银杏叶提取物预处理对胰腺移植受体大鼠 小肠肠黏膜屏障的影响

目的 ：探讨银杏叶提取物（EGb）对胰腺移植受体大鼠肠黏膜屏障的保护作用及其机制。方法 ：12只正常SD大鼠为对照组;糖尿病大鼠随机分为胰腺移植组（PT组， n =12）及银杏叶提取物预处理胰腺移植组（EGb组， n =12），大鼠均接受同系胰腺移植。EGb组于移植前1d和30min予受体静脉注射EGb （1.5mL/kg）。移植术后5 d测定小肠通透性和吸收功能，检测血清TNF-α，NO，SOD和淀粉酶活性。取受体回肠黏膜组织测定小肠黏膜湿重、微绒毛厚度及宽度、MDA含量及MPO活性。同时取肠系膜静脉血、肠系膜淋巴结、肝及脾组织行细菌培养，观察细菌易位情况。结果 ：EGb组血清TNF-α含量（ P <0.01）、淀粉酶活性（ P <0.01）、MDA含量（ P <0.05）、MPO活性（ P <0.05）、小肠通透性（ P <0.01）、细菌易位率（ P <0.01）和小肠黏膜损伤程度均低于PT组;血清NO和SOD含量、小肠吸收功能均高于PT组( P <0.01)。结论 ：EGb预处理可保护胰腺移植受体大鼠小肠肠黏膜屏障，降低细菌易位率，机制可能与抗氧化、清除自由基、减少TNF-α生成、减轻嗜中性粒细胞黏附与聚集、增加内源性NO的生成有关。     

参附注射液对大鼠胰腺移植受体小肠肠粘膜屏障的保护作用

目的探讨参附注射液（SF）对大鼠胰腺移植受体肠粘膜屏障的保护作用及机制。方法24只糖尿病大鼠随机分为缺血再灌注组（IR组。n=12），参附注射液预处理组（SF组．n=12），12只正常大鼠为对照组，IR组和SF组大鼠均接受胰腺移植，再灌注后5d检测小肠通透性和吸收功能，检测血清TNF-α、NO、SOD和淀粉酶活性，取受体空肠粘膜组织检测小肠粘膜粘膜湿重、微绒毛高度及宽度、MDA含量及MPO活性，同时取肠系膜静脉血、肠系膜淋巴结、肝及脾组织进行细菌培养，观察细菌易位情况。结果再灌注后SF组血清TNF—α含量（P〈0．01）、淀粉酶活性（P〈0．01）、MDA含量（P〈0．01）、MPO活性（P〈0．01）、小肠通透性（P〈0．01）、细菌易位率（P〈0．01）和小肠粘膜损伤程度均低于IR组；血清NO和SOD含量、小肠吸收功能均高于IR组（P〈0．01）。结论SF预处理可保护大鼠胰腺移植受体小肠肠粘膜屏障，降低细菌易位率，机制可能与降低胰酶活性、减少TNF—α生成、减轻PMNs粘附与聚集、增加NO和SOD含量有关。     

参附注射液对大鼠胰腺移植受体小肠肠粘膜屏障的保护作用

目的探讨参附注射液(SF)对大鼠胰腺移植受体肠粘膜屏障的保护作用及机制。方法24只糖尿病大鼠随机分为缺血再灌注组(IR组,n=12),参附注射液预处理组(SF组,n=12),12只正常大鼠为对照组,IR组和SF组大鼠均接受胰腺移植,再灌注后5d检测小肠通透性和吸收功能,检测血清TNF-α、NO、SOD和淀粉酶活性,取受体空肠粘膜组织检测小肠粘膜粘膜湿重、微绒毛高度及宽度、MDA含量及MPO活性,同时取肠系膜静脉血、肠系膜淋巴结、肝及脾组织进行细菌培养,观察细菌易位情况。结果再灌注后SF组血清TNF-α含量(P<0.01)、淀粉酶活性(P<0.01)、MDA含量(P<0.01)、MPO活性(P<0.01)、小肠通透性(P<0.01)、细菌易位率(P<0.01)和小肠粘膜损伤程度均低于IR组;血清NO和SOD含量、小肠吸收功能均高于IR组(P<0.01)。结论SF预处理可保护大鼠胰腺移植受体小肠肠粘膜屏障,降低细菌易位率,机制可能与降低胰酶活性、减少TNF-α生成、减轻PMNs粘附与聚集、增加NO和SOD含量有关。     

