卡托普利对大潮气量机械通气大鼠肺组织细胞凋亡的影响

Effect of captoprii on apoptosis induced by high tidal volume ventilation in lung tissue of rats

目的通过观察大潮气量机械通气大鼠肺组织细胞凋亡水平和肺内血管紧张素Ⅱ（AngⅡ）含量的变化，探讨血管紧张素转换酶抑制剂——卡托普利对呼吸机所致肺损伤（VILI）的防治作用。方法雄性Wistar大鼠30只，随机分为对照组、大潮气量机械通气组（H-Vt）和卡托普利干预组（CAP）。观察各组大鼠肺组织病理学改变，测定其急性肺损伤（ALl）评分、支气管肺泡灌洗液（BALF）总蛋白含量和肺湿／干重比值（W／D）。采用DNA断端末端标记法（TUNEL）检测肺组织细胞凋亡指数，采用ELISA法检测肺组织AngⅡ含量。结果H—V，组大鼠肺组织ALl评分、W／D、BALF总蛋白含量、肺组织AngⅡ含量及细胞凋亡指数均明显高于对照组（P值均〈0．01），且出现明显肺组织病理学改变。CAP组大鼠肺组织上述指标均较H-V，组明显降低（P值均〈0．01），同时肺组织病理学改变也较H—Vt组明显减轻。结论肺组织细胞凋亡在VILI发病中具有重要作用，卡托普利可通过降低大潮气量机械通气大鼠肺组织细胞凋亡水平，对VILI起一定保护作用。

Objective To explore the effect of captopril on ventilator induced lung injury （VILI） by observing the relationship between apoptosis and angiotensin Ⅱ （Ang Ⅱ ） in lungs of rats with high tidal volume ventilation. Methods Thirty male wistar rats were randomly divided into three groups： control group,high tidal volume ventilation （H-VT） group, captopril pretreatment group. Lung pathological changes were observed by macroscopy. The lung ALI scores,wet/dry weight ratio and the levels of protein （TP） in BALF were calculated. Apoptosis of the lung cells was detected by using terminal deoxynucleodityl transferase-mediated nick-end labeling （TUNEL）. Ang Ⅱ contents in lung tissues were detected by ELISA. Results The lung ALI scores, wet/dry weight ratio and the levels of TP in BALF, Ang Ⅱ contents and apoptotic index in H-VT group were remarkably elevated （all P〈0.01）, and followed by significant pathological changes of lung. Compared with H-VT group above all indexs showed marked decreased in captopril group （all P〈0.01 ）, and followed by lighter pathological changes of lung. Conclusions Apoptosis is a crucial mechanism of VILI. Captopril executes lung-protective effects during mechanical ventilation via apoptosis-suppressed with high tidal volume ventilation.