The effects of propofol on Ca2+ -induced mitochondrial dysfunction after focal cerebral ischemia-reperfusion injury in rats / 中华麻醉学杂志

ABSTRACT

Objective To investigate the effects of propofol on Ca2+ -induced mitochondrial dysfunction after focal cerebral ischemia-reperfusion(IR) injury in rats. Methods Eighty-four male Wistar ratsweighing 250-300 g were randomly divided into 4 groups (n= 21 each)group Ⅰ sham operation (group S); group Ⅱ IR; group Ⅲ CaCl2 and group Ⅳ propofol (group P). In group Ⅱ - Ⅳ focal cerebral IR was induced by 2 h middle cerebral artery occlusion (MCAO) followed by 24 h reperfusion. Neurological function was assessed at 2 h of ischemia and scored (0= no deficit, 5 = death). The animals were decapitated at the end of 24 h reperfusion. Left parietal and frontal cortex were immediately isolated and mitochondria were extracted. In group Ⅲ and Ⅳ mitochondria were incubated with 200 μmol/L CaCl2 for 5 min at 37 ℃, and were pretreated with propofol 200 μmol/L in group Ⅳ for 2 min before CaCl2. Morphological changes of mitochondria were examined by electron microscopy. Mitochondrial permeability transition pore (MPTP) activity was detected by ultraviolet visible absorption spectroscopy.Results Mitochondrial ultrastructure was normal in group Ⅰ . Significant mitochondrial swelling, disrupted cristae and membrane rupture were observed in group Ⅲ. Propofol significantly attenuated the Ca2+ -induced changes. The MPTP activity was significantly increased in group Ⅱ and Ⅲ as compared with group Ⅰ but were significantly decreased in group Ⅳ (propofol group). The decrease in MPTP activity was attenuated in group Ⅳ as compared with group Ⅲ. Conclusion Propofol can improve mitochondrial dysfunction induced by Ca2+ after focal cerebral IR by inhibiting MPTP opening in rats.