腑安汤对小鼠术后肠麻痹的影响及机制

目的：探讨腑安汤对术后肠麻痹的治疗作用及相关机制。方法：90只小鼠随机均分为假手术组、模型组和腑安汤预处理组后常规制作术后肠麻痹模型或行假手术。应用ELISA法测定小肠组织中类胰蛋白酶、组胺含量;光镜下观察经甲苯胺蓝染色的肠系膜肥大细胞计数及脱颗粒情况;利用比色法测定小肠组织中髓过氧化物酶（MPO）活性;检测小鼠肠道内碳末移行率。结果：与假手术组比较,模型组小肠组织类胰蛋白酶、组胺含量和MPO活性均明显升高（均P<0.01）,而腑安汤预处理组小肠组织类胰蛋白酶、组胺含量和MPO活性的升高受到明显抑制,与模型组比较,差异均有统计学意义（均P<0.01）;各组肥大细胞计数无统计学差异（P>0.05）,但模型组细胞脱颗粒明显,而腑安汤预处理组较弱;术后模型组碳末移行率明显降低（P<0.01）,腑安汤预处理组碳末移行率较模型组明显增加（P<0.01）;相关性分析显示,MPO活性与碳末移行率呈负明显相关（r=-0.885,P<0.01）。结论：腑安汤可减少术后小鼠肠道类胰蛋白酶和组胺的产生,抑制肥大细胞脱颗粒及其所介导的炎症反应,有预防和减轻术后肠麻痹的作用。     

缺血后处理对双后肢缺血-再灌注大鼠小肠的影响

目的 观察缺血后处理对肢体缺血-再灌注大鼠小肠损伤的保护作用.方法 雄性Wistar大鼠108只随机均分为双后肢缺血-再灌注组(LIR组)、缺血后处理组(IPo组)和假手术组(S组).检测再灌注即刻(T1)、1 h(T2)、3 h(T3)、6 h(T4)、12 h(T5)和24 h(T6)小肠组织中超氧化物歧化酶(SOD)活性、髓过氧化物酶(MPO)活性、丙二醛(MDA)含量和小肠组织的湿/干重比值(W/D),光镜下对小肠黏膜行Chiu's病理分级.结果 与S组比较,LIR组和IPo组各时点小肠黏膜Chiu's病理分级、MDA含量、MPO活性和W/D升高,SOD活性降低(P＜0.05),并随再灌注时间的变化而变化;与LIR组比较,T3～T6时IPo组Chiu's病理分级降低,T2～T6时MDA含量、MPO活性和W/D显著下降,而SOD活性升高(P＜0.05).结论 缺血后处理对大鼠双后肢缺血-再灌注小肠具有保护作用,其保护机制可能与抑制氧自由基及中性粒细胞活化有关.     

静脉输注高氧液对家兔小肠缺血再灌注损伤的影响

目的 评价静脉输注高氧液对家兔小肠缺血再灌注损伤的影响.方法 健康成年家兔24只,雌雄不拘,体重2.5 ～ 3.2 kg,采用随机数字表法,将家兔随机分为3组(n=8):假手术组(S组)、小肠缺血再灌注组(I/R组)和静脉输注高氧液组(HOS组).S组仅开腹游离但不夹闭肠系膜上动脉,I/R组和HOS组采用夹闭肠系膜上动脉1h恢复灌注2h的方法制备家兔小肠缺血再灌注模型,于夹闭肠系膜上动脉即刻HOS组耳缘静脉输注高氧液20 ml·kg-1 ·h-1,I/R组静脉输注等容量生理盐水.于再灌注2h时采集下腔静脉血样,检测血清乳酸浓度,处死家兔取小肠组织,测定丙二醛(MDA)含量、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧物酶(GSH-Px)的活性,光镜及电镜下观察肠上皮组织病理学结果,行肠黏膜损伤评分.取内脏组织,观察细菌移位情况.结果 与S组相比,I/R组和HOS组肠组织MDA含量、血清乳酸浓度和细菌移位率升高,SOD、CAT和GSH-Px活性降低(P＜0.05);与I/R组相比,HOS组肠组织MDA含量、血清乳酸浓度和细菌移位率降低,SOD、CAT和GSH-Px活性降低(P＜0.05).结论 静脉输注高氧液可减轻家兔小肠缺血再灌注损伤.     

