EFFECT OF HALOTHANE ON MYOCARDIAL REOXYGENATION INJURY IN THE ISOLATED RAT-HEART

Several studies have reported a protective effect of halothane on myoc ardial injury in an ischaemia-reperfusion situation. It is unclear if the protection is a result of the haemodynamic effects of halothane or if halothane has a specific action on ischaemia or reperfusion pathom echanisms. To examine this question, we have used an isolated rat hear t model where heart rate (300 beat min(-1)), ventricular volume and co ronary flow are constant. Left ventricular developed pressure (LVDP) a nd release of creatine kinase (CK) were measured as variables of myoca rdial performance and cellular injury, respectively. Five control hear ts were subjected to 35 min of low-flow (2 ml min(-1)) anoxic and subs trate-free perfusion and were then perfused for 1 h with the oxygenate d buffer. In the treatment groups, halothane 0.4 mmol litre(-1) was ad ded during the first 30 min of anoxic perfusion (n = 5) or during the first 30 min of reoxygenation (n = 5), in five additional hearts, the effect of halothane 0.4 mmol litre(-1) was under normoxic tested condi tions, Mean basal CK 0.29 (SEM 0.13) iu g(-1) min(-1) and 105.5 (4.0) mm Hg. Under normoxic conditions, halothane reduced LVDP to 52.0 (2.6) mm Hg. In control hearts, the major cell injury occurred at the onset of reoxygenation (CK release increased to 149.1 (9.1) iu g(-1) min(-1 )) and functional recovery after 1 h of reoxygenation was poor (contro l LVDP, 14.2 (2.)% of baseline). Halothane during anoxia attenuated my ocardial injury only moderately (CK release 50.2 (5.7) iu g(-1) min(-1 )) and LVDP recovered to 30.8 (3.0)% (each P < 0.05 vs control). When halothane was administered at reoxygenation, CK release was reduced to 10.1 (0.9) iu g(-1) min(-1) and LVDP recovered to 69.4 (4.9)% (each P < .05 vs control). We conclude that halothane not only attenuated isc haemic injury but had a specific protective action against reoxygenati on injury.