Effects of halothane, enflurane, isoflurane, sevoflurane and desflurane onmyocardial reperfusion injury in the isolated rat heart

A specific action against myocardial reperfusion injury of the oxygen parad ox type was recently characterized for halothane after anoxic perfusion in isolated rat hearts and isolated cardiomyocytes. In this study, we have cha racterized the protective effects of the clinically available inhalation an aesthetics during reperfusion after ischaemia. In isolated, isovolumically beating rat hearts perfused at a constant flow (10 mi min(-1), PO2 80 kPa) and paced at 350 beat min(-1), we determined left ventricular developed pre ssure (LVDP) and release of creatine kinase (CKR) as indices of myocardial performance and cellular injury, respectively. Seven control hearts underwe nt 30 min of no-flow ischaemia and 1 h of reperfusion. In the treatment gro ups, halothane, enflurane, isoflurane, sevoflurane or desflurane (each grou p n=6) was added to the perfusion medium for the first 30 min of reperfusio n at a concentration corresponding to 1.5 MAC in the rat. In the control gr oup, cellular injury occurred at early reperfusion (peak CKR 283 (SEM 57) i u litre(-1) at 10 min of reperfusion). Peak CKR to the coronary venous effl uent was attenuated by all anaesthetics (halothane group 156 (45), enfluran e group 134 (20), sevoflurane group 132 (20), desflurane group 159 (25) iu litre(-1); each P<0.05). Isoflurane did not differ from controls (303 (53) iu litre(-1); P=0.5). In the sevoflurane group, there was a delayed peak CK R after discontinuation of the anaesthetic at 30 min of reperfusion (260 (3 4) iu litre(-1)). Functional recovery was improved by all anaesthetics, but was seen much earlier with desflurane (LVDP 28 (3)% of baseline at 5 min r eperfusion compared with halothane (6 (1)%), enflurane (11(3)%), isoflurane (9 (6)%), sevoflurane (10(2)%) and controls (3 (1)% of baseline)). At 30 m in of reperfusion, recovery of LVDP was improved to a similar extent by all anaesthetics (halothane 30 (9)%, enflurane 36 (9)%, isoflurane 33 (5)%, se voflurane 30 (5)%, desflurane 36 (4)% of baseline values) compared with con trols (13 (5)%; each P<0.05). All inhalation anaesthetics protected against myocardial reperfusion injury, but showed differences in attenuation of ce llular injury and functional recovery. These differences may suggest differ ent protective mechanisms.