2004Zhonghua xinxueguanbing zazhiRequires access

Effects of angiotensin-(1-7) on prevention of left ventricular remodeling after acute myocardial infarction in rats

Zeng Wu-ta

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Abstract

Objective To assess the effects of angiotensin-(1-7) on prevention of left ventricular(LV) remodeling after acute myocardial infarction(AMI) in rats. Methods Thirty male Sprague Dawley rats surviving AMI, which was achieved by ligating coronary artery, were randomized to AMI control group (15) or angiotensin-(1-7) treatment group (15). Fifteen sham-operated Sprague Dawley rats were selected to serve as non-infarction controls. Two days after surgery, intravenous infusion of angiotensin-(1-7) (25 microgram/kg per hour, for treatment group) or saline (for AMI control and sham-operated groups) was started by minipump. After 4 weeks of treatment, hemodynamic measurement was performed, and left ventricular weight (LVW), ratio of left ventricular weight to body weight (LVW/BW), left ventricular diameter (LVD) and size of MI were determined. Plasma angiotensinⅡand myocardial angiotensinⅡlevels were also measured. Results Compared with sham-operated rats, LVW, LVW/BW, LVD and myocardial angiotensinⅡlevel in AMI control group were significantly increased (all P0.01), while the LV systolic pressure(LVSP), the maximum rising and dropping rates of LV pressure(±dp/dt) in AMI control group were significantly reduced(all P0.01). In contract, compared with AMI control group, LVW/BW and LVD in angiotensin-(1-7) treatment group were significantly decreased (P0.05 or 0.01), while LVSP and ±dp/dt in angiotensin-(1-7) treatment group were significantly increased (all P0.05). There was no significant difference in MI size and myocardial angiotensinⅡlevel between AMI control group and angiotensin-(1-7) treatment group. Conclusion Angiotensin-(1-7) is effective in preventing left ventricular remodeling after AMI in rats.

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Objective To assess the effects of angiotensin-(1-7) on prevention of left ventricular(LV) remodeling after acute myocardial infarction(AMI) in rats. Methods Thirty male Sprague Dawley rats surviving AMI, which was achieved by ligating coronary artery, were randomized to AMI control group (15) or angiotensin-(1-7) treatment group (15). Fifteen sham-operated Sprague Dawley rats were selected to serve as non-infarction controls. Two days after surgery, intravenous infusion of angiotensin-(1-7) (25 microgram/kg per hour, for treatment group) or saline (for AMI control and sham-operated groups) was started by minipump. After 4 weeks of treatment, hemodynamic measurement was performed, and left ventricular weight (LVW), ratio of left ventricular weight to body weight (LVW/BW), left ventricular diameter (LVD) and size of MI were determined. Plasma angiotensinⅡand myocardial angiotensinⅡlevels were also measured. Results Compared with sham-operated rats, LVW, LVW/BW, LVD and myocardial angiotensinⅡlevel in AMI control group were significantly increased (all P0.01), while the LV systolic pressure(LVSP), the maximum rising and dropping rates of LV pressure(±dp/dt) in AMI control group were significantly reduced(all P0.01). In contract, compared with AMI control group, LVW/BW and LVD in angiotensin-(1-7) treatment group were significantly decreased (P0.05 or 0.01), while LVSP and ±dp/dt in angiotensin-(1-7) treatment group were significantly increased (all P0.05). There was no significant difference in MI size and myocardial angiotensinⅡlevel between AMI control group and angiotensin-(1-7) treatment group. Conclusion Angiotensin-(1-7) is effective in preventing left ventricular remodeling after AMI in rats.

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Available abstract

Objective To assess the effects of angiotensin-(1-7) on prevention of left ventricular(LV) remodeling after acute myocardial infarction(AMI) in rats. Methods Thirty male Sprague Dawley rats surviving AMI, which was achieved by ligating coronary artery, were randomized to AMI control group (15) or angiotensin-(1-7) treatment group (15). Fifteen sham-operated Sprague Dawley rats were selected to serve as non-infarction controls. Two days after surgery, intravenous infusion of angiotensin-(1-7) (25 microgram/kg per hour, for treatment group) or saline (for AMI control and sham-operated groups) was started by minipump. After 4 weeks of treatment, hemodynamic measurement was performed, and left ventricular weight (LVW), ratio of left ventricular weight to body weight (LVW/BW), left ventricular diameter (LVD) and size of MI were determined. Plasma angiotensinⅡand myocardial angiotensinⅡlevels were also measured. Results Compared with sham-operated rats, LVW, LVW/BW, LVD and myocardial angiotensinⅡlevel in AMI control group were significantly increased (all P0.01), while the LV systolic pressure(LVSP), the maximum rising and dropping rates of LV pressure(±dp/dt) in AMI control group were significantly reduced(all P0.01). In contract, compared with AMI control group, LVW/BW and LVD in angiotensin-(1-7) treatment group were significantly decreased (P0.05 or 0.01), while LVSP and ±dp/dt in angiotensin-(1-7) treatment group were significantly increased (all P0.05). There was no significant difference in MI size and myocardial angiotensinⅡlevel between AMI control group and angiotensin-(1-7) treatment group. Conclusion Angiotensin-(1-7) is effective in preventing left ventricular remodeling after AMI in rats.

Key concepts: Myocardial infarction, Internal medicine, Cardiology, Angiotensin II, Medicine, Renin–angiotensin system, Saline, Ventricular remodeling

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