烟雾吸入致伤犬右侧肺引发左侧肺损伤的实验研究  

Experimental study on secondary injury of left lung induced by smoke inhalation of right lung in dogs

作　　者：李晓辉[1] 杨宗诚[2] 刘志远[2] 何保斌[2] 黎鳌[2] 

机构地区：[1]第三军医大学药理教研室,重庆400038 [2]第三军医大学烧伤研究所,重庆400038

出　　处：《中国危重病急救医学》2001年第12期718-720,共3页Chinese Critical Care Medicine

基　　金：国家自然科学基金资助重大项目 (No.392 90 70 0 )

摘　　要：目的 :探讨烟雾致伤犬一侧肺对另侧肺的影响及其机制。方法 :在 Olympus(型号 P1 0 )纤维支气管镜引导下直视行双腔管气道插管 ,烟雾吸入致伤犬右侧肺 ;分别采用 AVL 990型自动血气分析仪、干湿重法、过氧化氢还原法、微量酸滴定法、TBA法、生物测定法检测犬动脉血气、肺含水量、髓过氧化物酶 (MPO)活性、磷脂酶 A2 (PLA2 )活性、脂质过氧化物丙二醛 (MDA)及血小板活化因子 (PAF)含量。结果 :右侧肺烟雾吸入致伤后 ,犬呼吸频率明显增快 ,动脉血氧分压 (Pa O2 )进行性下降 ,2 4小时达 8.3 7k Pa(1 k Pa=7.5 mm Hg)。但动脉血二氧化碳分压 (Pa CO2 )仅 2 4小时点与伤前比较显著升高。进一步研究发现 ,烟雾致伤右侧肺后 2 4小时 ,左侧肺含水量明显增加 ,粒细胞标志酶 MPO活性、膜磷脂分解酶 PLA2 活性、炎性介质 PAF及 MDA含量与正常对照组比较均显著升高。病理检查见 ,致伤犬双肺弥漫性肺泡内水肿 ,间隔增厚 ,伴大量炎细胞浸润 ,惟左侧肺略轻。结论 :烟雾吸入致伤犬一侧肺可引起另侧肺水肿 ,其机制与另侧肺组织继发性的白细胞浸润、PLA2 活化、脂质过氧化损伤及炎性介质Objective:To explore the potential effect of unilateral smoke inhalation injury of the right lung on the contralateral lung in dogs.Methods:The smoke inhalation injury model of right lung in dogs was produced with dualchamber tracheal intubation under the guidance of Olympus (type P10) fiberobronchoscope.The arterial blood gas,lung water content,the activity of myeloperoxidase (MPO) and phospholipase A 2 (PLA 2),the contents of malondialdehyde (MDA) and platelet activating factor (PAF) were respectively determined by AVL990 blood gas analyzer,the wet/dry weight ratio,hydrogen peroxide reduction technique,microacid titration assay,TBA spectrometry,and biodetection method.Results:The respiratory rate was obviously increased,the partial pressure of oxygen in artery(PaO 2) was progressively lowered to 8 37 kPa (1 kPa= 7 5 mmHg ) at 24 hours after smoke inhalation injury of the right lung in dogs.However,partial pressure of carbon dioxide in artery(PaCO 2) was significantly elevated only at 24 hours.Also,the water content,the activity of MPO and PLA 2,the contents of MDA and PAF of the left lung were markedly elevated compared with normal controls.Pathologic examination revealed that both right and left lungs in injured group displayed diffuse alveolar edema,thickening of septum,and heavy infiltration of leukocytes,but the pathologic changes in the left lung were less severe than that in the right lung.Conclusions:Secondary pulmonary edema of the left lung may occur after unilateral smoke inhalation of the right lung in dogs,the mechanisms of which may be related to the secondary leukocyte infiltration,the activation of PLA 2,lipoperoxidation,and the increase of PAF in the left lung in dogs.

关 键 词：继发性肺损伤 髓过氧化物酶 磷脂酶A2 血小板活化因子 

分 类 号：R563.8[医药卫生—呼吸系统]