缺血预适应在大鼠肢体缺血再灌注后胃黏膜损伤中的作用

NAC对大鼠脑缺血再灌注引起胃黏膜损伤的影响郑金玉,嵇春妹(徐州医学院附属淮安市第二人民医院脑外科,江苏淮安223000)摘要:目的研究N-乙酰-L-半胱氨酸(N-ace t y lcyste i ne,NAC)对大鼠脑缺血再灌注引起应激性胃损伤的影响。

方法采用四动脉结扎法建立大鼠全脑缺血模型,缺血后静脉注射NAC(150mg/kg),取胃后计数胃黏膜损伤指数(gastr i c mucosa l da m age i ndex,G M D I),测定胃黏膜组织中丙二醛(m a l ona l dehyde,M DA)含量、超氧化物歧化酶(s uperox i de dis mutase,S OD)活性,采用原位检测(TUNEL)法检测胃黏膜细胞凋亡情况。

结果NA C 可以降低大鼠脑缺血再灌注引起应激性胃损伤时的胃黏膜损伤指数,使胃黏膜组织中M DA含量减少、S OD活性增强,抑制胃黏膜细胞凋亡。

结论NAC对大鼠脑缺血再灌注引起的应激性胃损伤具有保护作用,这种保护作用是通过抑制氧化应激、减少胃黏膜细胞凋亡而实现的。

关键词:N-乙酰-L-半胱氨酸;脑缺血再灌注;胃黏膜损伤指数;超氧化物歧化酶;丙二醛中图分类号:R651.1文献标志码:A文章编号:1000-2065(2010)10-0658-03Eeffect of N-acetylcystei n e on brain ische m ia/reperfusion-inducedgastric mucosa injury in ratsZ H EN Ji nyu,JI Chun m e i(D epart m ent o f Cerebra l Surgery,T he A ffiliated Hua i c an Second P eop l e c sH osp ita l o f Xuzhou M edical Co ll ege,H ua i c an,Ji angsu223002,Ch i na)Ab stract:O b jective T o i nvestigate the eff ec t o f an ti ox i dant N-acety lcy ste i ne(NAC)on bra i n i sche m i a/reper-fusi on-i nduced stress g astric mucosa i njury i n ra ts.M ethods R at mode l s o f brain ischem ia/reperf usion we re estab-lished by t he four vessel occ l usi on m ethod.Fo ll ow ing brain i sche m i a,NAC(150mg/kg)w as i n jected into the fe m oral ve i n.T he ra ts w ere fi nall y sacr ificed t o i nvesti ga te gastric m ucosal da m age i ndex(GMD I)and de ter m i ne the con tent o f m a l ondialdehyde(M DA)and the ac ti v ity o f s uperox i de d i s m utase(S OD)i n gastr ic muco sa.The apoptosis o f gastr ic mu-cosa l ce lls was detected by TUNEL.R es u lts In j ection ofNA C int o t he fe m ora l ve i n could decrease gastric mucosa l da m-ag e i ndex i n stress gastr i c i n j ury,reduce the content o fM DA and i ncrease t he acti v ity of S OD i n the gastr ic mucosa,and i nh i b it gastric m ucosal ce ll u lar apop t o si s f o ll ow i ng bra i n ische m i a/reperfusi on.Conc l u sion NAC cou l d pro tect aga i nst bra i n ischem ia/reperf usion-i nduced stress g astric inj ury by t he i nhi b iti on of ox i dati ve stress and redcti on of ce ll apopto-sis i n gastr i c mucosa.K ey w ords:N-acety l cyste i ne;bra i n ische m ia/repe rf usion;g astric mucosa l da m age i ndex;superox i de dis mutase; m a l ondialdehyde机体遭遇各种应激性反应如休克、脑损伤、严重外伤等情况时,胃通常是受累最早的器官。

中外医疗China &Foreign Medical TreatmentDOI:10.16662/ki.1674-0742.2017.30.006预适应联合后适应对大鼠缺血再灌注损伤的保护作用张涛,许文胜,郝冬梅,何宏伟,单新亮,李鑫瑶,孙旭,高彩凤包头医学院基础医学与法医学院免疫学教研室,内蒙古包头014040[摘要]目的探讨预适应联合后适应对大鼠脑缺血再灌注损伤的保护作用。

