Can isoflurane mimic ischaemic preconditioning in isolated rat heart?

Ischaemic preconditioning can protect the myocardium against ischaemic injury by opening of the adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channel. Isoflurane is also thought to open this channel. The present investigation tested the hypothesis that pre-ischaemic treatment with isoflurane mimics ischaemic preconditioning (producing chemical preconditioning) and thereby protects the myocardium against ischaemic injury in an isolated rat heart model. Control hearts underwent 30 min of global no-flow ischaemia followed by 60 min of reperfusion. The hearts of the preconditioning group underwent two 5 min periods of no-flow ischaemia interspersed with 5 min of reperfusion before the sustained ischaemia. In three additional groups, hearts were subjected to 15 min of 1.5 minimal alveolar concentration (MAC) of isoflurane (ISO-1), 15 min 3 MAC (ISO-2) or 25 min 1.5 MAC (ISO-3) of isoflurane followed by 5 min washout before the global ischaemia. Left ventricular (LV) developed pressure and creatine kinase release were measured as variables of myocardial performance and cellular injury, respectively. Recovery of LV developed pressure was improved after ischaemic preconditioning [after 60 min reperfusion, mean 63 (SEM 6)% of baseline] compared with the control group [18 (4)% P <0.01] but not by isoflurane, independently of concentration or duration of administration [ISO-1, 17 (2)%, P=0.99 vs control; ISO-2, 12 (3)%, P=0.64; ISO-3, 4 (1)%, P=0.06]. Total creatine kinase release over 1 h of reperfusion was not significantly different between control [251 (36) U g(-1) dry weight] and all isoflurane groups [ISO-1, 346 (24) U g(-1), P=0.30; ISO-2, 313 (33) U g(-1), P=0.73; ISO-3, 407 (40) U g(-1), P=0.03]. These results indicate that pre-ischaemic administration of isoflurane does not cause anaesthetic-induced preconditioning in the isolated rat heart