Sevoflurane and isoflurane protect the reperfused guinea pig heart by reducing postischemic adhesion of polymorphonuclear neutrophils

Background: Polymorphonuclear neutrophils (PMNs) contribute to reperfusion injury. Because volatile anesthetics can reduce PMN adhesion in the reperfu sed, nonworking heart, the authors analyzed whether this action of volatile anesthetics affects cardiac performance after ischemia and reperfusion and further clarified the underlying mechanism. Methods: Isolated guinea pig hearts perfused with crystalloid buffer and pe rforming pressure-volume work were used. Hearts were subjected to 15 min gl obal ischemia and 20 min reperfusion. In the intervention groups an intraco ronary bolus of 3 x 10(6) PMNs was applied in the second min of reperfusion , either in the absence or presence of 0.5 or 1 minimum alveolar concentrat ion sevoflurane or isoflurane. The number of sequestered PMNs was calculate d from the difference between coronary input and output (coronary effluent) of PMNs. Performance of external heart work, determined pre- and postische mically, served as criterion for recovery of myocardial function. Additiona lly, the expression of the integrin CD11b on the cell surface of PMN was me asured before and after coronary passage. Results: Injection of PMN in the reperfusion phase, but not under nonischem ic conditions, reduced recovery of external heart work significantly (from 55 +/- 7% to 19 +/- 11%). Addition of sevoflurane or isoflurane in concentr ations of 0.5 and 1 minimum alveolar concentration to the perfusate reduced postischemic PMN adhesion from 36 +/- 8% to basal values (20 +/- 7%) and p revented decline of cardiac function. CD11b expression on PMNs increased si gnificantly during postischemic coronary passage under control conditions. Again, both anesthetics in both concentrations inhibited that activation. Conclusions Volatile anesthetics reduce PMN adhesion in the reperfused coro nary system and thereby preserve cardiac function. Reduced expression of th e adhesion molecule CD11b on PMNs in the presence of sevoflurane or isoflur ane is, at least in part, responsible for the cardioprotective effect.