国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2012年
11期
842-846
,共5页
呼吸机所致肺损伤%血管紧张素Ⅱ%卡托普利%细胞凋亡
呼吸機所緻肺損傷%血管緊張素Ⅱ%卡託普利%細胞凋亡
호흡궤소치폐손상%혈관긴장소Ⅱ%잡탁보리%세포조망
Ventilator induced lung injury%Angiotensin Ⅱ%Captopril%Apoptosis
目的 通过观察大潮气量机械通气大鼠肺组织细胞凋亡水平和肺内血管紧张素Ⅱ(AngⅡ)含量的变化,探讨血管紧张素转换酶抑制剂——卡托普利对呼吸机所致肺损伤(VILI)的防治作用.方法 雄性Wistar大鼠30只,随机分为对照组、大潮气量机械通气组(H-VT)和卡托普利干预组(CAP).观察各组大鼠肺组织病理学改变,测定其急性肺损伤(ALI)评分、支气管肺泡灌洗液(BALF)总蛋白含量和肺湿/干重比值(W/D).采用DNA断端末端标记法(TUNEL)检测肺组织细胞凋亡指数,采用ELISA法检测肺组织AngⅡ含量.结果 H-VT组大鼠肺组织ALI评分、W/D,BALF总蛋白含量、肺组织AngⅡ含量及细胞凋亡指数均明显高于对照组(P值均＜0.01),且出现明显肺组织病理学改变.CAP组大鼠肺组织上述指标均较H-VT组明显降低(.P值均＜0.01),同时肺组织病理学改变也较H-Vr组明显减轻.结论 肺组织细胞凋亡在VILI发病中具有重要作用,卡托普利可通过降低大潮气量机械通气大鼠肺组织细胞凋亡水平,对V1LI起一定保护作用.
目的 通過觀察大潮氣量機械通氣大鼠肺組織細胞凋亡水平和肺內血管緊張素Ⅱ(AngⅡ)含量的變化,探討血管緊張素轉換酶抑製劑——卡託普利對呼吸機所緻肺損傷(VILI)的防治作用.方法 雄性Wistar大鼠30隻,隨機分為對照組、大潮氣量機械通氣組(H-VT)和卡託普利榦預組(CAP).觀察各組大鼠肺組織病理學改變,測定其急性肺損傷(ALI)評分、支氣管肺泡灌洗液(BALF)總蛋白含量和肺濕/榦重比值(W/D).採用DNA斷耑末耑標記法(TUNEL)檢測肺組織細胞凋亡指數,採用ELISA法檢測肺組織AngⅡ含量.結果 H-VT組大鼠肺組織ALI評分、W/D,BALF總蛋白含量、肺組織AngⅡ含量及細胞凋亡指數均明顯高于對照組(P值均＜0.01),且齣現明顯肺組織病理學改變.CAP組大鼠肺組織上述指標均較H-VT組明顯降低(.P值均＜0.01),同時肺組織病理學改變也較H-Vr組明顯減輕.結論 肺組織細胞凋亡在VILI髮病中具有重要作用,卡託普利可通過降低大潮氣量機械通氣大鼠肺組織細胞凋亡水平,對V1LI起一定保護作用.
목적 통과관찰대조기량궤계통기대서폐조직세포조망수평화폐내혈관긴장소Ⅱ(AngⅡ)함량적변화,탐토혈관긴장소전환매억제제——잡탁보리대호흡궤소치폐손상(VILI)적방치작용.방법 웅성Wistar대서30지,수궤분위대조조、대조기량궤계통기조(H-VT)화잡탁보리간예조(CAP).관찰각조대서폐조직병이학개변,측정기급성폐손상(ALI)평분、지기관폐포관세액(BALF)총단백함량화폐습/간중비치(W/D).채용DNA단단말단표기법(TUNEL)검측폐조직세포조망지수,채용ELISA법검측폐조직AngⅡ함량.결과 H-VT조대서폐조직ALI평분、W/D,BALF총단백함량、폐조직AngⅡ함량급세포조망지수균명현고우대조조(P치균＜0.01),차출현명현폐조직병이학개변.CAP조대서폐조직상술지표균교H-VT조명현강저(.P치균＜0.01),동시폐조직병이학개변야교H-Vr조명현감경.결론 폐조직세포조망재VILI발병중구유중요작용,잡탁보리가통과강저대조기량궤계통기대서폐조직세포조망수평,대V1LI기일정보호작용.
Objective To explore the effect of captopril on ventilator induced lung injury (VILI) by observing the relationship between apoptosis and angiotensin Ⅱ (Ang Ⅱ) in lungs of rats with high tidal volume ventilation.Methods Thirty male wistar rats were randomly divided into three groups:control group,high tidal volume ventilation (H-VT) group,captopril pretreatment group.Lung pathological changes were observed by macroscopy.The lung ALI scores,wet/dry weight ratio and the levels of protein (TP) in BALF were calculated.Apoptosis of the lung cells was detected by using terminal deoxynueleodityl transferasc-mediated nick-end labeling (TUNEL).AngⅡ contents in lung tissues were detected by ELISA.Results The lung ALI scores,wet/dry weight ratio and the levels of TP in BALF,Ang Ⅱ contents and apoptotic index in H-VT group were remarkably elevated (all P＜0.01),and followed by significant pathological changes of lung,Compared with H-VT group above all indexs showed marked decreased in captopril group (all P＜0.01),and followed by lighter pathological changes of lung.Conclusions Apoptosis is a crucial mechanism of VILI.Captopril executes lung-protective effects during mechanical ventilation via apoptosis-suppressed with high tidal volume ventilation.
