Calmodulin antagonist reduces release of malondialdehyde from isolated ischemic/reperfused rat heart.

To investigate the role of Ca-calmodulin complex in the development of myocardial injury caused by ischemia and reperfusion, an isolated working rat hearts were subjected to ischemia/reperfusion with and without calmodulin antagonist, trifluoperazine (TFP 5 x 10(-7)M) in the perfusion medium. In TFP-treated hearts postischemic recovery of hemodynamic function was markedly improved and the release of LDH and malondialdehyde (MDA) significantly reduced as compared with control hearts. It is concluded that: 1) calmodulin-dependent mechanism seems to be involved in peroxidative injury of cellular membranes, 2) cardioprotective effect of TFP results at least in part from prevention of membrane damage caused by lipid peroxidation.