after the surgical performance,the surviving rats were randomly assigned to the following treatment groups: (1) MI rats with no therapy; (2) MI rats treated with TCV116 2 mg/kg per day; (3) Sham-operated control and (4) Sham-operated rats treated with TCV116 2 mg/kg per day. At 22 weeks, left ventricular function and cardiac histomorphometric parameters were measured, mRNA expression of cardiac genes such as beta myosin heavy chain, B-type natriuretic peptide, transforming growth factor beta1, collagen I and III quantified, and survival rates calculated. RESULTS: Treatment with TCV116 significantly improved LV function, suppressed mRNA expression of cardiac genes,and extended the survival period compared with MI rats with no therapy (P<0.05). CONCLUSION: Treatment with long-term angiotensin II type 1 receptor blocker may improve LV function and prolong the survival of rats after MI.

Key concepts: Myocardial infarction, Cardiac function curve, Medicine, Internal medicine, Candesartan, Ligation, Cardiology, Left coronary artery

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