缺血后处理对小肠缺血再灌注损伤的保护作用

目的：观察缺血后处理减轻肠缺血再灌注引起的小肠及远隔脏器损伤的效果,并探讨其机制。方法将家兔48只随机分为假手术组、缺血再灌注组、缺血后处理组,每组16只。再灌注2 h 后采集各组动脉血、静脉血及部分肠道组织、肝、肺组织,测动脉血中 TNF-α、IL-1β、IL-6、IL-10水平,测静脉血中 ALT、AST、BUN,Cr、LDH、CK-MB 活性,测内毒素水平,测定血清及小肠、肝、肺组织 MDA、MPO、CAT、SOD 水平,HE 染色,观察肠黏膜损伤情况,细菌培养观察细菌易位率。结果与缺血再灌注组比较,缺血后处理组血清及小肠、肝、肺组织中 MDA、MPO 水平明显降低, SOD、CAT 水平明显升高,静脉血 ALT、AST、LDH、CK-MB、BUN 下降;动脉血中 TNF-α、IL-1β、IL-6、内毒素降低,IL-10水平升高,肠黏膜损伤评分明显降低。结论缺血后处理可以减轻肠黏膜损伤,减少内毒素易位,促进抗炎因子的激活,抑制炎性介质的过度释放,提升小肠组织及远隔脏器的氧自由基的抗氧化能力,减轻小肠及远隔脏器组织损伤。     

Nrf2/HO-1信号通路在阿托伐他汀减轻小鼠肠缺血再灌注损伤中的作用

目的评价核因子NF-E2相关因子2(Nrf2)/血红素加氧酶-1(HO-1)信号通路在阿托伐他汀减轻小鼠肠缺血再灌注损伤中的作用。方法健康雄性C57BL/6小鼠24只,6～8周龄,体重18～22 g。采用随机数字表法分为4组(n=6):假手术组(S组)、肠缺血再灌注组(I/R组)、阿托伐他汀组(ATV组)和阿托伐他汀+Nrf2抑制剂ML385组(AM组)。采用夹闭肠系膜上动脉45 min恢复灌注的方法建立小鼠肠缺血再灌注损伤模型。ATV组和AM组造模前3 d每天灌胃给予阿托伐他汀10 mg/kg,S组和I/R组灌胃给予等容量生理盐水;AM组于造模前1 h腹腔注射Nrf2抑制剂ML385 30 mg/kg。于再灌注2 h时处死小鼠,取小肠组织,光镜下观察病理学结果,并对肠黏膜损伤程度进行Chiu评分;计算小肠组织湿重/干重比值(W/D比值),分别采用黄嘌呤氧化酶法和硫代巴比妥酸缩合法检测肠组织SOD活性和MDA含量,采用Western blot法测定Nrf2和HO-1表达水平。结果与S组比较,其余3组小肠组织Chiu评分、W/D比值和MDA含量升高,SOD活性降低,Nrf2和HO-1表达...     

HMGB1对急性坏死性胰腺炎大鼠肠上皮细胞紧密连接相关蛋白表达的影响

目的：观察急性坏死性胰腺炎（ANP）大鼠肠黏膜中高迁移率族蛋白B1（HMG81）的表达对肠黏膜上皮细胞紧密连接功能的影响。方法：24只Wistar大鼠随机分为正常对9帚组、ANP组和丙酮酸乙酯（EP）处理组,分别于建模后24h取材。测定血浆淀粉酶（AMY）、血浆D-乳酸、肠黏膜髓过氧化物酶（MPO）水平变化;应用Westernblot法检测ANP大鼠肠黏膜中HMGBl和occludin蛋白水平的变化。结果：在建模后24h,大鼠AMY、D-乳酸与肠黏膜MPO水平ANP组明显高于正常对照组和EP处理组（P〈0．05）,但EP处理组仍高于正常对照组（P〈0．05）;ANP组大鼠肠黏膜HMGBl表达水平明显高于正常对照组和EP处理组（P〈005）,EP处理组高于正常对照组（P〈0．05）;而肠黏膜上皮细胞紧密连接蛋白occludin的表达ANP组较正常对照组和EP处理组下降（P〈0．05）,EP处理组低于正常对照组（P〈0．05）。结论：ANP大鼠肠黏膜中HMGBl表达增高,可通过降低occludin蛋白表达,增加肠黏膜屏障通透性。EP能显著抑制HMGBl表达,使occludin蛋白表达升高,对ANP肠黏膜损伤有明显保护作用。     