方法该实验于2015年10月—2016年9月进行。

选取清洁级雄性SD 大鼠50只,体重(270±30)g(内蒙古科技大学包头医学院动物中心提供,合格证号:201407413,ddY 系SPF 级);随机分为假手术组、模型组、预适应组、后适应组和预适应+后适应组,每组10只,除假手术组外,其余各组大鼠均制作为脑缺血/再灌注损伤模型,在再灌注48h 后,检测各组大鼠神经功能、脑梗死灶体检、脑组织氧化应激损伤生化指标及神经元凋亡情况。

结果再灌注12、24h 和48h 模型组神经功能缺陷评分(3.10±0.23)分、(3.53±0.15)分、(3.32±0.16)分明显高于其他处理组(P <0.05);再灌注12、24h 和48h 处理组中,预适应+后适应组神经功能缺陷评分最低(1.89±0.11)分、(1.75±0.12)分、(1.22±0.13)分(P <0.05);预适应+后适应组脑梗死灶体积为(100.41±33.26)mm 3,明显低于模型组、预适应组和后适应组(P <0.05);预适应组(182.43±50.10)mm 3和后适应组(185.10±52.33)mm 3脑梗死灶体积较模型组(100.41±33.26)mm 3降低(P <0.05);假手术组超氧化物歧化酶(SOD)活性(122.41±24.61)μn/mgprot 明显高于模型组(45.56±10.31)μn/mgprot,而丙二醛(MDA)(43.51±9.64)nmol/mgprot 低于模型组(113.43±21.07)nmol/mgprot(P <0.05);后适应组(76.81±9.83)μn/mgprot 和预适应后适应组SOD 活性较模型组升高(110.13±12.16)μn/mgprot,而MDA(61.51±12.15)nmol/mgprot 较模型组(113.43±21.07)nmol/mgprot 降低(P <0.05);假手术组细胞凋亡数(15.20±7.62)个明显低于模型组(84.11±8.42)个(P <0.05);各处理组细胞凋亡数较模型组有所降低(73.04±9.01)个、(61.12±10.17)个(P <0.05),其中预适应+后适应组神经元细胞凋亡数最少,为(47.20±9.21)个。

缺血后处理抗大鼠肠缺血-再灌注损伤的作用及其机
制研究的开题报告
一、研究背景
肠缺血-再灌注（intestinal ischemia-reperfusion，I/R）损伤是一种
常见的临床情况，在胃肠道缺血性疾病、肠道手术、外伤等情况下常常
发生。

