中文摘要：

目的观察急性肺损伤（acute lungin iury，ALI）大鼠脑组织中Gq／11蛋白的动态改变，从分子水平研究油酸（0A）性ALI导致脑损伤以及ALI导致多器官功能障碍综合征的可能机制，为ALI和多器官功能障碍综合征的发病机制提供实验和理论依据。方法用尾静脉注射OA法复制ALI大鼠模型，将40只健康雄性Wistar大鼠随机分为对照组（C组）和实验组（OA组），OA组又根据不同时限将其分为30min、60min、90min和120min4个亚组。观察检测各组大鼠血气（pH、Pa02、PaCO2）、平均动脉压（MABP）、血浆及脑组织乳酸脱氢酶（LDH）、肌酸激酶（CK）、丙二醛（MDA）。免疫印迹法检测各组大鼠脑组织中的Gq／11蛋白含量。结果Gq／11蛋白含量：除OA30min组外，其余OA各组随着时间延长较C组分别增加至（141．85±33．82）％、（165．84±30．27）％、（174．31±32．52）％（P〈0．01）。除OA30min组外，其余OA各组血浆MDA含量均较C组升高（P〈0．01）；OA30min组和OA60min组脑组织MDA含量与C组比较差异无统计学意义，OA 90min组和OA 120min组脑组织MDA含量较C组升高（P〈0．01）。OA各组血浆LDH活性均较C组升高（P〈0．01）；除OA30min组外，其余OA各组脑组织LDH活性均较C组升高（P〈0．01）。脑组织CK活性在60min时达到峰值（P〈0．01），以后呈下降趋势。结论ALI可导致远隔器官脑的损伤，引起细胞信号转导功能异常和脑代谢及形态的变化，Gq／11蛋白的高表达变化可能参与了ALI过程及脑损害的病理性信号转导。

英文摘要：

Objective To observe the change of Gq/11 protein concentration in the brain of rats during acute lung injury（ALI） and explore the pathophysiological mechanism of multiple organ dysfunction syndrome caused by ALI in terms of signal conduction. Methods ALI rat model was reproduced by intravenous injection of oleic acid （OA）. Forty male Wistar rats were randomly divided into control group（C group） and experiment group （OA group）. OA group included four＇subsections： OA30, 60, 90,120 min group. Blood gas indexes （pH, PaO2, PaCO2 ）, mean arterial blood pressure and lactate dehydrogenase （LDH）, creatine kinase （CK）, malondialdehyde （MDA） of plasma and brain were measured. Gq/11 protein concentration was examined by Western blot. Results Gq/11 protein concentration in the brain of OA groups （except OA 30 min group） respectively increased to （141.85 ± 33.82）%, （165.84±30. 27）%, （174.31± 32.52） % （ P 〈0. 01）. MDA content in the plasma of OA groups （except OA 30 min group） was higher than that of C group（ P 〈0.01）. MDA content in the brain of OA 90 min group and OA 120 rain group was higher than that of C group（ P 〈0.01）. LDH activity in the plasma of OA groups was higher than that of C group（ P 〈0.01）. LDH activity in the brain of OA groups （except OA 30 rain group） was higher than that of C group（ P 〈0.01）. CK activity in the brain reached peak at OA60 min group（ P 0.01） and then decreased. Conclusions Upregulation of Gq/11 protein concentration in the brain may play a role in ALl.