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.