title: Cardioprotective effect of fluvastatin on isoproterenol-induced myocardial infarction in rat.
abstract: The present study was designed to investigate whether fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, would attenuate the acute myocardial infarction in isoproterenol-treated rat model via maintaining activities of endogenous antioxidant enzymes. Hemodynamic and electrocardiograph parameters were monitored and recorded continuously, cardiac marker enzymes and antioxidative parameters of plasma and heart tissues were measured, and histopathological examination of heart tissues was performed. Isoproterenol-treated rats showed lower of left-ventricular systolic pressure (LVSP), maximum (LVdP/dtmax) and minimum rate of developed left ventricular pressure (LVdP/dtmin), and higher of left ventricular end-diastolic pressure (LVEDP), in addition, a significant rise in ST-segment and increase in content of lactate dehydrogenase, glutamic oxalacetic transaminase, creatine kinase and malondialdehyde, as well as fall in activities of glutathione peroxidase, superoxide dismutase and catalase were observed. Oral administration of fluvastatin (5, 10 and 20 mg/kg, respectively) significantly prevented almost all the parameters of isoproterenol-induced heart failure and myocardial injury that mentioned above. The protective role of fluvastatin on isoproterenol-induced myocardial damage was further confirmed by histopathological examination. There was no significant change in heart rate in all experimental groups. Compared with control group, any indexes in sham rats treated with fluvastatin (20 mg/kg) alone were unaltered (all P>0.05). Our results suggest that fluvastatin has a significant effect on the protection of heart against isoproterenol-induced myocardial infarction through maintaining endogenous antioxidant enzyme activities.
authors.affiliation: Department of Pharmacology, School of Basic Medical Science, Ningxia Medical College, 692 Shengli Street, Yinchuan, Ningxia, 750004, PR China.
authors.forename: Ru
authors.initials: R
authors.lastname: Zhou
authors.forename: Qingbin
authors.initials: Q
authors.lastname: Xu
authors.forename: Ping
authors.initials: P
authors.lastname: Zheng
authors.forename: Lin
authors.initials: L
authors.lastname: Yan
authors.forename: Jie
authors.initials: J
authors.lastname: Zheng
authors.forename: Guidong
authors.initials: G
authors.lastname: Dai
mesh_terms: D000318:Adrenergic beta-Agonists; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D004562:Electrocardiography / Q000187:drug effects; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology*; D000077340:Fluvastatin; D006334:Heart Function Tests; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D007150:Immunohistochemistry; D007211:Indoles / Q000494:pharmacology*; D007545:Isoproterenol; D008297:Male; D009203:Myocardial Infarction / Q000139:chemically induced / Q000517:prevention & control*; D009206:Myocardium / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000318:Adrenergic beta-Agonists; D000975:Antioxidants; D005229:Fatty Acids, Monounsaturated; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D000077340:Fluvastatin; D007545:Isoproterenol