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1A). Moreover, acute intravenous administration of rosiglitazone significantly reduced the time interval from LAD ligation to the onset of the first spontaneous VF occurrence during ischaemia�Creperfusion compared with that in the saline group (Fig. 1B). However, the dispersion of refractoriness as shown by the standard deviation of the three ERPs measured at three different sites was not different between the saline- and the rosiglitazone-treated group (Fig. 2). Unlike the effect Selleckchem Small molecule library on VF incidence, the areas of myocardial infarction (i.e. the ratio of infarct size to AAR) in the rosiglitazone group were decreased (P?Ficain mitochondrial membrane potential changes (Fig. 4A). Moreover, rosiglitazone could not reduce the level of ROS production in the ischaemic myocardium (Fig. 4B). In rat isolated cardiac mitochondria treated with rosiglitazone at 10, 25 and 50 ��m, the drug did not alter cardiac mitochondrial ROS level or membrane potential changes, in comparison to the control group (Fig. 5). When cardiac mitochondria were under severe oxidative stress caused by H2O2, i.e. conditions that mimic ischaemia�Creperfusion injury, cardiac mitochondrial dysfunction was observed as indicated by a decrease in the red/green fluorescence ratio, indicating cardiac mitochondrial membrane depolarization (Fig. 5A) and an increase in ROS level (Fig. 5B). None of the three concentrations of rosiglitazone could prevent or attenuate cardiac mitochondrial dysfunction caused by oxidative stress in these isolated cardiac mitochondria (Fig. 5). The major findings of the present study are as follows. In ischaemia�Creperfusion of the swine heart, acute intravenous administration of rosiglitazone had the following effects: (1) it facilitated mTOR inhibitor the occurrence of ventricular fibrillation; (2) it reduced the myocardial infarction area; and (3) it failed to prevent cardiac mitochondrial ROS production and mitochondrial depolarization caused by ischaemia�Creperfusion injury. Furthermore, acute intravenous administration of rosiglitazone did not alter the basic cardiac electrophysiology and haemodynamic parameters both in normal hearts and in hearts during ischaemia�Creperfusion. In the present study, our finding that acute administration of rosiglitazone did not alter haemodynamic parameters in swine is consistent with a previous report that rosiglitazone did not alter the blood pressure (Lu?et al.?2008). In addition to haemodynamics, our study also demonstrated for the first time that the basic cardiac electrophysiological parameters as well as the defibrillation efficacy and the VFT were not altered by rosiglitazone in both normal conditions and ischaemia�Creperfusion in swine hearts.