الفهرس 
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Abstract
Cardiovascular disease is the most common leading cause of mortality worldwide. Acute myocardial infarction is the most severe manifestation of cardiovascular disease. The pathophysiology of MI comprises different mechanisms in which RAS play an effective role. The RAS are more complex than previously known. It could be considered that Ang II is a ‘devil’ while Ang (1–7) is an angel as regard to their effects on the heart. The cardioprotective effects of Ang (1–7) include vasorelaxation of the coronary vessels, prevention of arrhythmia, inhibition of cardiac remodeling and cardiomyocytes apoptosis, inhibition of sympathetic activity, and prevention of inflammation. The cardioprotective effect of Ang (1–7) is thought to be mediated by NO and PGs. In the present study we aimed to investigate the possible cardioprotective effect of Ang-(1-7) Also, possible role of NO and PGs in this probable cardioprotective effect of Ang- (1-7) was studied through evaluation of cardiac enzyme, lipid profile, ECG changes, caspase 3 expression, cardiomyocyte hypertrophy and histopathological changes in rat model of isoprenaline induced MI. Forty eight adult male Sprague Dawely rats were allocated into six groups: 1) group I(control): normal rats, 2) group II (ISO): received isoprenaline (150 mg/kg subcutaneously) for 2 successive days with 24 hours interval 3) group III (ISO+Ang 1-7): received isoprenaline for 2 days followed by administration of Ang 1-7 (576µg/kg/day )subcutaneously for 6 days, 4) group IV (ISO- + Ang (1-7)+ L NAME): received isoprenaline for 2 days followed by Ang (1-7) the same dose and L NAME in the drinking water (80 mg/l) for 6days 5) group V (ISO + Ang (1-7) +Indomethacin): received isoprenaline for 2 days followed by administration of Ang 1-7 the same dose and Indomethacin 5 mg/kg/day IP for 6days 6)group VI (ISO+ Ang (1-7)+Indomethacin+ L NAME): received isoprenaline for 2 days followed by administration of Ang (1-7), Indomethacin and L NAME in the same doses for 6 days.The results of the present study were analyzed and the following conclusions were concluded:The high dose of ISO induces myocardial damage similar to that occurs in acute MI. This finding ensured by significant increase in the level of cardiac enzymes (CK-MB, LDH, and AST) as well as lipid profile changes (decreased level of HDL-CL with increased level of total cholesterol, TGs, and LDL-CL). 2.Treatment with Ang1-7 resulted in protection of the heart against ISO induced MI in rats. This was ensured by improvement in all studied parameters as significant decrease in the level of cardiac enzymes (CK-MB, LDH, AST and ALT), improved lipid profile(increased level of HDL-CL with decreased level of total cholesterol, TGs, and LDL-CL), improved pathological changes of MI, decreased hypertrophied cardiomyocytes, and decreased expression of caspase 3..Synchronous treatment with Ang1-7 and LNAME decreased the cardioprotective effect of Ang1-7 against ISO induced MI in rats.4.Synchronous treatment with Ang1-7 and indomethacin decreased the cardioprotective effect of Ang1-7 against ISO induced MI in rats.Cardioprotective effects of Ang1-7 is mediated mainly by NO and PGs