下胸段硬膜外阻滞对失血性休克-复苏大鼠肠黏膜上皮细胞凋亡的影响

目的探讨下胸段硬膜外阻滞对失血性休克-复苏大鼠肠黏膜上皮细胞凋亡的影响。方法健康成年雄性SD大鼠64只,3月龄,体重280~320 g,硬膜外置管成功,随机分为四组,每组16只:假手术组(Sham组)、休克-复苏组(HSR组)、下胸段硬膜外注射生理盐水+休克-复苏组(NS组)、下胸段硬膜外阻滞+休克-复苏组(TEA组)。Sham组仅行硬膜外置管,不实施失血性休克,其余三组均采用改良Chaudry法制备失血性休克-复苏模型,放血前30 min TEA组硬膜外注射0.075%罗哌卡因100μl/kg,NS组注入等量生理盐水,HSR组不给予硬膜外注射。复苏后2 h采用化学反应法测定肠黏膜丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性,采用TUNEL、免疫组化法分别测定肠黏膜细胞凋亡和Bcl-2、Bax蛋白含量。结果与Sham组比较,HSR组、NS组和TEA组肠黏膜Chiu评分、MDA含量、Bax蛋白含量、上皮细胞凋亡指数明显增高(P0.05),SOD活性明显降低(P0.05)。与HSR组和NS组比较,TEA组Chiu评分、MDA含量、Bax蛋白含量、上皮细胞凋亡指数明显降低(P0.05),SOD活性和Bcl-2蛋白含量明显升高(P0.05)。结论下胸段硬膜外阻滞可增强肠黏膜抗氧化、抗凋亡能力,从而抑制黏膜上皮氧化应激和细胞凋亡,保护肠黏膜屏障功能,以促进失血性休克-复苏后生存。     

血红素氧合酶-1/一氧化碳在高动力循环大鼠肝脏缺血/再灌注肺损伤中的保护作用

目的 研究血红素氧合酶-1(HO-1)对高动力循环大鼠肝脏缺血/再灌注引起肺损伤的保护作用,以及其与一氧化碳(CO)的关系.方法 32只雄性SD大鼠,随机分为4组:假手术组(sham operation,S组),高动力循环组(hyperdynamic,HC组)是对门静脉结扎大鼠隔日皮下注射脂多糖(10μg/100 g)三周,每组8只.肝脏缺血/再灌注组(hepatic ischemia-leper-fusion,HIR)是对高动力循环大鼠处死前行全肝缺血20 min后再灌注1 h.血晶素组是对高动力循环大鼠肝脏缺血/再灌注前1 h腹腔注射血晶素50 mg/kg.所有大鼠在处死前静脉注射伊文思蓝30 mg/kg.大鼠处死前取动脉血测碳氧血红蛋白含量,通过测量肺组织含水率(肺叶湿重/干重×100%)和伊文思蓝含量来评估肺微循环通透性,取肺组织测伊文思蓝含量,丙二醛(malondialdehyde,MDA)含量,髓过氧化物酶(myeloperoxidase,MPO)含量和超氧化物歧化酶(superoxide,SOD)活力变化以及肺组织血红素氧合酶(hemeoxygenase-1,HO-1)活性变化.结果 与S组和HC组相比,HIR组和血晶素组肺叶湿/干重比、伊文思蓝含量、MDA含量、MPO含量均显著增加,而SOD活力则显著下降(P<0.01).与HIR组相比,血晶索组伊文思蓝含量、MDA含量、MPO含量降低(P<0.05).与S组和HC组相比,HIR组和血晶素组碳氧血红蛋白(carboxyhemoglobin,CO-Hb)含量和HO-1活性增加(P<0.01).与HIR组相比,血晶素组碳氧血红蛋白(carboxyhemoglobin,COHb)含量和HO-1活性增加(P<0.05).门静脉压力在各组之间均有统计学意义(P<0.01).结论 CO产生增加参与高动力循环大鼠肝脏缺血/再灌注肺损伤保护,这与HO-1活性增加相关.血晶素可以上调肝脏缺血/再灌注期肺组织HO-1/CO系统,这可能是对损伤的内源性代偿反应.     

