摘要
目的动态观察一氧化碳(CO)中毒大鼠血浆血栓素(thromboxane B_2,TXB_2)和前列腺素(6-k- PGF_(1α))变化,观察脑组织毛细血管内皮细胞超微结构。方法Sprague-Dawley(SD)大鼠42只,随机分为对照组和染毒后即刻组、1、4、7、14、21d组,每组6只。建立CO中毒大鼠模型,用放射免疫法测定各组血浆中TXB_2和6-k- PGF_(1α)水平,电镜观察毛细血管内皮细胞超微结构变化。结果CO中毒后大鼠血浆中TXB_2和6-k-PGF_(1α)水平均升高,TXB_2/6-k-PGF_(1α)先降低后升高。中毒大鼠脑组织毛细血管内皮细胞紧密连接松弛,线粒体水肿,管腔皱缩变形。结论CO中毒后大鼠TXA_2/PGI_2的平衡被打破,脑组织毛细血管内皮细胞损伤、血脑屏障破坏,脑组织微血栓形成,可能与CO中毒迟发性脑病的发生有关。
Objective To study TXB2 and 6-k-PGFzolevel of plasma in rats in order to provide theoretical evidence for the treatment of acute carbon monoxide poisoning(ACOP) and delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Meanwhile to observe cerebral vascular endothelial cell ultrastrueture alteration and situation of blood brain barrier (BBB). Methods 42 Sprague-Dawley rats were.divided into control group and operated groups (the moment, 1st day,4th day,7th day, 14th day,21st day group). 6 rats in every group. Carbon monoxide poisoning model of rats was established with letting rats absorbing CO. The control group inhaled the atmosphere. Venous blood samples were obtained at the certain time according the different groups to determine TXB2 and 6-k-PGF1α level. Pathological slices were prepared. Results Compared with the control group,the TXB2 and 6-k-PGF1α level of operated groups elevated. The level of TXB2/6-k-PGF1α oraised first ,then went down. It was observed capillary vessel joint of rats' tissue became slack ,mitochondrial swelled ,the blood vessel crimpled and was transfigured. Conclusion The balance of TXB2 and 6-k-PGF1α was broken after ACOP. The BBB was damaged. It was possible to related with DEACMP.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2007年第3期340-342,386,共4页
Journal of Apoplexy and Nervous Diseases