I/R损伤可导致肠道黏膜损伤、肠道壁破坏、肠道菌群异常、免疫系统异常等一系列不良反应，严重者可导致全身炎症反应综合征（SIRS）和多器官功能障碍（MOF）。

因此，对I/R损伤的预防和治疗具有重要的临床意义。

二、研究目的
本研究旨在探讨抗大鼠肠缺血-再灌注损伤的作用，并研究其作用机制，以期为临床治疗提供科学的理论依据。

三、研究内容
（一）建立I/R模型
本研究选用大鼠作为研究对象，采用经典的artery夹闭-再灌注方法建立I/R模型。

（二）给予抗缺血剂处理
在模型建立后，将大鼠随机分为对照组和处理组。

对照组不做任何
处理，处理组给予抗缺血剂处理。

（三）观察指标
观察指标包括：肠道形态学改变、肠道血流灌注改变、血清丙二醛（MDA）含量、血清超氧化物歧化酶（SOD）活性、血清炎症因子水平等。

（四）机制研究
从抗缺血剂处理的角度出发，探讨其作用机制。

包括：抗氧化作用、抗炎作用、改善肠道微环境等。

四、研究意义
本研究对于深入理解肠缺血-再灌注损伤的机制、探究抗缺血剂的作用机制、提高临床治疗水平具有重要的意义。

同时，本研究可为抗I/R损伤药物的研究提供新的思路和方向。

缺血预适应在大鼠肢体缺血再灌注后胃粘膜损伤中的作用要瑞莉;张连元;门秀丽;董淑云;杨全会;张一兵;王保强;孙树勋【期刊名称】《中国病理生理杂志》【年(卷),期】2004(020)008【摘要】目的:观察肢体缺血再灌注(LIR)对胃粘膜的损伤,探讨肢体缺血再灌注对胃粘膜损伤的作用及其部分机制,以及短暂多次肢体缺血在胃粘膜损伤发生中的作用.方法:按Rosenthal方法复制大鼠LIR模型,观察并测定肢体缺血4 h再灌注4 h后以及应用缺血预适应干预对胃粘膜损伤的影响:取各组胃粘膜制作切片于光学显微镜和电子显微镜下进行观察,测定各组胃粘膜损伤指数、胃粘膜血流量(GMBF)、胃结合粘液量、胃粘液中磷脂、氨基己糖的含量、血浆和胃组织一氧化氮含量以及胃粘膜一氧化氮合酶(NOS)活性.结果:光学显微镜和电子显微镜观察结果显示大鼠LIR后胃粘膜损伤严重,IPC组各类细胞损伤较LIR组轻;LIR后GMBF及胃结合粘液量、胃粘液中磷脂、氨基己糖的含量均低于对照组,虽然IPC组大部分指标与对照组有差异,但与LIR组对比GMBF及胃结合粘液量、胃粘液中磷脂、氨基己糖的含量均较高于LIR组;LIR组血浆与胃粘膜组织NO含量及NOS活性显著高于对照组,而IPC组血浆与胃粘膜组织NO含量和胃粘膜的NOS活性又显著高于LIR组.结论:肢体缺血再灌注可导致胃粘膜损伤;缺血预适应可减轻肢体缺血再灌注后的胃粘膜损伤.【总页数】4页(P1468-1471)【作者】要瑞莉;张连元;门秀丽;董淑云;杨全会;张一兵;王保强;孙树勋【作者单位】唐山职业技术学院生理学教研室,河北,唐山,063000;华北煤炭医学院病理生理学教研室,河北,唐山,063000;华北煤炭医学院病理生理学教研室,河北,唐山,063000;华北煤炭医学院病理生理学教研室,河北,唐山,063000;华北煤炭医学院病理生理学教研室,河北,唐山,063000;华北煤炭医学院病理生理学教研室,河北,唐山,063000;华北煤炭医学院病理生理学教研室,河北,唐山,063000;华北煤炭医学院病理生理学教研室,河北,唐山,063000【正文语种】中文【中图分类】R363【相关文献】1.内质网应激诱导的细胞凋亡在大鼠肢体缺血再灌注后肺损伤中的作用及牛磺酸的影响 [J], 成兰云;门秀丽;张连元;李宏杰;孔小燕;赵利军2.缺血预适应对大鼠肢体缺血再灌注后小肠损伤的保护效应及NO的作用 [J], 刘燕;彭海兵;张博;周洪霞;杨秀红;张连元3.缺血预适应在大鼠肢体缺血再灌注后胃黏膜损伤中的作用 [J], 要瑞莉;张连元;董淑云;门秀丽;杨全会;张一兵;王保强;孙树勋4.Bach1/Nrf2通路调控HO-1在大鼠肢体缺血再灌注后肺损伤中的作用机制研究[J], 李艳艳;孙克玉;邱志云;龚霞;王继芹5.内质网应激在大鼠肢体缺血再灌注后肺损伤中的作用 [J], 门秀丽;张连元;李宏杰因版权原因，仅展示原文概要，查看原文内容请购买。

Ｖ０１．２６Ｎｏ．９Ｓｅｐ．２００６上海交通大学学报（医学版）ＪｏｕｒｎａｌｏｆＳｈａｎｇｈａｉＪｉａｏｔｏｎｇＵｎｉｖｅｒｓｉｔｙ（ＭｅｄｉｃａｌＳｃｉｅｎｃｅ）・１０３９・【文章编号】０２５８—５８９８（２００６）０９—１０３９一０３・基础研究・缺血预适应对高血脂大鼠心肌缺血一再灌注损伤的保护作用郭竹英，徐芒华（上海交通大学医学院第三人民医院实验中心，上海２０１９００）【摘要】目的研究缺血预适应对高血脂大鼠心肌缺血一再灌注损伤的保护作用。

