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  • Title: Cardioprotective effect of melatonin against isoproterenol induced myocardial infarction in rats: A biochemical, electrocardiographic and histoarchitectural evaluation.
    Author: Patel V, Upaganlawar A, Zalawadia R, Balaraman R.
    Journal: Eur J Pharmacol; 2010 Oct 10; 644(1-3):160-8. PubMed ID: 20624385.
    Abstract:
    The present study was designed to investigate the cardioprotective effect of melatonin against isoproterenol induced myocardial infarction in rats by studying myocyte injury markers, antioxidant defense system, serum and heart lipid profile, inflammatory markers, electrocardiographic and histopathological changes. Male Sprague Dawley (SD) rats were randomly divided into four groups, namely control, melatonin, isoproterenol and melatonin+isoproterenol treated group. Melatonin treatment group received melatonin (10mg/kg/day, i.p.) for 7days. Myocardial infarction in rats was induced by isoproterenol administration (150mg/kg, s.c.) at an interval of 24h on 6th and 7th day. On 8th day ECG, gravimetric, biochemical and histopathological parameters were assessed. Isoproterenol administration showed changes in ECG pattern, including ST-segment elevation (diagnostic of myocardial infarction) increase in the serum levels of cardiac injury markers (creatine kinase-MB, lactate dehydrogenase, aspartate transaminase and alanine transaminase), decreased antioxidant defense system in the heart and altered lipid profile in the serum and heart. Isoproterenol administration also resulted in release of inflammatory markers and neutrophil infiltration along with histopathological changes. Melatonin pre-co-treatment prevented almost all the parameters of isoproterenol induced myocardial infarction in rats. The above finding was confirmed by the histopathological examination. In the baseline group (melatonin alone treated group) no significant change was observed. Results of the present study suggest that melatonin has a significant effect on the protection of the heart against isoproterenol induced myocardial infarction through maintaining endogenous antioxidant enzyme activities.
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