ATP sparing effect of isoflurane during ischaemia and reperfusion of the canine heart

Abstract

Sustained dysfunction of myocardial contractility after short periods of coronary artery occlusion and reperfusion has been termed "stunned myocardium". Isoflurane may improve the recovery of regional myocardial contractility in stunned myocardium. The purpose of the present study was to determine if isoflurane prevents depletion of high energy phosphates after myocardial ischaemia-reperfusion and if the reduction in cardiac work during isoflurane anaesthesia contributes to the preservation of high energy phosphate metabolism in an acute canine model. Mongrel dogs were allocated to one of three groups: controls, anaesthetized with urethane and chloralose; ISO group, isoflurane administered before ischaemia; and ISOc group, heart rate and mean arterial pressure controlled to approximately match baseline values. The left anterior descending (LAD) coronary artery was occluded for 15 min and then reperfused for 60 min during 1.5% end-tidal isoflurane anaesthesia. Full thickness samples of myocardium were obtained from the reperfused area (supplied by the LAD) and the non-ischaemic area (supplied by the left circumflex coronary artery). The concentrations of adenosine monophosphate (AMP), adenosine diphosphate (ADP), adenosine triphosphate (ATP), creatine phosphate (CP) and lactate in the endocardial portion of the myocardium were measured. Arterial pressure, aortic flow in the ascending aorta and rate-pressure product decreased significantly after isoflurane. Although the concentration of ATP of the reperfused area in the control group showed a significant reduction 60 min after reperfusion, the ISO and ISOc groups had significantly greater concentrations. Isoflurane anaesthesia maintained myocardial high energy phosphate metabolism in reperfused myocardium. We conclude that the reduction in cardiac work played only a minor role in the ATP-sparing effect of isoflurane.