香烟烟雾所致肺动脉高压大鼠模型的肺小血管肌化程度及意义  

Changes and Significance of Muscularization of Pulmonary Arterioles in a Rat Model of Pulmonary Hypertension Induced by Cigarette Smoke

作　　者：孙得胜 刘虹延 刘先胜[3] 欧阳瑶 徐永健[3] SUN Desheng;LIU Hongyan;LIU Xiansheng;OUYANG Yao;XU Yongjian(Department of Respiratory and Critical Care Medicine,Affiliated Hospital of Zunyi Medical University,Zunyi 563003,China;Department of Acupuncture and Moxibustion,Affiliated Hospital of Zunyi Medical University,Zunyi 563003,China;Department of Respiratory and Critical Care Medicine,Tongji Hospital,Tongji Medical College,Huazhong University of Science&Technology/Key Laboratory of Pulmonary Diseases of National Health Commission of the People's Republic of China,Wuhan 430030,China)

机构地区：[1]遵义医科大学附属医院呼吸与危重症医学科,贵州省遵义市563003 [2]遵义医科大学附属医院针灸科,贵州省遵义市563003 [3]华中科技大学同济医学院附属同济医院呼吸与危重症医学科卫生部呼吸系统疾病重点实验室,湖北省武汉市430030

出　　处：《中国全科医学》2021年第8期964-967,976,共5页Chinese General Practice

基　　金：国家自然科学基金资助项目(81960016);贵州省科技计划项目(黔科合基础[2019]1349号);遵义医科大学博士科研启动资金项目(院字(2018)04号)。

摘　　要：背景肺动脉高压是常见的肺血管疾病,香烟烟雾能否直接导致肺动脉高压目前存在争议,有研究发现部分吸烟人群在早期,甚至在肺功能仍正常且未发生明显缺氧表现时已发生肺小血管重塑,但是其中的具体机制尚不清楚。肺小血管的重塑是肺动脉高压的主要病理机制,有研究显示,实验小鼠的肺血管重塑与其肺小血管的肌化有关。目的探讨单纯香烟烟雾所致肺动脉高压大鼠的肺小动脉肌化程度及意义。方法 2018年1—5月,选用16只健康SD大鼠,随机分为对照组、模型组各8只,用香烟烟雾刺激的方法诱导肺动脉高压模型,用时4个月。造模满4个月时,观察大鼠活动、饮食、毛发等一般状况并检测右心室收缩压和平均右心室压,计算右心室肥厚指数、右心室重量和体质量的比值(RV/BW),免疫组织化学法检测肺小血管中α-SMA的表达以评估肺血管肌化程度(完全肌化、部分肌化、未肌化)。结果造模4个月后,对照组大鼠活动、饮食、毛发等一般状况未见异常,而模型组大鼠明显表现出倦怠状态,常蜷缩于角落,不积极寻觅食物,毛发也变得比较枯黄。模型组大鼠右心室收缩压和平均右心室压高于对照组,体质量低于对照组(P<0.05)。模型组右心室肥厚指数和RV/BW高于对照组(P<0.05)。对照组大鼠的肺小血管肌化比例低于模型组(P<0.05);模型组肺小血管中未肌化比例低于对照组,部分肌化和完全肌化比例高于对照组(P<0.05)。结论香烟烟雾刺激可直接导致肺动脉高压,其发病可能与肺小动脉肌化程度加重有关。Background It is controversial that whether there is a direct causal association between cigarette smoke and pulmonary hypertension,a common pulmonary vascular disease.Studies have found that some smokers have remodeling of pulmonary small vessels in the early stage,even when the lung function is normal and there is no obvious hypoxia.However,the specific mechanism is still unclear.The remodeling of pulmonary small vessels is the main pathological mechanism of pulmonary hypertension.Some studies have shown that pulmonary vascular remodeling in experimental mice is related to the muscularization of pulmonary small vessels.Objective To investigate the degree and significance of pulmonary arterioles muscularization in a rat model of pulmonary hypertension induced by cigarette smoke.Methods This experiment was carried out from January to May 2018,16 healthy SD rats were randomly and equally divided into control group and model group.Rats in the model group received the intervention with cigarette smoke for 4 months for establishing.a pulmonary hypertension model,while those in the control group did not.At the end of 4 months,the activity,diet,hair and other general conditions of both groups of rats were observed,and the right ventricular systolic pressure and mean right ventricular pressure were measured.Right ventricular hypertrophy index,right ventricular weight to body weight(RV/BW)ratio were calculated.The expression ofα-SMA in pulmonary small vessels was detected by immunohistochemistry to evaluate the degree of muscularization(non,partial and complete)of pulmonary arterioles.Results The control group showed no abnormalities in their activities,diet,hair and other general conditions,while the model group showed obvious tiredness,often curled up in the corners,did not actively seek food,and their hair became more withered.The model group had higher mean right ventricular systolic pressure and average right ventricular pressure,and lower,average body weight than the control group(P<0.05).The model group also show

关 键 词：高血压 肺性 烟雾吸入损伤 肺血管重塑 肌化 大鼠 

分 类 号：R544[医药卫生—心血管疾病]