Effect of isoproterenol on tissue defense enzymes, hemodynamic and left ventricular contractile function in rats.

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.