Fig. 2.  Area of infarct as percentage of the ischemic region at risk by triphenyltetrazolium chloride staining. Bars indicate the mean ± SD of the following sets of experiments: control (C) ischemia-reperfusion (I/R), ischemic postC (isch-postC; I), sevoflurane postC (sevo-postC; S), 5-hydroxy decanoate sodium (5-HD) as a mitochondrial adenosine triphosphate–dependent potassium channel antagonist, and wortmannin as a phosphatidylinositol 3-kinase antagonist. Each was given to nondiabetic and diabetic animals. Insulin (Ins) experiments were performed after 48-h treatment in the diabetic animals. *  P < 0.002 (control experiments: isch- and sevo-postC vs.  control I/R). *  P < 0.05 (diabetic experiments with Ins [control and isch-postC]vs.  diabetic without Ins and diabetic sevo-postC with and without Ins). *  P = 0.028 for wortmannin action on isch- and sevo-postC in the diabetic group.