方ａｔＳＤ大鼠，造模高血脂后随机分成缺血预适应组（ＩＰ），缺血一再灌注组（Ｉ／Ｒ）以及对照组，每组８只。

取缺氧前及复灌后冠脉流出液测肌酸激酶（ＣＫ）活性，心肌组织测脂质过氧化产物丙二醛（ＭＤＡ）、氧自由基清除剂超氧化物歧化酶（ＳＯＤ）、谷胱苷肽转移酶（ＧＳＨ—Ｐｘ），线粒体测ＡＴＰ酶活性。

结果ＩＰＣ组较Ｉ／Ｒ组冠脉流出液中的ＣＫ生成减少，ＭＤＡ明显降低，ＳＯＤ、ＧＳＨ—Ｐｘ活性增强，Ｎａ＋＿Ｋ＋ＡＴＰａｓｅ、Ｃａ“一ＡＴＰａｓｅ、Ｃａ“一Ｍｇ“．ＡＴＰａｓｅ活性明显升高。

结论心肌缺血预适应对高血脂大鼠心肌缺血一再灌注的损伤同样有保护作用。

【关键词】缺血预适应；再灌注；高血脂；ＡＴＰ酶；大鼠【中图分类号】Ｒ一３３；Ｒ５８９．２；Ｒ５４【文献标识码】ＡＥｆｆｅｃｔｏｆＭｙｏｃａｒｄｉａｌＩｓｃｈｅｍｉｃＰｒｅｃｏｎｄｉｔｉｏｎｉｎｇｏｎＩｓｃｈｅｍｉｃ／ＲｅｐｅｒｆｕｓｉｏｎＩｎｊｕｒｙｉｎＨｉｇｈＢｌｏｏｄＦａｔＲａｔＧＵＯＺｈｕ－ｙｉｎｇ，ＸＵＭａｎｇ－ｈｕａ（ＥｘｐｅｒｉｍｅｎｔａｌＣｅｎｔｅｒ，ＴｈｅＴｈｉｒｄＰｅｏｐｌｅ’ＳＨｏｓｐｉｔａｌ，ＳｃｈｏｏｌｏｆＭｅｄｉｃｉｎｅ，ＳｈａｎｇｈａｉＪｉａｏｔｏｎｇＵｎｉｖｅｒｓｉｔｙ，Ｓｈａｎｇｈａｉ２０１９００，Ｃｈｉｎａ）Ａｂｓｔｒａｃｔ：ＯｂｊｅｃｔｉｖｅＴｏｓｔｕｄｙｔｈｅｅｆｆｅｃｔｏｆｍｙｏｃａｒｄｉａｌｉｓｃｈｅｍｉｃｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇｏｎａｃｔｉｖｉｔｙｏｆＡＴＰａｓｅａｎｄｃｒｅａ—ｔｉｎｅｋｉｎａｓｅ（ＣＫ）ｉｎｈｉｇｈｂｌｏｏｄｆａｔｒａｔ．ＭｅｔｈｏｄｓＨｉｇｈｂｌｏｏｄｆａｔｒａｔｍｏｄｅｗａｓｅｓｔａｂｌｉｓｈｅｄｆｒｏｍＳＤｒａｔｓ．