Effect of Isoproterenol on Tissue Defense Enzymes, Hemodynamic and Left Ventricular Contractile Function in Rats

Abstract

Present study investigated the effects of isoproterenol-induced oxidative stress on hemodynamic and ventricular functions in rats. Subcutaneous injections of isoproterenol (85 mg/kg for two consecutive days at 24 h interval) significantly decreased myocardial antioxidant enzymes; superoxide dismutase, catalase and glutathione peroxidase in heart. Isoproterenol-induced oxidative stress was also evidenced by significant depletion of reduced glutathione and increased formation of lipid peroxidation product, thiobarbituric acid reactive substances along with depletion of myocyte injury specific marker enzymes; creatine phosphokinase isoenzyme and lactate dehydrogenase. The deleterious outcome of oxidative stress on hemodyanmic parameters and ventricular function were further evidenced by decreased systolic, diastolic and mean arterial blood pressure, heart rate, ventricular contractility; [(?)LVdP/dt] and relaxation; [(-)LVdP/dt], along with an increased left ventricular end diastolic pressure (LVEDP). Subsequent to changes in heart rate and arterial pressure, isoproterenol also decreased rate pressure product. Present study findings clearly demonstrate the detrimental outcome of isoproterenol induced-oxidative stress on cardiac function and tissue antioxidant defense and substantiate its suitability as an animal model for the evaluation of cardioprotective agents.

Protective effects of low‐dose rosuvastatin on isoproterenol‐induced chronic heart failure in rats by regulation of DDAH‐ADMA‐NO pathway

“…However, rosuvastatin (5 mg/kg) significantly alleviated the pathophysiological and morphologic changes including cardiac myocyte hypertrophy, inflammatory cell infiltration, interstitial fibrosis which strongly demonstrated the protective effect of rosuvastatin on ventricular remodeling and hypertrophy in isoproterenol‐induced heart failure rats. The changes of LVSP, LVdP/dt max and LVdP/dt min reflected an overall dysfunction between myocardial contractility and relaxation . Present investigation demonstrated that treatment with 5 mg/kg isoproterenol for 7 days caused significant changes in levels of LVSP, LVdP/dt max , SAP, MAP, HR and LVdP/dt min in rats, which were in line with previous research results .…”

Inhibition of TGF-β by a novel PPAR-γ agonist, chrysin, salvages β-receptor stimulated myocardial injury in rats through MAPKs-dependent mechanism

“…The myocardial damage produced by isoproterenol is irreversible in nature and occurs via free radical generation due to auto-oxidation and positive inotropic and chronotropic effect. Since hemodynamic, ventricular, biochemical, morphological, and histopathological changes following high dose isoproterenol administration in rats resemble closely to those occurring in patients with myocardial infarction, the isoproterenol-induced MI serves as a well-standardized model to study the beneficial effects and mechanism of many drugs [ 19 , 21 - 23 ]. As anticipated, in the present study, isoproterenol administered rats showed hemodynamic and ventricular dysfunction as evident by decreased contractility and relaxability and elevated preload as compared to sham group.…”

Dietary Phenolic Acids ofMacrotyloma uniflorum(Horse Gram) Protect the Rat Heart Against Isoproterenol-Induced Myocardial Infarction

“…Reduction in arterial pressure values, viz., systolic blood pressure, diastolic blood pressure and MABP against an increasing HR indicates deranged sympathetic and parasympathetic inputs to the heart. It is possible that a deteriorating myocardial contractility following ISO administration might be responsible for a significant fall in MABP, a marker of afterload (Ojha et al ., ). Similarly, a deterioration in myocardial relaxation followed by ISO administration is responsible for an increase in LVEDP that is a surrogate marker of preload.…”