To determine whether sevoflurane, like isoflurane, protects against consequences of prolonged coronary artery occlusion, Toller et al.  assigned 75 dogs to one of seven experimental groups. All dogs were anesthetized with barbiturates, intubated, ventilated, and instrumented for measurement of aortic and left ventricular pressures and maximum rate of increase of left ventricular pressure (+dP/dtmax). They first underwent a 60-min left anterior descending coronary artery occlusion, followed by 3 h of reperfusion. In four experiments designed to test whether sevoflurane reduces myocardial infarct size by adenosine triphosphate–sensitive potassium channel activation, dogs received either intravenous drug vehicle (50% polyethylene glycol and 50% ethyl alcohol) or adenosine triphosphate–sensitive potassium channel antagonist glyburide in the presence or absence of a 30-min administration of 1 minimum alveolar concentration end-tidal concentration of sevoflurane.

Another set of experiments was designed to determine whether sevoflurane is associated with an acute memory phase and whether it reduces the time threshold to ischemic preconditioning. For these additional studies, sevoflurane was either discontinued 30 min (memory) before the 60-min left anterior descending occlusion, or a 2-min left anterior descending occlusion as an ischemic preconditioning stimulus was used with or without subsequent sevoflurane (with memory) pretreatment.

At the end of each experiment, regional myocardial perfusion was measured with radioactive microspheres, and infarct size was measured with triphenyltetrazolium staining. Vehicle and glyburide had equivalent effects on myocardial infarct size. Sevoflurane significantly decreased infarct size, an effect that was abolished by glyburide. Discontinuing sevoflurane 30 min before the prolonged left anterior descending occlusion did not afford myocardial protection, but sevoflurane enhanced the effects of the brief ischemic stimulus and reduced infarct size.