Effect of chlorpromazine on myocardial damage in the calcium paradox.
Prevention of myocardial cell death is an important goal in the treatment of myocardial infarction. The potential benefit of chlorpromazine in myocardial injury was assessed in the isolated rabbit heart under conditions of the calcium paradox. A period of 20 min of calcium-free perfusion followed by reintroduction of calcium was associated with myocardial damage, as indicated by severe impairment in left ventricular contractile function and marked loss of protein and enzymes (aspartate aminotransferase) from the myocardium. Chlorpromazine, 15 or 25 mg/kg, was given intravenously 30 min before excision of the heart. Chlorpromazine was associated with significant (p less than 0.05) improvement in left ventricular function, as indicated by larger developed pressure, greater peak positive and negative dP/dt, and lower left ventricular end-diastolic pressures. Chlorpromazine pretreatment was associated with significant (p less than 0.05) reduction in the amount of enzyme and protein lost from the myocardium. Thus, chlorpromazine can reduce the severity of myocardial cell injury.
D000818:Animals; D002118:Calcium / Q000633:toxicity*; D002746:Chlorpromazine / Q000494:pharmacology*; D005260:Female; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D011817:Rabbits
D002118:Calcium; D002746:Chlorpromazine