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目的观察丙泊酚在沙土鼠全脑缺血–再灌注后对脑损伤的保护作用及脑组织组胺浓度的影响。方法雄性清洁级蒙古沙土鼠27只,随机分为假手术组(S组)、模型组(M组)和丙泊酚组(P组),每组9只。M组及P组建立大鼠全脑缺血–再灌注模型(夹闭双侧颈总动脉缺血10min,再灌注2h),S组仅游离双侧颈总动脉但不阻断;P组在再灌注即刻经舌静脉泵注丙泊酚10mg·kg-1·h-1,持续2h。各组于再灌注2h处死大鼠。光镜观察脑皮质病理损伤并评分,测定脑组织含水量及组胺浓度,电镜观察皮质神经元超微结构的变化。结果光镜显示,S组脑组织神经元正常,M组神经元变性坏死,P组神经元基本正常。病理损伤评分M组最高,P组明显减低(P<0.05)。M组脑组织含水量及组胺含量较S组显著升高,P组较M组明显降低(P<0.01)。电镜显示,M组神经元固缩,线粒体肿胀,P组神经元内的线粒体肿胀减轻。结论全脑缺血-再灌注后应用丙泊酚可减轻大鼠脑缺血–再灌注损伤,其机制可能与降低组胺浓度有关。
Objective To observe the protective effect of propofol on brain injury and the effect of histamine on cerebral injury after global cerebral ischemia / reperfusion in gerbils. Methods Twenty-seven male Mongolian gerbils were randomly divided into sham operation group (S group), model group (M group) and propofol group (P group), with 9 rats in each group. The model of global cerebral ischemia-reperfusion was established in M group and P group (occluded bilateral common carotid artery 10 min ischemia, reperfusion 2 h), only the free bilateral common carotid artery was not found in group S; Immediately after reperfusion, propofol 10 mg · kg-1 · h-1 was injected via the lingual vein for 2 h. Rats were sacrificed at 2h after reperfusion. The pathological changes of cerebral cortex were observed with light microscope, the water content of brain tissue and histamine concentration were measured. The ultrastructure of cortical neurons was observed by electron microscope. Results Light microscopy showed that the neurons in normal brain tissue of group S were normal, the neurons in group M degenerated and necrotic, and the neurons in group P were almost normal. The score of pathological injury was the highest in group M, while it was significantly lower in group P (P <0.05). M group brain water content and histamine content was significantly higher than the S group, P group was significantly lower than the M group (P <0.01). Electron microscopy showed that in group M, neurons were pyknotic and mitochondria were swollen, and mitochondria swelling in neurons of group P was alleviated. Conclusion Propofol can reduce cerebral ischemia-reperfusion injury after global cerebral ischemia-reperfusion in rats. The mechanism may be related to the decrease of histamine concentration.