中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2008年
11期
678-680,插2
,共4页
黄幸青%饶文霖%刘晓燕%钟延东%林拓%张昌瑞%朱飚
黃倖青%饒文霖%劉曉燕%鐘延東%林拓%張昌瑞%硃飚
황행청%요문림%류효연%종연동%림탁%장창서%주표
溃疡,应激性%脑出血%内皮素,内源性%内皮素抗体%内皮素受体拮抗剂
潰瘍,應激性%腦齣血%內皮素,內源性%內皮素抗體%內皮素受體拮抗劑
궤양,응격성%뇌출혈%내피소,내원성%내피소항체%내피소수체길항제
acute stress ulcer%cerebral hemorrhage%endogenous endothelin%endothelin antibody%endotbelin receptor antagonist
目的 观察内皮素(ET)抗体、ET受体拮抗剂对大鼠脑出血致应激性溃疡的干预作用,并比较其效果.方法 将SD大鼠随机分为对照组(A组)、模型组(B组)、ET抗体组(C组)、ET受体拮抗剂组(D组),每组10只.用非精确定位穿刺法将实验组大鼠自体尾静脉血200μl注入右脑实质内制备大鼠尾状核脑出血致应激性溃疡模型.B、C、D组分别于尾静脉注射0.2 ml生理盐水、ET抗体、ET受体拮抗剂(阿魏酸钠),每日1次,连用3 d.处死大鼠,观察其胃黏膜溃疡发生率、溃疡指数,血清ET-1,血清、脑、胃黏膜的丙二醛(MDA)、超氧化物歧化酶(SOD),光镜和电镜下观察脑、胃黏膜病理变化并进行超微结构电脑图像定量分析线粒体比表面(Rsv)和体积密度(Vv).结果 制模后,血清ET-1无明显变化;血清、脑、胃黏膜MDA显著升高,SOD显著下降,脑组织含水量也明显升高;脑、胃壁细胞Rsv及胃壁细胞Vv均显著下降(P<0.05或P<0.01).B组胃黏膜溃疡发生率为30%,溃疡指数为15,其他组肉眼均未见溃疡灶.与B组比较,C、D组血清、脑、胃黏膜的MDA显著降低.SOD显著升高;C组脑含水量较B组显著下降,差异均有统计学意义(P均<0.01),C、D组间上述指标差异均无统计学意义.B、C、D组间脑神经细胞、胃壁细胞超微结构电脑图像定量分析中的Rsv、Vv变化及各组间血清ET-1差异亦均无统计学意义.结论 ET抗体、ET受体拈抗剂均可有效减轻大鼠脑出血致应激性溃疡的发生发展,ET抗体的干预效果似乎稍优于ET受体拮抗剂.
目的 觀察內皮素(ET)抗體、ET受體拮抗劑對大鼠腦齣血緻應激性潰瘍的榦預作用,併比較其效果.方法 將SD大鼠隨機分為對照組(A組)、模型組(B組)、ET抗體組(C組)、ET受體拮抗劑組(D組),每組10隻.用非精確定位穿刺法將實驗組大鼠自體尾靜脈血200μl註入右腦實質內製備大鼠尾狀覈腦齣血緻應激性潰瘍模型.B、C、D組分彆于尾靜脈註射0.2 ml生理鹽水、ET抗體、ET受體拮抗劑(阿魏痠鈉),每日1次,連用3 d.處死大鼠,觀察其胃黏膜潰瘍髮生率、潰瘍指數,血清ET-1,血清、腦、胃黏膜的丙二醛(MDA)、超氧化物歧化酶(SOD),光鏡和電鏡下觀察腦、胃黏膜病理變化併進行超微結構電腦圖像定量分析線粒體比錶麵(Rsv)和體積密度(Vv).結果 製模後,血清ET-1無明顯變化;血清、腦、胃黏膜MDA顯著升高,SOD顯著下降,腦組織含水量也明顯升高;腦、胃壁細胞Rsv及胃壁細胞Vv均顯著下降(P<0.05或P<0.01).B組胃黏膜潰瘍髮生率為30%,潰瘍指數為15,其他組肉眼均未見潰瘍竈.與B組比較,C、D組血清、腦、胃黏膜的MDA顯著降低.SOD顯著升高;C組腦含水量較B組顯著下降,差異均有統計學意義(P均<0.01),C、D組間上述指標差異均無統計學意義.B、C、D組間腦神經細胞、胃壁細胞超微結構電腦圖像定量分析中的Rsv、Vv變化及各組間血清ET-1差異亦均無統計學意義.結論 ET抗體、ET受體拈抗劑均可有效減輕大鼠腦齣血緻應激性潰瘍的髮生髮展,ET抗體的榦預效果似乎稍優于ET受體拮抗劑.