Ｔｈｅｒａｔｓｗｅｒｅｒａｎｄｏｍｌｙｄｉｖｉｄｅｄｉｎｔｏｔｈｒｅｅｇｒｏｕｐｓ：ｉｓｃｈｅｍｉｃｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇ（ＩＰＣ），ｉｓｃｈｅｍｉｃ／ｒｅｐｅｒｆｕｓｉｏｎ（Ｉ／Ｒ）ａｎｄｃｏｎｔｒｏｌｇｒｏｕｐ．ＴｈｅａｃｔｉｖｉｔｙｏｆＣＫｉｎｃｏｒｏｎａｒｙｏｕｔｆｌｏｗ，ｔｈｅａｃｔｉｖｉｔｙｏｆｍａｌｏｎｙｌｄｉａｌｄｅｈｙｄｅ（ＭＤＡ），ｓｕｐｅｒｏｘｉｄｅｄｉｓｍｕｔａｓｅ（ＳＯＤ），ｇｌｕｔａｔｈｉｏｎｅｐｅｒｏｄｘｉｄａｓｅ（ＧＳＨ－Ｐｘ）ａｎｄＡＴＰａｓｅｉｎｍｙｏｃａｒｄｉｕｍｗｅｒｅｄｅｃｔｅｃｔｅｄ．ＲｅｓｕｌｔｓＣＫａｎｄＭＤＡｗｅｒｅｓｉｇｎｉｆｉｃａｎｔｌｙｌｅｓｓｉｎＩＰＣｇｒｏｕｐｔｈａｎｔｈｏｓｅｉｎＩ／Ｒｇｒｏｕｐ．ＩｎＩＰＣｇｒｏｕｐ，ｔｈｅａｃｔｉｖｉｔｙｏｆＳＯＤ，ＧＳＨ－Ｐｘ，Ｎａ＋一Ｋ＋一ＡＴＰａｓｅ．Ｃａ２＋一ＡＴＰａｓｅａｎｄＣａ２＋一Ｍ９２＋一ＡＴＰａｓｅｗｅｒｅｍｕｃｈｈｉｇｈｅｒｔｈａｎｔｈｏｓｅｉｎＩ／Ｒｇｒｏｕｐ．ＣｏｎｃｌｕｓｉｏｎＭｙｏｃａｒ—ｄｉａｌｉｓｃｈｅｍｉｃｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇｃａｎｐｒｏｔｅｃｔｈｉｇｈｂｌｏｏｄｆａｔｒａｔｆｒｏｍｉｓｃｈｅｍｉｅ／ｒｅｐｅｒｆｕｓｉｏｎｉｎｊｕｒｙ．Ｋｅｙｗｏｒｄｓ：ｉｓｃｈｅｍｉｃｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇ；ｒｅｐｅｒｆｕｓｉｏｎ；ｈｉｇｈｂｌｏｏｄｆａｔ；ＡＴＰａｓｅ；ｒａｔ１９８６年Ｍｕｒｒｙ等¨。

