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作 者:陈贤明[1] 许瑞令[1] 任杰[2] 赵元昌[3] 尹镭[4] 王蕊[4] 马学惠[4] 韩德五[4]
机构地区:[1]山西医学院病理生理教研室 [2]第一附属医院儿科 [3]山西医学院病理生理教研室 太原 030001 [4]山西医学院肝病研究室
出 处:《中国病理生理杂志》1993年第6期674-677,共4页Chinese Journal of Pathophysiology
摘 要:本实验对硫代乙酰胺所致暴发性肝损伤大鼠肺血管壁通透性及血气的变化进行了观察。结果表明,肝损伤大鼠出现暴发性肝功能衰竭症状时,其肺血管对伊文思蓝的通透性增加(P<0.05),血浆内毒素水平亦较正常动物为高(P<0.05)。血气分析表现为动脉血CO_2分压增高(P<0.05);pH降低,且其水平与血浆内毒素浓度呈负相关(r=-0.730,P<0.05),70%大鼠出现混合性酸中毒,但动脉血氧分压及血氧饱和度无变化。Changes of pulmonary vascular permeability and blood gas were measuredin rats of experimental fulminant hepatic failure induced by thioacetamide. The resultsshowed that the pulmonary vascular permeability to Evans Blue in rats of fulminant he-patic failure with hepatic enphalopathy was markedly increased than that of normalcontrols (P<0.05), level of endotoxins in plasma also increased (P<0.05). Analysis ofblood gas indicated that the arterial partial pressure of CO_2 bacame significantly higher,and pH became lower (which was negatively correlated with levels of endotoxins in theplasma, r=-0.730, P<0.05). Some of the rats of fulminant hepatic failure showedmixed acid-base imbalance, but their arterial partial pressure of O_2 and oxygen carryingcapacity of the blood remained normal. It was suggested that the pulmonary vascular permea-bility increased when fulminant hepatic failure developed, and that alteration, as well asthe disturbance of acid-base in blood, was related with the endotoxiemia resulted fromserious liver failure.
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