Tangshang Clinical College of Hebei Medical University, Tangshan-063000, Hebei, China.
Pain Clinics, Xuanwu Hospital Capital Medical University, Beijing-100053, China.
Asian Pac J Trop Med. 2014 Nov;7(11):905-8. doi: 10.1016/S1995-7645(14)60158-9. Epub 2014 Oct 22.
To observe the effect of captopril on the tumor necrosis factor-α (TNF-α) level and arterial blood gases in acute lung injury (ALI) induced by HCL in rats, and to analyze its protective mechanism.
Fifty Wistar rats were selected and randomly divided into three groups, with 20 rats in Group I and II, respectively and 10 animals in Group III. ALI model was constructed by intratracheal injection of diluted hydrochloric acid (pH=1.25, 1.2 mL/kg). Group I rats received not any treatment after construction of ALI model. Group II rats were treated with captopril (5 mg/kg, i.p.) 5 min after induction of ALI. Group III served as normal control without any treatment. Ninety minutes after construction of ALI model, all the rats were sacrificed. Blood was withdrawn for detection of TNF-α level and arterial blood gases index. And lung tissue slices of the three groups were prepared for observation of pathologic histology changes.
TNF-α level in serum of Group I and II rats was significantly higher than that in Group III (P<0.05), while TNF-α level in serum of Group II was significantly lower in Group I (P<0.05). PaCO2 level was significantly higher (P<0.05), while PaO2 was significantly lower (P<0.05) in Group I and II rats than those in Group III. PaCO2 was significantly lower (P<0.05) and PaO2 was significantly higher (P<0.05) in Group II than those in Group I. Histological observation showed diffuse congestion and severe edema of lung tissue, obvious thickening and structure damage of alveolar walls and a large amount of neutrophil infiltration in Group I rats. Group II rats showed mild edema of lung tissue; only a small portion of alveolar walls showed thickening and only a few of neutrophil infiltration could be observed. The degree of injury was remarkably slighter than that of Group I rats. Group III rats showed clear lung tissue structure and normal morphology; alveolar walls were uniform and the margin was smooth and few neutrophil could be observed.
Captopril can significantly reduce serum TNF-α level, elevate PaO2 and reduce PaCO2 in rats with ALI. It has a protective effect on ALI rats.
观察卡托普利对盐酸致大鼠急性肺损伤（ALI）时肿瘤坏死因子-α（TNF-α）水平及动脉血气的影响，分析其保护机制。
选取 50 只 Wistar 大鼠，随机分为三组，每组 20 只，另设 10 只大鼠作为正常对照组。采用气管内注入稀释盐酸（pH=1.25，1.2 mL/kg）法制备 ALI 模型。模型制备后，Ⅰ组大鼠不给予任何干预；Ⅱ组大鼠于 ALI 模型制备后 5 min 给予卡托普利（5 mg/kg，腹腔注射）；Ⅲ组大鼠不给予任何干预作为正常对照组。ALI 模型制备 90 min 后处死所有大鼠，取血检测 TNF-α 水平及动脉血气指标，取三组大鼠肺组织切片观察病理组织学改变。
Ⅰ组和Ⅱ组大鼠血清 TNF-α水平明显高于Ⅲ组（P<0.05），Ⅱ组明显低于Ⅰ组（P<0.05）。Ⅰ组和Ⅱ组大鼠 PaCO2 明显升高（P<0.05），PaO2 明显降低（P<0.05），Ⅱ组 PaCO2 明显低于Ⅰ组（P<0.05），PaO2 明显高于Ⅰ组（P<0.05）。光镜下观察，Ⅰ组大鼠肺组织弥漫性淤血、水肿明显，肺泡壁明显增厚，结构破坏，大量中性粒细胞浸润；Ⅱ组大鼠肺组织水肿较轻，仅部分肺泡壁增厚，少量中性粒细胞浸润，损伤程度明显轻于Ⅰ组；Ⅲ组大鼠肺组织结构清晰，形态正常，肺泡壁均匀，边缘光滑，仅少量中性粒细胞浸润。
卡托普利可明显降低 ALI 大鼠血清 TNF-α水平，升高 PaO2，降低 PaCO2，对 ALI 大鼠具有保护作用。
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