无创性延迟肢体缺血预适应对大鼠脑缺血再灌注损伤的保护作用赵会颖;杨永刚;张建平;李贵琴;钱玉中;李倩倩【期刊名称】《河北医科大学学报》【年(卷),期】2017(38)11【摘要】目的观察无创性肢体缺血预适应(noninvasive delayed limbischemic preconditioning,NDLIP)对大鼠脑缺血再灌注损伤的保护作用.方法将30只健康雄性SD大鼠随机分成假手术组、缺血再灌注组和NDLIP组各10只.NDLIP组大鼠给予左侧后肢缺血5 min、再灌注5 min,每天1次,连续操作3d,然后再制作缺血模型;假手术组大鼠给予同样的麻醉和操作,但不进行颈总动脉的闭塞;假手术组和缺血再灌注组不进行NDLIP操作.检测各组大鼠海马超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)含量和Bax、Bcl 2、Caspase-3蛋白表达水平.结果缺血再灌注组和NDLIP组大鼠海马MDA含量明显高于假手术组,SOD含量明显低于假手术组,Bax、Caspase-3表达水平明显高于假手术组,Bcl-2表达水平明显低于假手术组;NDLIP组大鼠海马MDA含量明显低于缺血再灌注组,SOD含量明显高于缺血再灌注组,Bax、Caspase-3表达水平明显低于缺血再灌注组,Bcl-2的表达水平明显高于缺血再灌注组.结论 NDLIP能显著减少脑缺血再灌注损伤后凋亡的发生和氧化应激损伤,对脑缺血再灌注损伤具有保护作用.%Objective To study the protective effectof noninvasive delayed limb ischemia preconditioning(NDLIP) on cerebral ischemia reperfusion injury in rats.Methods Thirty healthy male SD rats randomly divided into 3 groups,Sham-operated group,ischemic-reperfusion group and NDLIPgroup(n =10/group).Rats in NDLIP group were subjected to 5 minutes ischemia/5 minutes reperfusion on the left hind limb once a day for 3 consecutive days,then all rats were subjected to cerebral ischemia reperfusion injury.The Sham-operated group gave the same anesthesia an.d operation,but did not carry out the occlusion of the common carotid artery.The sham-operated group and ischemic-reperfusion group were not performed NDLIP operation.The expression of superoxide dismutase(SOD) and malondialdehyde(MDA) was detected by the kit.The protein expression of Bax,Bcl-2 and Caspase-3 were detected by Western blotting.Results Compared with the rats in the Sham-operation group,the contents of the hippocampal MDA,Bax and Casaspe-3 were significantly higher in the ischemic-reperfusion pared with the rats in the ischemic-reperfusion group,the contents of the hippocampal MDA,Bax and Casaspe3 were significantly decreased in the NDLIP pared with the rats in the Sham-operation group,the contents of the hippocampal SOD and Bcl-2 were significantly decreased in the ischemic-reperfusion pared with the rats in the ischemic-reperfusion group,the contents of the hippocampal SOD and Bcl-2 were significantly increased in the NDLIP group.Conclusion NDLIP could significantly reduce the occurrence of apoptosis and oxidative stress damage after cerebral ischemia reperfusion injury,it has protective effect on cerebral ischemia reperfusion injury.【总页数】4页(P1244-1247)【作者】赵会颖;杨永刚;张建平;李贵琴;钱玉中;李倩倩【作者单位】河北省石家庄市第一医院老年病科,河北石家庄050011;河北省石家庄市第一医院老年病科,河北石家庄050011;河北省石家庄市第一医院老年病科,河北石家庄050011;河北省石家庄市第一医院老年病科,河北石家庄050011;河北省石家庄市第一医院中医科,河北石家庄050011;河北省石家庄市第一医院老年病科,河北石家庄050011【正文语种】中文【中图分类】R743.31【相关文献】1.无创性延迟肢体缺血预适应减轻大鼠脑缺血/再灌注损伤 [J], 罗琼;袁恒杰;吴艳娜;康毅;高卫真;刘艳霞;娄建石2.无创性延迟肢体缺血预适应对大鼠缺血再灌注损伤心肌持续保护效应 [J], 高建波;张颖;娄建石3.无创性肢体缺血预适应的早期及延迟效应对中年大鼠心肌缺血再灌注损伤的保护作用和差异 [J], 宋二飞;陈敏;张轩萍;王微;刘飞君;梁月琴;张明升4.无创性延迟肢体缺血预适应对脑缺血再灌注大鼠存活素和血管内皮生长因子表达的影响 [J], 鲁慧;王彬成;崔宁宁;张艳春;杨兰5.无创性延迟肢体缺血预适应对大鼠脑缺血再灌注皮层的保护作用 [J], 袁恒杰;罗琼;朱学慧;于培;李玉梅;吴艳娜;康毅;焦建杰;娄建石因版权原因，仅展示原文概要，查看原文内容请购买。

