Fig. 4. Ethidium (ETH) fluorescent intensity in arbitrary units, measured in real time at the left ventricular free wall by spectrofluorometry. Hearts are loaded with dihydroethidium, which is converted to fluorescent ETH by intracellular reactive oxygen species, particularly superoxide. APC = anesthetic preconditioning; APC+CHE = APC and chelerythrine; APC+PP101 = APC and protein kinase C–δ isoform inhibitor; APC+PP149 = APC and protein kinase C–ε isoform inhibitor; CHE = chelerythrine alone; PP101 = PP101 alone; PP149 = PP149 alone. Averaged signal intensity during 5 min of perfusion with Krebs-Ringer's solution (baseline) and during exposure to sevoflurane alone (APC) or with protein kinase C inhibitors (APC+CHE, APC+PP101, APC+PP149) and during Krebs-Ringer's solution perfusion with protein kinase C inhibitors in the absence of sevoflurane (CHE, PP101, PP149). Values are mean ± SEM; n = 4 for each group. *P < 0.05 versus  baseline.

Fig. 4. Ethidium (ETH) fluorescent intensity in arbitrary units, measured in real time at the left ventricular free wall by spectrofluorometry. Hearts are loaded with dihydroethidium, which is converted to fluorescent ETH by intracellular reactive oxygen species, particularly superoxide. APC = anesthetic preconditioning; APC+CHE = APC and chelerythrine; APC+PP101 = APC and protein kinase C–δ isoform inhibitor; APC+PP149 = APC and protein kinase C–ε isoform inhibitor; CHE = chelerythrine alone; PP101 = PP101 alone; PP149 = PP149 alone. Averaged signal intensity during 5 min of perfusion with Krebs-Ringer's solution (baseline) and during exposure to sevoflurane alone (APC) or with protein kinase C inhibitors (APC+CHE, APC+PP101, APC+PP149) and during Krebs-Ringer's solution perfusion with protein kinase C inhibitors in the absence of sevoflurane (CHE, PP101, PP149). Values are mean ± SEM; n = 4 for each group. *P < 0.05 versus  baseline.

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