Abstract
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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Bulletin of Egyptian Society for Physiological Sciences
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
