Shereen M. Samir, Mahmoud Elalfy, Eman Mohamad El Nashar, Mansour A. Alghamdi, Eman Hamza, Mohamed Saad Serria, and Mona G. Elhadidy. Korean J Physiol Pharmacol 2021;25:341-54. https://doi.org/10.4196/kjpp.2021.25.4.341

Background: Myocardial infarction (MI) is a necrosis of cardiomyocytes due to prolonged myocardial ischemia, the injured heart characterized by activation of the renin-angiotensin system (RAS). The cardiac effect of enalapril and losartan was determined in Isoproterenol (ISO) induced MI rat model. Methods: Twenty-four adult male rats were randomly divided into four groups of six rats each, Group-I- Normal rats, group II-ISO (150 mg/kg once daily for two successive days), Group-III-Enalapril pretreated, and Group-IV-Losartan pretreated rats. Enalapril and losartan were given by gavage at dose 10 mg/kg and 30 mg/kg, respectively the treatment started 3 days before ISO injection and continue for 5 days after 2nd ISO dose. Results: ISO-induced group showed significant increase in the cardiac enzymes lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB), accompanied with marked decrease in the catalase (CAT) and glutathione (GSH) and Bcl2. Both enalapril and losartan induce significant reduction of cardiac enzymes and systolic blood pressure and improve oxidative stress which confirmed by reduction of Malondialdehyde (MDA) and elevation of antioxidant enzymes and markedly upregulated the expression of Bcl2, Nrf-2 and HO-1. Moreover, Both enalapril and losartan reversed the histopathological changes induce by ISO and thus exhibits its cardioprotective activity. Moreover, treated rats partially minimize myocardial necrosis and interstitial edema. In conclusion: Enalapril and losartan ameliorates oxidative stress, inhibit apoptosis and improve cardiac dysfunction by alteration of Nrf2/HO-1 signaling pathway. It also reduces cardiac enzymes and improves blood pressure without affection of serum K on short term therapy in MI.

The aim of this study was to find out the possible role nitric oxide (NO) due to its nature as a second messenger in stress responses in the cardioprotective effect of the abscisic acid (ABA) in isoproterenol (ISO) -induced myocardial infarction in rats. Material and method: Thirty male rats distributed into: normal control group, myocardial infarction (MI) group, and MI group treated with ABA for one week. The cardiac effect of ABA on ISO-induced MI was evaluated by ECG, measuring mean arterial pressure, markers of heart injury in serum, levels of lipid peroxidation, and antioxidants in heart tissue, observing pathological changes of tissue, and indirect detection of NO was performed. Results: Compared with the MI group, it was found that ABA could ameliorated ISO-induced disturbances in the ECG pattern and in mean arterial pressure. Moreover, the concentration of creatine kinase MB (CK-MB), lactate dehydrogenase (LDH), troponinI (CTn-I), nitrite and nitrate in the serum all decreased in the MI+ABA group. The activities of catalase (CAT), and the content of reduced glutathione (GSH) in heart increased, on the contrary, the content of malondialdehyde (MDA) and iNOS was decreased. In addition, the histopathologic examination showed that pathological changes in the myocardium that was observed in the MI group, was reduced in the group treated with ABA. Conclusion: ABA protected myocardium against damage caused by an ISO through inhibition of lipid peroxidation, prevent the cytotoxic actions of the excessive NO release, and restored near normal architecture and function of myocardial.