BACKGROUND: Ischemic preconditioning (IPC) and some volatile anesthetics have been shown to attenuate ischemia-reperfusion injury in an isolated-heart model. The aim of this study was to determine whether sevoflurane has a cardioprotective effect on isolated-heart models when given before prolonged periods of global ischemia.

METHODS: 48 male Sprague-Dawley rat hearts were randomly subdivided into four groups. Rats were anesthetized with 25 mg ketamine. After hearts had been removed, and perfused with a modified Krebs solution gassed with 5% CO₂ balanced O₂ at a constant temperature (37℃) and pressure (55 mmHg), a latex balloon was placed into the left ventricle to obtain isovolumetric contraction. After 20 min of equilibration, hearts were randomly allocated to 1) a control group, 2) an IPC group, two 5 min ischemic periods interspersed with 5 min normal perfusion, 3) an SPC (sevoflurane preconditioning) group, two 5 min sevoflurane periods interspersed with 5 min normal perfusion, 4) an SPC with Glibenclamide group. All groups were subjected to 30 min of global ischemia and 75 min of reperfusion. Left ventricular pressure, dP/dt max, and coronary flow were measured. Also flow responses to bradykinin were tested 15 min before IPC or SPC and 60 min after reperfusion.

RESULTS: Sevoflurane administration before global ischemia was found to have protective effects like IPC on functional recovery, to reduce infarct size, and to conserve coronary endothelial function. LVP was less depressed in the SPC and IPC groups. dP/dt max in both the IPC and SPC groups recovered after global ischemia. Coronary flow was depressed in the control and in the SPC with Glibenclamide groups, but it was slightly depressed in the IPC and SPC groups. Smaller infarct sizes were observed in IPC and SPC groups. Flow increases due to bradykinin were greater after SPC and IPC. Moreover, these beneficial effects of sevoflurane were blocked by glibenclamide administration.

CONCLUSIONS: Preconditioning with sevoflurane, like IPC, improves post ischemic contractility basal flow, and bradykinin-induced flow increases. Moreover, the protective effects of SPC and IPC were reversed by K_ATP channel antagonism.