缺血预适应在大鼠肢体缺血再灌注后胃黏膜损伤中的作用要瑞莉;张连元;董淑云;门秀丽;杨全会;张一兵;王保强;孙树勋【期刊名称】《中国组织工程研究》【年(卷),期】2007(011)004【摘要】背景:肢体缺血再灌注作为应激原而引起胃黏膜损伤,导致应激性溃疡的发生.目的:观察肢体缺血再灌注对胃黏膜的损伤,了解肢体缺血再灌注对胃黏膜损伤的作用及其部分机制,以及短暂多次肢体缺血在胃黏膜损伤发生中的作用.设计:随机分组设计、对照动物实验.单位:华北煤炭医学院病理生理学教研室.材料:实验于2002-01/06在华北煤炭医学院病理生理学实验室完成.选择健康成年的雄性Wistar大鼠54只随机数字表法分为3组,每组18只.缺血再灌注组:按Rosenthal方法复制模型,乙醚浅麻醉下以橡皮带环绕结扎大鼠双后肢根部,阻断血流4 h后松解,恢复血流灌注4 h后自腹主动脉放血处死.缺血预适应组:如上法预先阻断双后肢血流5 min,然后恢复血流灌注5 min,反复4次,其后操作同缺血再灌注组.对照组:操作同缺血再灌注组,但松弛结扎双后肢,不阻断血流.方法:取各组胃黏膜制作切片于光学显微镜和电子显微镜下进行观察,按Guth标准测定各组胃黏膜损伤指数,在721型分光光度计上于650 nm波长比色,计算胃结合黏液量,同时测定胃黏膜血流量、胃黏液中磷脂、氨基己糖的含量、血浆和胃组织一氧化氮含量及胃黏膜一氧化氮合酶活性.主要观察指标:胃黏膜损伤指数、胃结合黏液量、胃黏膜血流量、胃黏液中磷脂、氨基己糖的含量、血浆和胃组织一氧化氮含量及胃黏膜一氧化氮合酶活性.结果:纳入动物54只,均进入结果分析.①缺血再灌注组大鼠胃黏膜损伤严重,光镜下可见黏膜腺体水肿、充血,糜烂、解体,在黏膜基底部及黏膜下层可见炎细胞浸润,即溃疡形成.缺血预适应组胃黏膜较完整,损伤程度较缺血再灌注组轻;电镜下缺血再灌注组胃壁细胞、主细胞细胞器结构不完整,遭到破坏.同样缺血预适应组各类细胞损伤轻于缺血再灌注组[损伤指数分别为18.00±10.71,34.00±15.01,P＜0.01].②缺血再灌注组和缺血预适应组大鼠胃黏膜血流量及胃结合黏液量、胃黏液中磷脂、氨基己糖的含量均明显低于对照组[分别为(2.12±0.56),(10.84±2.56),(25.52±2.97)mL/(kg·h);(2.01±0.91),(2.79±0.73),(3.9 9±0.87)mg;(7.68±1.95),(9.74±1.04),(11.98±1.98)mg/g;(3.83±1.18),(5.42±0.4 7),(5.76±1.21)mg/g,P＜0.05,0.01].缺血预适应组胃黏膜血流量及胃结合黏液量、胃黏液中磷脂、氨基己糖的含量均高于缺血再灌注组.③缺血再灌注组和缺血预适应组血浆与胃黏膜组织一氧化氮含量及一氧化氮合酶活性显著高于对照组[分别为(250.0±5.6),(270.0±11.3),(210.0±7.4)μmol/L;(9.34±0.67),(11.34±1.00),(7.50±0.67)μkat/g,P＜0.01],缺血预适应组血浆与胃黏膜组织一氧化氮含量和胃黏膜的一氧化氮合酶活性又显著高于缺血再灌注组.结论:肢体缺血再灌注作为应激原可导致胃黏膜损伤,引起应激性溃疡;缺血预适应可减轻肢体缺血再灌注后的胃黏膜损伤.%BACKGROUND: Limb ischemia reperfusion (LIR) as a stressor leads to gastric mucosal injury, and then results in the occurrence of stress ulcer.OBJECTIVE: To observe the effects of LIR on gastric mucosal injury, investigate part of the mechanism, and the role of several transient limb ischemia in the occurrence of gastric mucosal injury.DESIGN: A randomized grouping design and controlled animal experiment.SETTING: Department of Pathophysiology of North China Coal MedicalCollege.MATERIALS: The experiment was carried out in the pathophysiological laboratory of North China Coal Medical College from January to June 2002. Fifty-four healthy adult male Wistar rats were randomly divided into three groups with 18 rats in each group. Ischemiareperfusion (I/R) group: The rats were duplicated into models according to the Rosenthal method that under superficial anesthesia with ether, the roots of both hindlimbs were ligated by wrapping with rubber strap, blood flow was blocked for 4 hours and then recovered to perfusion for 4 hours, and finally killed by bleeding from abdominal aorta. Ischemic preconditioning group: Before model establishment, blood flow of both hindlimbs was blocked for 5 minutes, and then recovered to perfusion for 5 minutes, which was repeated for four times, and the following operations were the same as those in the I/R group. Control group: The operations were the same as those in the I/R group,but both hindlimbs were ligated at relaxation without blocking the blood flow.METHODS: Sections of gastric mucosa were prepared, and then observed under light microscope and electron microscope, and the index of gastric mucosal injury was determined according to the Guth