国际外科学杂志
國際外科學雜誌
국제외과학잡지
INTERNATIONAL JOURNAL OF SURGERY
2011年
8期
532-534
,共3页
丁冠男%刘缚鲲%田鸣%李树人
丁冠男%劉縳鯤%田鳴%李樹人
정관남%류박곤%전명%리수인
二异丙酚%肝脏病学%再灌注损伤
二異丙酚%肝髒病學%再灌註損傷
이이병분%간장병학%재관주손상
Propofol%Gastroenterology%Reperfusion injury
目的 观察肝脏缺血再灌注后急性肺损伤的发病机制及丙泊酚的保护作用.方法 成年封闭群SD雄性大鼠48只,采用随机数字表法随机分为:假手术组(Sham):假手术2 h(Sham2)组;假手术6 h(Sham6)组;缺血再灌注组(IR):缺血再灌注2 h(IR2)组;缺血再灌注6 h(IR6)组及丙泊酚组(P):丙泊酚2 h(P2)组;丙泊酚6 h(P6)组.P组自缺血前30min静脉输注丙泊酚1mg·kg-1·min-1.Sham组及IR组按0.1 mL·kg-1·min-1速率输注乳酸钠林格氏液,时间30 min.在再灌注后2 h、6 h测定肺灌洗液肿瘤坏死因子-α(TNF-α),超氧化物歧化酶(SOD),丙二醛(MDA),肺组织髓过氧化物(MPO)浓度及肺组织湿/干重(W/D)比值并计算肺组织学评分.结果 IR组及P组大鼠缺血再灌注后肺泡灌洗液TNF-a的水平较Sham组明显升高,但P组再灌注2 h、6 h时均明显低于IR组.Sham组SOD水平与P组相比差异无统计学意义.IR各组SOD值均显著降低,P组SOD值与IR组相比明显升高.在大鼠肝脏缺血/再灌注后,IR各组MDA值均显著升高,在再灌注后6 h达到高峰.P组MDA轻度升高,但明显低于IR组,与Sham组相比差异无统计学意义.IR组大鼠的肺W/D值、MPO及组织学评分均明显高于Sham组及P组.结论 丙泊酚通过抑制炎性因子的分泌,减轻氧化应激损伤等机制,对肝脏缺血再灌注损伤后肺部的继发性损伤有明显的保护作用.
目的 觀察肝髒缺血再灌註後急性肺損傷的髮病機製及丙泊酚的保護作用.方法 成年封閉群SD雄性大鼠48隻,採用隨機數字錶法隨機分為:假手術組(Sham):假手術2 h(Sham2)組;假手術6 h(Sham6)組;缺血再灌註組(IR):缺血再灌註2 h(IR2)組;缺血再灌註6 h(IR6)組及丙泊酚組(P):丙泊酚2 h(P2)組;丙泊酚6 h(P6)組.P組自缺血前30min靜脈輸註丙泊酚1mg·kg-1·min-1.Sham組及IR組按0.1 mL·kg-1·min-1速率輸註乳痠鈉林格氏液,時間30 min.在再灌註後2 h、6 h測定肺灌洗液腫瘤壞死因子-α(TNF-α),超氧化物歧化酶(SOD),丙二醛(MDA),肺組織髓過氧化物(MPO)濃度及肺組織濕/榦重(W/D)比值併計算肺組織學評分.結果 IR組及P組大鼠缺血再灌註後肺泡灌洗液TNF-a的水平較Sham組明顯升高,但P組再灌註2 h、6 h時均明顯低于IR組.Sham組SOD水平與P組相比差異無統計學意義.IR各組SOD值均顯著降低,P組SOD值與IR組相比明顯升高.在大鼠肝髒缺血/再灌註後,IR各組MDA值均顯著升高,在再灌註後6 h達到高峰.P組MDA輕度升高,但明顯低于IR組,與Sham組相比差異無統計學意義.IR組大鼠的肺W/D值、MPO及組織學評分均明顯高于Sham組及P組.結論 丙泊酚通過抑製炎性因子的分泌,減輕氧化應激損傷等機製,對肝髒缺血再灌註損傷後肺部的繼髮性損傷有明顯的保護作用.
목적 관찰간장결혈재관주후급성폐손상적발병궤제급병박분적보호작용.방법 성년봉폐군SD웅성대서48지,채용수궤수자표법수궤분위:가수술조(Sham):가수술2 h(Sham2)조;가수술6 h(Sham6)조;결혈재관주조(IR):결혈재관주2 h(IR2)조;결혈재관주6 h(IR6)조급병박분조(P):병박분2 h(P2)조;병박분6 h(P6)조.P조자결혈전30min정맥수주병박분1mg·kg-1·min-1.Sham조급IR조안0.1 mL·kg-1·min-1속솔수주유산납림격씨액,시간30 min.재재관주후2 h、6 h측정폐관세액종류배사인자-α(TNF-α),초양화물기화매(SOD),병이철(MDA),폐조직수과양화물(MPO)농도급폐조직습/간중(W/D)비치병계산폐조직학평분.결과 IR조급P조대서결혈재관주후폐포관세액TNF-a적수평교Sham조명현승고,단P조재관주2 h、6 h시균명현저우IR조.Sham조SOD수평여P조상비차이무통계학의의.IR각조SOD치균현저강저,P조SOD치여IR조상비명현승고.재대서간장결혈/재관주후,IR각조MDA치균현저승고,재재관주후6 h체도고봉.P조MDA경도승고,단명현저우IR조,여Sham조상비차이무통계학의의.IR조대서적폐W/D치、MPO급조직학평분균명현고우Sham조급P조.결론 병박분통과억제염성인자적분비,감경양화응격손상등궤제,대간장결혈재관주손상후폐부적계발성손상유명현적보호작용.
Objective To investigate the mechanism of acute lung injury after hepatic ischemia / reperfusion and the protective effect of propofol.Method s Forty-eight male SD rats were randomly divided into Sham2 group,Sham6 group; IR2 group (IR2),IR6 group (IR6); P2 group (P2),P6 group (P6).The 1 mg·kg-1·min-1 propofol was infused from 30min before ischemia in P groups,and the same volume sodium lactate Ringer's solution was infused in Sham and IR groups.The concentration of TNF-α,superoxidedimutase(SOD),malondialdehyde(MDA),myeloperosidase(MPO),lung wet/dry weight ratio and lung histological scores were measured at the points of 2 and 6 hour after reperfusion.Results TNF-α levels were higher in IR and P groups than those in sham groups but the values in P groups were lower than those in IR groups.SOD levels decreased greatly in IR groups,there were great difference between P and IR groups.MDA levels increased greatly in IR groups and reached the peak value at 6 hour after reperfusion.MDA levels in P groups were lower than those in IR groups and there were no difference between P and sham groups.The ratio of Wet/dry levels,MPO and lung histological scores were increased greatly after reperfusion in IR and P groups.But the value in P groups was lower than those in IR groups.Conclusions Acute lung injury after hepatic ischemia / reperfusion is mainly induced by the oxidant stress and neutrophil infiltration in lung tissues.Propofol may have effects of antioxidation and decrease neutrophil infiltration which attenuate lung injury induced by hepatic ischemia/reperfusion.