Post-infarct morphine treatment reduces apoptosis and myofibroblast density in a rat model of cardiac ischemia-reperfusion.

Following myocardial ischemia, the cardiac tissue undergoes both, physiological and pathological changes to compensate the initial loss of function. Long-term continuous adjustments often take a drastic picture indicated by deteriorated ventricular function. Morphine is commonly used for rescuing patients suffering a heart attack. Recent results from our laboratory showed the anti-remodeling potential of morphine. Here, we explored the effect of morphine treatment on gelatinolytic activity, apoptosis and myofibroblast density. The male Sprague - Dawley rats underwent ischemia via ligation of left anterior descending coronary artery and received morphine (3 mg/kg; i.p.) for five consecutive days. Seven days post-MI, morphine led to significant reduction in MMP - 2 activity, apoptotic cell death and fibroblast density. Morphine also reduced MI-induced rise in serum pro-oxidant antioxidant balance and nitrite levels on day 28th following the surgery. These results provide mechanistic insight for morphine - induced anti-remodeling effects.