Observation on activation of mitochondrial calcium activated potassium channel to potentiate the cardioplegic solution of cardioplegia

Objective: To investigate whether the activation of mitochondrial calcium activated potassium channel (mitoKCa) can potentiate the cardioplegic solution of modified St.Thomas cardioplegia in isolated rat hearts subjected to ischemia and reperfusion.Methods: The isolated perfused rat hearts were subjected to 30 min global ischemia and 120 min reperfusion.The rats were divided into four groups:ischemia and reperfusion group;modified St.Thomas cardioplegia group;modified St.Thomas cardioplegia+NS1619 group and modified St.Thomas cardioplegia+NS1619+Paxilline group.The ventricular hemodynamic parameters,lactate dehydrogenase (LDH) release from coronary flow during reperfusion and myocardial water content were measured.Results: In contrast to ischemia and reperfusion group,modified St.Thomas cardioplegia decreased the elevation of left ventricular end-diastolic pressure (P<0.01),increased rate-pressure product (P<0.01) and coronary flow (P<0.05),reduced LDH release (P<0.01) and mycardical water content (P<0.01).Administration of NS1619,an activator of mitoKCa channel potentiated the role of modified St.Thomas cardioplegia,LDH release and mycardical water content further decreased (P<0.01),and the improvement of left ventricular performance was more significant (P<0.01).The inhibitor of mitoKCa channel Paxilline abolished the role of NS 1619 (P<0.05-P<0.01).Conclusions: These findings indicate that activation of mitochondrial calcium activated potassium channel can potentiate the cardioplegic solution of cardioplegia.