Cardioprotective Eflects of Propofol and Sevoflurane in Ischemic and Reperfused Rat Hearts

Background: Sodium ionhydrogen ion (Na+-H+) exchange inhibitors are effective cardioprotective agents. The N+-H+ exchange inhibitor HOE 642 (cariporide) has undergone clinical trials in acute coronary syndromes, including bypass surgery. F'ropofol and sevoflurane are also cardioprotective v i a unknown mechanisms. The authors investigated the interaction between propofol and HOE 642 in the ischemic reperfused rat heart and studied the role of adenosine triphosphate-sensitive potassium (KAT,,) channels in the myocardial protection associated with propofol and sevoflurane. Methods: Isolated rat hearts were perfused by the Iangendorff method at a constant flow rate, and left ventricular function and coronary pressures were assessed using standard methods. Energy metabolites were also determined. To assess the role of KAN channels, hearts were pretreated with the KAlp blocker @wide (10 p ~ ) . Hearts were then exposed to either control buffer or buffer containing HOE 642 (5 p ~ ) , propofol(35 p ~ ) , sevoflurane (2.15 vol0/o), the KAw opener pinacidil(1 p ~ ) , or the combination of propofol and HOE 642. Each heart was then subjected to 1 h of global ischemia followed by 1 h of reperfusion. Results: Hearts treated with propofol, sevoflurane, pinacidil, or HOE 642 showed significantly higher recovery of left ventricular developed pressure and reduced end-diastolic pressures compared with controls. The combination of propofol and HOE 642 provided superior protection toward the end of