الفهرس 
Introduction
Myocardial InfarctionOnly 14 pages are availabe for public view
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Abstract
Coronary heart disease (CHD) remains the leading cause of morbidity and mortality worldwide, despite the significant advances that have been achieved in the treatment and understanding of its pathogenesis (Yusuf & Ounpuu, 2003). Myocardial infarction (MI) is the main cause of death from CHD, and results from prolonged myocardial ischemia with necrosis of myocytes due to interruption of blood supply to an area The aim of this study is to: The aim of the present study is to investigate the effects of: Isoproterenol induced myocardial injury on the cardiac functions and morphology, ECG parameters, oxidative stress markers, and expression of connexin-43 and heat shock protein 70 in myocardial muscles HO-1 induction on the cardiac functions and morphology, ECG changes, oxidative stress markers, and expression of connexin-43 and heat shock protein 70 in myocardial muscles in ISO-induced myocardial infarction Materials & methods: study involved Thirty-two adult male Sprague Dawely rats divided in four groups eight rats in each. The rats of group Ⅰ served as normal control. group Ⅱ received Isoproterenol (ISO) 150 mg/kg body weight intraperitoneally for 2 successive days at (day 0 and day1) to induce myocardial infarction. group Ⅲ a Vehicle group, received (ISO) as group II and trizma (5 mg/ kg) intraperitoneal injection 2 days before injection of ISO, with ISO at day 0 and at day 2 after ISO injections. group Ⅳ (Cobalt protoporphyrin group) received ISO as group II and CoPP (5 mg/ kg) dissolved in Trizma intraperitoneal injection (5 mg/ kg) 2 days before injection of ISO, with ISO at day 0 and at day 2 after ISO injections. Before induction of MI, basal ECG and blood samples were collected for biochemical analysis (CK-MB and LDH) then it was repeated 24 hours after second ISO injection and finally at day 5 before sacrifice. After rat sacrifice, the cardiac tissues were collected for oxidative stress, real time PCR for HO-1 mRNA expression and histopathological and immunostaining studies (Cx-43 and Hsp70). Recommendations: Isoproterenol administration at a dose of 150 mg/Kg caused marked deteriorations in cardiac functions and morphology, which was associated with signs of myocardial infarction in ECG, reduction of myocardial antioxidants, Connexin-43 proteins and upregulation of heat shock protein 70. Upregulation of heme oxygenase-1 by Cobalt protoporphyrin IX had a cardioprotective action against isoproterenol induced myocardial injury, which might be due to increased myocardial antioxidant capacity and upregulation of gap junction proteins (Connexin-43) and heat shock protein 70.