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卡托普利对通气相关肺损伤的保护作用
Angiotensin-converting enzyme inhibitor captopril attenuates ventilator-induced lung injury in rats
【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。
【Abstract】 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.
- 【文献出处】 第三军医大学学报 ,Acta Academiae Medicinae Militaris Tertiae , 编辑部邮箱 ,2009年21期
- 【分类号】R965
- 【被引频次】3
- 【下载频次】58