Can isoflurane mimic ischaemic preconditioning in isolated rat heart?

Ischaemic preconditioning can protect the myocardium against ischaemic inju ry by opening of the adenosine triphosphate (ATP)-sensitive potassium (K-AT P) channel. Isoflurane is also thought to open this channel. The present in vestigation tested the hypothesis that pre-ischaemic treatment with isoflur ane mimics ischaemic preconditioning (producing chemical preconditioning) a nd thereby protects the myocardium against ischaemic injury in an isolated rat heart model. Control hearts underwent 30 min of global no-flow ischaemi a followed by 60 min of reperfusion. The hearts of the preconditioning grou p 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 b 5 min washout before the global ischaemia. Left ventr icular (LV) developed pressure and creatine kinase release were measured as variables of myocardial performance acid cellular injury, respectively. Re covery of LV developed pressure was improved after ischaemic preconditionin g [after 60 min reperfusion, mean 63 (SEM 6)% of baseline] compared with th e control group [18 (4)% P<0.01] but not by isoflurane, independently of co ncentration or duration of administration [ISO-1, 17 (2)%, P=0.99 vs contro l; ISO-2, 12 (3)%, P=0.64; ISO-3, 4 (1)%, P=0.06]. Total creatine kinase re lease over I h of reperfusion was not significantly different between contr ol [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 isof lurane does not cause anaesthetic-induced preconditioning in the isolated r at heart.