15-F2t-isoprostane在大鼠肠缺血再灌注损伤中的作用

目的 评价异构前列腺素15-F2t-isoprostane在大鼠肠缺血再灌注损伤中的作用.方法 健康雄性SD大鼠32只,体重230 ～ 255 g,采用随机数字表法,将其随机分为4组(n=8):假手术组(S组)、肠缺血再灌注组(I/R组)、血栓烷A2(TXA2)受体拮抗剂SQ-29548组(SQ组)和二甲基亚砜组(DMSO组).采用阻断肠系膜上动脉60 min,再灌注120 min的方法制备肠缺血再灌注损伤模型.SQ组及DMSO组分别于夹闭肠系膜上动脉前30 min腹部皮下注射SQ-29548或二甲基亚砜2μmol/kg.于再灌注120 min时取肠段,观察肠粘膜形态学,并行Chiu评分,取肠粘膜组织,检测髓过氧化物酶(MPO)、超氧化物歧化酶(SOD)活性和丙二醛(MDA)、乳酸(LD)含量;采集动脉血样,检测血清二胺氧化酶( DAO)活性及15-F2t-isoprostane、内皮素-1(ET-1)和血栓烷B2(TXB2)浓度.结果 与S组比较,其余各组Chiu评分、DAO活性、15-F2t-isoprostane及TXB2浓度均升高(P＜0.05),SQ组LD和MDA含量、MPO和SOD活性及ET-1浓度差异无统计学意义(P＞0.05);与I/R组比较,SQ组Chiu评分、LD含量、DAO和MPO活性及ET-1浓度降低,SOD活性升高(P＜0.05).结论 15-F2t-isoprostane可通过激活TXA2受体,增加ET-1生成及促进中性粒细胞在肠粘膜聚集参与大鼠肠缺血再灌注损伤过程.     

The effect of heme oxygenase-1 induction by glutamine on radiation-induced intestinal damage: the effect of heme oxygenase-1 on radiation enteritis

BACKGROUND: Radiation enteritis is a significant clinical problem in patients receiving ionizing radiation directed at the abdomen or pelvis. The small intestine is the most radiosensitive gastrointestinal organ. Myeloperoxidase (MPO) activity and malondialdehyde (MDA) levels of the small intestine were measured to determine the oxidative damage caused by radiation. In addition, caspase-3 activity of the small intestine was measured to define the degree of apoptosis. The present study was undertaken to investigate the effect of glutamine administration on heme oxygenase-1 (HO-1) expression of the radiation enteritis model. METHODS: Rats received 1 g/kg/d glutamine (HO-1-inducer) for 7 days before irradiation and continued for 3 days after irradiation. Zn-prothoporphyin (Zn-PP) 40 micromol/kg was delivered subcutaneously for 1 day before irradiation. Intestinal MPO activities and MDA levels are indicators of oxidative damage, whereas caspase-3 activities show the degree of apoptosis of the small intestine. At histopathologic examination, terminal ileum tissue was analyzed for morphologic changes. Also, the nuclear factor-kappa (NF-kappa) expression level of the terminal ileum was determined with immunohistochemistry methods to show the mucosal inflammatory process. RESULTS: Irradiation significantly increased the intestinal MPO and caspase-3 activities, MDA levels, and HO-1 expression in comparison with the sham group. Glutamine treatment was associated with increased HO-1 expression, decreased MPO activity, caspase-3 activity, and MDA levels. Inhibition of HO-1 activity by Zn-PP completely eliminated the protective effects of glutamine. Histopathologic examination showed that the intestinal mucosal structure was preserved in the glutamine-treated group. In the irradiation group, NF-kappaB overexpression was detected. NF-kappaB positivity was strongest in the intestine of animals in the radiation alone group and the Zn-PP-treated irradiation group. CONCLUSIONS: Glutamine appears to have protective effects against radiation-induced intestinal damage. This protective effect is mediated in part by the induction of HO-1 activity because inhibition of Zn-PP resulted in the complete abolishment of the protective effect of glutamine.     