standard. The colorimetric assay was performed with 721 spectrophotometer at 650 nm, and the amount of gastric combining mucus was calculated.Meanwhile, the blood flow of gastric mucosa, contents of phospholipid and hexosamine in gastric mucus, content of nitric oxide in plasma and gastric tissue and activity of nitric oxide synthase (NOS) in gastric mucosa were determined.MAIN OUTCOME MEASURES: Index of gastric mucosal injury, amount of gastric combining mucus, blood flow of gastric mucosa, contents of phospholipid and hexosamine in gastric mucus, contents of nitric oxide in plasma and gastric tissue and NOS activity in gastric mucosa.RESULTS: All the 54 rats were involved in the analysis of results. ① In the I/R group, gastric mucosalinjury was serious, edema, hyperemia, erosion and disintegration of gland of mucosal glands were observed, infiltration of inflammatory cells (formation of ulcer) was observed in basal and inferior mucosa. In the ischemic preconditioning group, the gastric mucosa was complete, and the damaged severity was milder than that in the I/R group; Under electron microscope, the organell structures of gastric parietal and chief cells were incomplete and destroyed. The cell injuries in the ischemic preconditioning group were milder than those in the I/R group (index of injury:18.00±10.71, 34.00±15.01, P＜ 0.01). ② The blood flow and combining mucosal amount of gastric mucosa, contents of phospholipid and hexosamine in gastric mucus in the ischemic preconditioning group andI/R group were all obviously lower than those in the control group [(2.12±0.56), (10.84±2.56), (25.52±2.97) mL/(kg·h); (2.01±0.91), (2.79±0.73), (3.99±0.87) mg;(7.68±1.95), (9.74±1.04), (11.98±1.98) mg/g; (3.83±1.18), (5.42±0.47), (5.76±1.21) mg/g, P ＜ 0.05, 0.01], those the above indexes were all higher in the ischemic preconditioning group than in the I/R group. ③ The contents of nitric oxide in plasma and gastric tissue and NOS activity in gastric mucosa in the ischemic preconditioning group and I/R group were significantly lower than those in the control group [(250.0±5.6), (270.0±11.3), (210.0±7.4) μmol/L; (9.34±0.67), (11.34±1.00), (7.50±0.67) μ kat/g, P ＜ 0.01], those were also signficantly higher in the ischemic preconditioning group than in the I/R group.CONCLUSION: As a stressor, LIR can lead to gastric mucosal injury, and cause stress ulcer.Ischemic preconditioning can alleviate the gastric mucosal injury following LIR【总页数】4页(P791-794)【作者】要瑞莉;张连元;董淑云;门秀丽;杨全会;张一兵;王保强;孙树勋【作者单位】华北煤炭医学院病理生理学教研室,河北省唐山市,063000;华北煤炭医学院病理生理学教研室,河北省唐山市,063000;华北煤炭医学院病理生理学教研室,河北省唐山市,063000;华北煤炭医学院病理生理学教研室,河北省唐山市,063000;华北煤炭医学院病理生理学教研室,河北省唐山市,063000;华北煤炭医学院病理生理学教研室,河北省唐山市,063000;华北煤炭医学院病理生理学教研室,河北省唐山市,063000;华北煤炭医学院病理生理学教研室,河北省唐山市,063000【正文语种】中文【中图分类】R5【相关文献】1.内质网应激诱导的细胞凋亡在大鼠肢体缺血再灌注后肺损伤中的作用及牛磺酸的影响 [J], 成兰云;门秀丽;张连元;李宏杰;孔小燕;赵利军2.缺血预适应在大鼠肢体缺血再灌注后胃粘膜损伤中的作用 [J], 要瑞莉;张连元;门秀丽;董淑云;杨全会;张一兵;王保强;孙树勋3.缺血预适应对大鼠肢体缺血再灌注后小肠损伤的保护效应及NO的作用 [J], 刘燕;彭海兵;张博;周洪霞;杨秀红;张连元4.Bach1/Nrf2通路调控HO-1在大鼠肢体缺血再灌注后肺损伤中的作用机制研究[J], 李艳艳;孙克玉;邱志云;龚霞;王继芹5.内质网应激在大鼠肢体缺血再灌注后肺损伤中的作用 [J], 门秀丽;张连元;李宏杰因版权原因，仅展示原文概要，查看原文内容请购买。