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卡托普利对通气相关肺损伤的保护作用 被引量:1

Angiotensin-converting enzyme inhibitor captopril attenuates ventilator-induced lung injury in rats
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摘要 目的探讨通气相关肺损伤(ventilator induced lung injury,VILI)中的肺部炎症反应和肺内血管紧张素Ⅱ的关系,并研究血管紧张素转换酶抑制剂(卡托普利)在大鼠通气相关肺损伤模型中的作用。方法将21只雄性SD大鼠分成3组:高潮气量、零呼气末正压(HVZP)组;卡托普利治疗组(HVZP+CAP)组;空白对照组。行动脉插管和气管插管后测定动脉血气分析和平均动脉压,同时测定支气管肺泡灌洗液中的总蛋白数、巨噬细胞炎性蛋白-2(MIP-2)的浓度及肺组织血管紧张素Ⅱ的水平,并观察肺组织形态学的变化。结果HVZP+CAP组大鼠的平均动脉压明显低于HVZP组(P<0.05)。HVZP大鼠肺泡灌洗液中的总蛋白水平明显高于对照组(P<0.05),且灌洗液中的MIP-2和肺血管紧张素Ⅱ明显高于对照组和HVZP+CAP组(P<0.05)。肺血管紧张素Ⅱ的水平与肺泡灌洗液中的蛋白水平和MIP-2的水平呈正相关。结论卡托普利通过下调炎症因子可以降低机械通气中肺损伤的程度,机械通气相关肺损伤的发生与肺部的血管紧张素系统相关。 Objective To study the relationship between lung inflammation and lung angiotensin Ⅱ ( ANG Ⅱ) in ventilator-induced lung injury ( VILI) and assessed the efficiency of the angiotensin-converting enzyme inhibitor captopril to attenuate VILI in rats. Methods Totally 21 adult male Sprague-Dawley rats were randomly assigned into 3 groups,high-volume,0 positive end-expiratory pressure ( HVZP) group; captopril injection ( 100 mg/kg i. p. ) in 30 min before HVZP ventilation ( HVZP + CAP group) ; no ventilation group ( control) . The blood gas tensions and mean arterial pressure were measured after a polyethylene catheter was placed in one carotid artery and a plastic cannula was inserted into the trachea. The protein contents and contents of macrophage inflammatory protein-2 ( MIP-2) in bronchoalveolar lavage fluid ( BALF) and lung ANGⅡ were determined by ELISA. The changes of lung pathology were observed by HE staining. Results Mean arterial pressure was significantly lower in the HVZP + CAP group than in the HVZP group after 2 hour’s ventilation. Total protein levels were significantly higher in BALF recovered from HVZP-ventilated rats than from controls. BALF MIP-2 and lung ANG Ⅱ were significantly higher in the HVZP group than in the control and HVZP + CAP groups. Lung ANG Ⅱ level was correlated positively with BALF contents of total protein and MIP-2. Conclusion Captopril has the efficiency to attenuate VILI by reducing inflammatory cytokines. Our results suggest that VILI is partly mediated by the local angiotensin system.
作者 钟贞 张婷
出处 《第三军医大学学报》 CAS CSCD 北大核心 2009年第21期2134-2136,共3页 Journal of Third Military Medical University
关键词 机械通气相关肺损伤 卡托普利 支气管肺泡灌洗液 巨噬细胞炎性蛋白 血管紧张素Ⅱ ventilator-induced lung injury captopril bronchoalveolar lavage fluid macrophage inflam- matory protein-2 angiotensin Ⅱ
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