中文摘要：

目的通过观察不同时间段机械通气大鼠肺组织中小窝蛋白-1（caveolin-1，cav-1）的表达水平，探讨cav-1在呼吸机所致肺损伤（VILI）发病中的作用。方法雄性SD大鼠32只，随机分为对照组、通气0.5h组（H-VT0.5h组）、通气1h组（H-VT1h组）和通气2h组（H-VT2h组）。采用免疫组织化学染色法测定各组大鼠肺组织cav-1的表达水平，测定其肺湿／干重（W／D）比值和支气管肺泡灌洗液（BALF）中总蛋白含量，并在光镜下观察各组大鼠肺组织的病理学改变。结果①肺组织cav-1表达结果显示，H-V0.5h组和对照组均明显高于H-VT2h组和H-VT1h组（P值均〈O．001），H-VT0.5h组明显高于对照组（P〈0．001），H-VT1h组明显高于H-VT2h组（P〈O．01）。②肺组织W／D比值和BALF总蛋白含量测定结果显示，H-VT2h组和H-VT1h组均明显高于对照组和H-VT0.5h组（P值均〈0．001），H-VT2h组明显高于H-VT1h组（P〈O．001），H-VT0.5h组与对照组比较差异无统计学意义（P〉O．05）。③肺组织病理学结果显示，随着机械通气时间延长，大鼠肺组织损伤程度呈逐渐加重趋势。结论肺组织cav-1在机械通气不同时间段表达水平明显不同，表现为先增高后降低。提示肺组织cav-1高表达对VILI起一定保护作用；大潮气量机械通气可通过抑制肺组织cav-1表达，诱发和加重肺组织损伤。

英文摘要：

Objective To observe the expression of the caveolin-1 induced by high tidal volume ventilation in lung tissue of rats during different time periods,and therefore to explore the role of caveolin-1 in ventilator induced lung injury. Methods Thirty-two healthy male Sprague-Dawley rats were randomly divided into four groups： control group, ventilation for half an hour group （H-VT0.5h group） ,ventilation for one hour group （H-VTlh group）,and ventilation for two hours group （H-VT2h group）. The expression of caveolin-1 in lung tissues of rats was detected by immunohistochemistry. The level of total protein （TP） in bronchoalveolar lavage fluid （BALF） was measured by bicinchoninic acid method. The lung wet/dry weight ratio （W/D） was calculated. The pathological changes of the lungs were observed under light microscope. Results ①The expression of caveolin-1 in lung tissues in H-VT0.5h group and control group was respectively higher than that in H-VTlh group and H-VT2h group （all P 〈0.001）, that in H-VT0.5h group was higher than that in control group （ P〈0.001）,that in H-VTlh group was higher than that in H-VT2h group （ P〈0.01）. ②W/D of lung tissues and the level of TP in BALF in H-VTlh group and H-VT2h group were respectively higher than those in H-VT0.5h group and control group （all P〈0. 001）, those in H-VT2h group were higher than those in H-VTlh group （ P 〈0. 001）. There was no statistical difference in W/D and the level of TP in BALF between control group and H-V〈0.5h group （ P〉0.05）. ③ Histopatholosical findings under light microscope demonstrated that diffused alveolar damage induced bymechanical ventilation was worse with time. Conclusions With the extension of the duration of mechanical ventilation, the expression of caveolin-1 increases at first, then reduces. The high expression of caveolin-1 plays a protective role in ventilator induced lung injury. The high tidal volume ventilation can induce and aggravate the lung injury by inhibiting the ex