CAJ | 학술논문

目的探讨山莨菪碱预处理对兔肺缺血再灌注后肺水肿的保护作用及作用机制.方法建立在体兔肺缺血再灌注动物模型,10～12周龄健康家兔24只,雌雄不拘,体重2 200～2 600 g,随机分为3组,每组8只.山莨菪碱组于左肺缺血再灌注处理前静脉给予山莨菪碱3 mg/kg预处理,对照组进行左肺缺血再灌注处理,假手术组只开胸并套带不行缺血再灌注处理.各组左肺缺血1 h,再灌注3 h后结扎并切取左肺下叶,部分行组织学观察,部分通过测量肺湿干重的方法计算肺含水量,余肺组织按试剂盒说明书检测组织髓过氧化酶(MPO)含量.最后经兔股静脉注射2%伊文思蓝(1.5 mL/kg),然后取左肺上叶,参照Udaka的方法比较3组肺血管通透性.结果缺血再灌注处理后,对照组肺含水量、MPO含量及伊文思蓝含量分别为(6.59±0.53) g/g干重、(1.16±0.14) U/g·prot和(172.8±15.5) μg/g湿重,明显高于假手术组的(4.34±0.37) g/g干重、(0.53±0.09) U/g·prot和(103.3±11.2) μg/g湿重(P均<0.05),组织损伤严重并可见严重的肺水肿,山莨菪碱组上述指标水平分别为(5.62±0.43) g/g干重、(0.82±0.11) U/g·prot和(123.9±18.2) μg/g湿重,较对照组明显下降(P均<0.05),组织损伤轻微,肺水肿程度很轻.结论山莨菪碱通过抑制中性粒细胞生成、降低肺血管通透性等作用显著减轻了肺缺血再灌注后肺水肿的程度.
목적 탐토산랑탕감예처리대토폐결혈재관주후폐수종적보호작용급작용궤제.방법 건립재체토폐결혈재관주동물모형,10～12주령건강가토24지,자웅불구,체중2 200～2 600 g,수궤분위3조,매조8지.산랑탕감조우좌폐결혈재관주처리전정맥급여산랑탕감3 mg/kg예처리,대조조진행좌폐결혈재관주처리,가수술조지개흉병투대불행결혈재관주처리.각조좌폐결혈1 h,재관주3 h후결찰병절취좌폐하협,부분행조직학관찰,부분통과측량폐습간중적방법계산폐함수량,여폐조직안시제합설명서검측조직수과양화매(MPO)함량.최후경토고정맥주사2%이문사람(1.5 mL/kg),연후취좌폐상협,삼조Udaka적방법비교3조폐혈관통투성.결과 결혈재관주처리후,대조조폐함수량、MPO함량급이문사람함량분별위(6.59±0.53) g/g간중、(1.16±0.14) U/g·prot화(172.8±15.5) μg/g습중,명현고우가수술조적(4.34±0.37) g/g간중、(0.53±0.09) U/g·prot화(103.3±11.2) μg/g습중(P균<0.05),조직손상엄중병가견엄중적폐수종,산랑탕감조상술지표수평분별위(5.62±0.43) g/g간중、(0.82±0.11) U/g·prot화(123.9±18.2) μg/g습중,교대조조명현하강(P균<0.05),조직손상경미,폐수종정도흔경.결론 산랑탕감통과억제중성립세포생성、강저폐혈관통투성등작용현저감경료폐결혈재관주후폐수종적정도.
Objective To investigate the protective efficacy of anisodamine against lung edema after ischemia-reperfusion in rabbits, and to explore the possible mechanism. Methods Rabbit lung in vivo ischemia-reperfusion model was developed, twenty-four Chinese rabbits of either gender, aged 10～12 weeks, weighting 2 200～2 600 g were divided into 3 groups randomly: anisodamine group, control group and sham group, and each group had eight rabbits. In anisodamine group the left pulmonary hilum was occluded for 1 hour and released for 3 hours, anisodamine 3 mg/kg was administered intravenously injection before occlusion. In control group, the left pulmonary hilum was occluded for 1 hour and then released for 3 hours, did ischemia-reperfusion. In sham group, left lung received no ischemia-reperfusion. Left lung tissues in each group were harvested for histopathology analysing, the lung water content determining and myeloperoxidase (MPO) level checking at the same time. At last 2% Evens blue (1.5 mL/kg) was injected into femoral venous in order to measure lung vascular permeability by the method of Udaka. Results After ischemia-reperfused, the lung tissue water content, MPO level and Evens blue level in control group were (6.59±0.53) g/g dry weight, (1.16±0.14) U/g·prot and (172.8±15.5) μg/g wet weight respectively, significantly higher than that in sham group, which were(4.34±0.37) g/g dry weight, (0.53±0.09) U/g·prot and 103.3±11.2 μg/g wet weight)(P<0.05). Those items in anisodamine group were (5.62±0.43) g/g dry weight, (0.82±0.11) U/g·prot and (123.9±18.2) μg/g wet weight, obviously lower than that in control group(P<0.05). Left lung revealed prominent edema, septal swelling, hemorrhage and neutrophil infiltration in control, anisodamine group was significantly improved compared with control. Conclusion Anisodamine can significantly prevent lung from lung edema after ischemia-reperfusion in rabbits. The mechanism may be ascribed to inhibiting neutrophil infiltration and depressing vascular permeability.