Melatonin reduces cardiac remodeling and improves survival in rats with isoproterenol-induced heart failure
Abstrakt
Melatonin was previously shown to reduce blood pressure and left ventricular remodeling in several models of experimental heart damage. Isoproterenol-induced heart failure with hypertrophy of the left and right ventricles, lowered systolic blood pressure and elevated pulmonary congestion.
Fibrotic rebuilding was accompanied by alterations of tubulin level in the LV and oxidative stress development. Melatonin failed to reduce the weight of the LV or RV; however, it curtailed the weight of the lungs and attenuated the decline in SBP.
Moreover, melatonin decreased the level of oxidative stress and insoluble and total collagen. Most importantly, melatonin reduced mortality and prolonged the average survival time.
In conclusion, melatonin exerts cardioprotective effects and improves outcome in a model of isoproterenol-induced heart damage.