2011Guoji mazuixue yu fusu zazhiRequires access

The protective effect of propofol against global cerebral ischemia/reperfusion injury in rats

Chun yu Song, Tao Tao, Xiao guang Cui, Hong jie Xi, Zi yong Yue, Nan Wang

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Abstract

Objective To investigate the protective effects of propofol on global cerebral ischemia-reperfusion injury (I/RI)in rats and the underlying mechanism. Methods 65 male Wistar rats weighting 250 g-300 g were randomly divided into 5 groups (n=13): group S sham operation, group ischemia/reperfusion (I/R), group P1 propofol (0.5 mg·kg1·min-1)+I/R, group P2 propofol (1.0 mg·kg-1·min-1)+I/R and group P3 propofol (1.5 mg·kg-1·min-1)+I/R. I/R group was induced by occlusion of bilateral common carotid arteries combined with controlled hypotension for 10 min. In group P1, P2and P3, propofol was continued intravenous infusion for 60 min before FR. The neurological behavior was evaluated at 6, 24, 48, 72 h, 4, 5, 6 d and 7 d after I/R. Rats were killed at 7 d in each group and the brains were removed for pathomorphologic examination of the survived pyramidal neurons in the area of CA1 hippocampus. Flow cytometric was applicated for detection apoptosis at 24 h of reperfusion in each group. Results The rats subjected to ischemic and reperfusion appeared behavioral defects. The behavior of animals was significantly better in group P2 and in groups P3 than that of in groups P1 and I/R. The HG scores of normal neurons in CA1 of hippocampus in S group, I/R group, P1 group, P2 group, P3 group was 0, 2.8±0.4, 2.6±0.5, 2.0±0.7, 1.4±0.5, respectively. The apoptosis rates in S group, I/R group, P1 group, P2 group, P3group was (6.5±0.6), (51.5±2.8), (48.2±0.6), (24.7±1.2), (18.6±0.8)%, respectively. Conclusion Propofol confers dose-dependent protection against cerebral I/R injury, and this effect may be involved in the anti-apoptosis effect of propofol. Key words: Ischemia/reperfusion injury;  Propofol;  Neurological behavior;  Apoptosis

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Objective To investigate the protective effects of propofol on global cerebral ischemia-reperfusion injury (I/RI)in rats and the underlying mechanism. Methods 65 male Wistar rats weighting 250 g-300 g were randomly divided into 5 groups (n=13): group S sham operation, group ischemia/reperfusion (I/R), group P1 propofol (0.5 mg·kg1·min-1)+I/R, group P2 propofol (1.0 mg·kg-1·min-1)+I/R and group P3 propofol (1.5 mg·kg-1·min-1)+I/R. I/R group was induced by occlusion of bilateral common carotid arteries combined with controlled hypotension for 10 min. In group P1, P2and P3, propofol was continued intravenous infusion for 60 min before FR. The neurological behavior was evaluated at 6, 24, 48, 72 h, 4, 5, 6 d and 7 d after I/R. Rats were killed at 7 d in each group and the brains were removed for pathomorphologic examination of the survived pyramidal neurons in the area of CA1 hippocampus. Flow cytometric was applicated for detection apoptosis at 24 h of reperfusion in each group. Results The rats subjected to ischemic and reperfusion appeared behavioral defects. The behavior of animals was significantly better in group P2 and in groups P3 than that of in groups P1 and I/R. The HG scores of normal neurons in CA1 of hippocampus in S group, I/R group, P1 group, P2 group, P3 group was 0, 2.8±0.4, 2.6±0.5, 2.0±0.7, 1.4±0.5, respectively. The apoptosis rates in S group, I/R group, P1 group, P2 group, P3group was (6.5±0.6), (51.5±2.8), (48.2±0.6), (24.7±1.2), (18.6±0.8)%, respectively. Conclusion Propofol confers dose-dependent protection against cerebral I/R injury, and this effect may be involved in the anti-apoptosis effect of propofol. Key words: Ischemia/reperfusion injury;  Propofol;  Neurological behavior;  Apoptosis

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Available abstract

Objective To investigate the protective effects of propofol on global cerebral ischemia-reperfusion injury (I/RI)in rats and the underlying mechanism. Methods 65 male Wistar rats weighting 250 g-300 g were randomly divided into 5 groups (n=13): group S sham operation, group ischemia/reperfusion (I/R), group P1 propofol (0.5 mg·kg1·min-1)+I/R, group P2 propofol (1.0 mg·kg-1·min-1)+I/R and group P3 propofol (1.5 mg·kg-1·min-1)+I/R. I/R group was induced by occlusion of bilateral common carotid arteries combined with controlled hypotension for 10 min. In group P1, P2and P3, propofol was continued intravenous infusion for 60 min before FR. The neurological behavior was evaluated at 6, 24, 48, 72 h, 4, 5, 6 d and 7 d after I/R. Rats were killed at 7 d in each group and the brains were removed for pathomorphologic examination of the survived pyramidal neurons in the area of CA1 hippocampus. Flow cytometric was applicated for detection apoptosis at 24 h of reperfusion in each group. Results The rats subjected to ischemic and reperfusion appeared behavioral defects. The behavior of animals was significantly better in group P2 and in groups P3 than that of in groups P1 and I/R. The HG scores of normal neurons in CA1 of hippocampus in S group, I/R group, P1 group, P2 group, P3 group was 0, 2.8±0.4, 2.6±0.5, 2.0±0.7, 1.4±0.5, respectively. The apoptosis rates in S group, I/R group, P1 group, P2 group, P3group was (6.5±0.6), (51.5±2.8), (48.2±0.6), (24.7±1.2), (18.6±0.8)%, respectively. Conclusion Propofol confers dose-dependent protection against cerebral I/R injury, and this effect may be involved in the anti-apoptosis effect of propofol. Key words: Ischemia/reperfusion injury;  Propofol;  Neurological behavior;  Apoptosis

Key concepts: Propofol, Ischemia, Anesthesia, Medicine, Hippocampus, Reperfusion injury, Occlusion, Apoptosis

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