목적 관찰내피소(ET)항체、ET수체길항제대대서뇌출혈치응격성궤양적간예작용,병비교기효과.방법 장SD대서수궤분위대조조(A조)、모형조(B조)、ET항체조(C조)、ET수체길항제조(D조),매조10지.용비정학정위천자법장실험조대서자체미정맥혈200μl주입우뇌실질내제비대서미상핵뇌출혈치응격성궤양모형.B、C、D조분별우미정맥주사0.2 ml생리염수、ET항체、ET수체길항제(아위산납),매일1차,련용3 d.처사대서,관찰기위점막궤양발생솔、궤양지수,혈청ET-1,혈청、뇌、위점막적병이철(MDA)、초양화물기화매(SOD),광경화전경하관찰뇌、위점막병리변화병진행초미결구전뇌도상정량분석선립체비표면(Rsv)화체적밀도(Vv).결과 제모후,혈청ET-1무명현변화;혈청、뇌、위점막MDA현저승고,SOD현저하강,뇌조직함수량야명현승고;뇌、위벽세포Rsv급위벽세포Vv균현저하강(P<0.05혹P<0.01).B조위점막궤양발생솔위30%,궤양지수위15,기타조육안균미견궤양조.여B조비교,C、D조혈청、뇌、위점막적MDA현저강저.SOD현저승고;C조뇌함수량교B조현저하강,차이균유통계학의의(P균<0.01),C、D조간상술지표차이균무통계학의의.B、C、D조간뇌신경세포、위벽세포초미결구전뇌도상정량분석중적Rsv、Vv변화급각조간혈청ET-1차이역균무통계학의의.결론 ET항체、ET수체념항제균가유효감경대서뇌출혈치응격성궤양적발생발전,ET항체적간예효과사호초우우ET수체길항제.
Objective To observe the respective effects of intervention either with endothelin (ET) antibody or with ET receptor antagonist on acute stress ulcer (ASU) subsequent to cerebral hemorrhage in rats.Methods Forty Sprague-Dawley (SD) rats were randomly divided into control group (group A,n=10),model group (group B,n=10),ET antibody (group C,n=10),and ET receptor antagonist group (group D,n=10).Right intracerebral hemorrhage was reproduced by injection of 200 μl autologous venous blood.Normal saline,ET antibody,or ET receptor antagonist was respectively administered intravenously per day for designated group.The rats were saerified at 3 days of the experiment.The incidence of ASU and ulcer index were assessed,serum ET-1 level,malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in serum,Rsvmit (Rsv) and Vvmit (Vv) of cerebral and gastric mucosa were measured,and pathological examination of the cerebral tissue and gastric mucosa was performed with light microscopy and electron microscopy.Results In group B,serum ET-1 level did not changed.MDA content were markedly increased in serum,cerebral and gastric mucosa,SOD activity were markedly decreased,cerebral water content were markedly increased; Rsv in neuron and gastric parietal cell,Vv in gastric parietal cell both were markedly decreased (P<0.05 or P<0.01).ASU was only observed in group B (the incidence was 30%,ulcer index was 15).It was not observed in other groups.Compaired with group B,MDA content were significantly decreased,and SOD activity were significantly increased in serum,cerebral and gastric mucosa in grougs C and D,cerebral water content in group C were dramatically decreased (all P<0.01),but these were not statistically different between groups C and D.Rsv and Vv in neuron and gastric parietal cell in groups B,C and D were not statistically different,and serum ET-1 level were not statistically different among the groups (all P>0.05).Conclusion Intervention of ET antibody and ET receptor antagonist can both reduce occurrence and development of ASU subsequent to cerebral hemorrhage in rats.