对一氧化碳中毒迟发性脑病相关因素的研究

摘要

Objective　To observe the changes in nitric oxide synthases in brain,endothelium count,platelet volume,the expression of leukocyte adhesion molecules (CD11b/18)in peripheral blood,tPA and PAI in plasma and percentage of apoptotic cells in hippocampus following carbon monoxide poisoning and to evaluate the significance of these factors to delayed brain disease.Methods　48 Wistar adult rats were divided evenly into six groups.Rats were exposed to CO environment (2950 ppm,60 min) except those in the control group.Samples obtained from rats were measured immediately after CO exposure and at 5th，10th，15th and 20th day.A detailed analysis were made by flow cytometry and spectrophotometer.Results　In the CO poisoned rats,the platelet activity,the expression of leukocyte adherence molecules and the percentage of apoptotic cells are higher,and the mitochondrial membrane potential of hippocampus neurons are lower than those in the control rats.Fibrinolysis system has a slight change yet.Conclusions　The factors observed are involved in cerebral tissue injury in rats after onset of acute carbon monoxide poisoning.They seem to be associated with the occurrence of delayed brain disease.%目的观察一氧化碳中毒(COP)后大鼠脑组织一氧化氮合酶(NOS)、外周血内皮细胞计数、血小板体积变化、血小板CD61表达、多形核白细胞粘附分子(CD11b/CD18)表达、海马神经细胞凋亡细胞百分比及线粒体膜电位的改变。方法 Wistar大鼠共16只随机分成正常对照组及一氧化碳中毒组各8只。制作COP动物模型。用流式细胞仪测定大鼠脑组织一氧化氮合酶(NOS)、外周血内皮细胞计数、血小板体积变化、血小板CD61表达、多形核白细胞粘附分子(CD11b/CD18)表达的动态变化，海马神经细胞凋亡细胞百分比及线粒体膜电位的改变。用分光光度法测定血浆组织型纤溶酶原激活剂(tPA)和抑制剂(PAI)。结果 COP后NOS水平降低，血小板活性增高，纤溶系统变化不明显，细胞粘附分子表达增加，线粒体膜电位降低，凋亡细胞数增加。结论 COP后血小板活性增高，细胞粘附分子表达增加，导致脑微小动脉血栓形成趋势并引起白细胞浸润造成脑组织损伤，是COP迟发性脑病的重要发病因素之一。