The effects of methylene blue on lung injury in septic rats

PURPOSE: We aimed to investigate the effects of methylene blue (MB) on NO production, myeloperoxidase (MPO) activity, antioxidant status and lipid peroxidation in lung injury during different stages of sepsis in rats. MATERIAL AND METHODS: Rats were randomly divided into 4 groups (n = 20): group C, sham operated; group CMB, sham operated and receiving MB (25 mg/kg, i.p.); group S, sepsis; group SMB, sepsis and receiving MB (25 mg/kg, i.p.). Sepsis was induced by cecal ligation and puncture (CLP). The MB dose was administered after CLP. Each group was subdivided into two subgroups (n = 10) which were sacrificed at 9 or 18 h after the surgical procedure. The levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) and MPO activity, total nitrite/nitrate and malondialdehyde (MDA) in the lung tissue were measured. Lung injury was graded from 1 (injury to 25% of the field) to 4 (diffuse injury) by the pathologist. RESULTS: In group SMB, while SOD and CAT increased in both early and late sepsis periods, GSH-PX increased significantly only in the early sepsis period when compared with group S. Increase in lung MPO activity after CLP-induced sepsis was prevented by MB administration. MB significantly decreased to nitrite/nitrate and MDA levels both in early and late sepsis periods when compared with group S (p < 0.05). Group S showed a marked increase in neutrophil infiltration into the interstitial space and thickening of the alveolar septa, whereas the alveolar damage score was lower in the SMB group (p < 0.05). CONCLUSION: MB reduced the MPO activity and lipid peroxidation by both decreasing oxidative stress and NO overproduction in the lungs, which resulted in the attenuation of lung injury after CLP-induced sepsis in rats.     

维生素C减轻重度烧伤休克犬肠内补液时过氧化损伤的观察

目的 了解维生素c对重度烧伤休克犬肠内补液时过氧化损伤的影响. 方法 将18只雄性Beagle犬行颈动、静脉置管和十二指肠造几后24 h造成50%TBSAⅢ度烧伤.伤后按随机数字表法分为不补液组(伤后无治疗)、肠内补液组和肠内补液+维生素C组,每组6只.肠内补液组和肠内补液+维生素C组于伤后30 min开始从十二指肠造口管分别注入葡萄糖-电解质溶液(GES)、含维生素C的GES液(250 mg/kg维生素C溶于GES),依据Parkland公式计算输液量和速率.于伤前(0 h)和伤后2、4、8 h抽取犬静脉血检测血浆二胺氧化酶(DAO)活性.伤后8 h处死犬,取空肠组织测定丙二醛(MDA)含量以及髓过氧化物酶(MPO)、黄嘌呤氧化酶(XOD)和超氧化物歧化酶(SOD)活性,干湿质量法测定小肠组织含水率. 结果 伤后各组犬血浆DAO活性均较伤前显著升高,伤后6、8 h肠内补液组明显高于不补液组(P<0.05);肠内补液+维生素C组从伤后2 h起DAO活性均明显低于不补液组和肠内补液组(P<0.05或P<0.01).伤后8 h肠内补液组MDA含量,MPO、XOD活性和肠组织含水率分别为(5.74±0.51)nmol/mg、(2.08±0.46)U/g、(58.4±3.8)U/mg、(81.5±1.8)%,均显著高于不补液组[(5.43±0.25)nmol/mg、(1.55±0.21)U/g、(50.1±2.8)U/mg、(78.3±1.5)%,P<0.05或P<0.01],而SOD活性(72±12)U/mg低于不补液组(97±20)U/mg(P<0.01).肠内补液+维生素C组MDA含量,MPO、XOD活性和小肠组织含水率低于肠内补液组,而SOD活性高于肠内补液组(P<0.01). 结论 维生素C能改善烧伤休克犬缺血再灌注过程引起的过氧化损伤和肠组织水肿,减轻口服补液时的肠道并发症.     

A monoclonal antibody against cytokine-induced neutrophil chemoattractant attenuates injury in the small intestine in a model of ruptured abdominal aortic aneurysm

PURPOSE: Ruptured abdominal aortic aneurysm (RAAA) continues to be a major source of aneurysm-related morbidity and mortality. Neutrophils have been implicated in RAAA repair-induced organ injury; however, the agents responsible for neutrophil activation and organ sequestration have not been identified. This study investigated the role of cytokine-induced neutrophil chemoattractant (CINC) in organ injury in an RAAA model. METHODS: Rats were subjected to 1 hour of hemorrhagic shock with resuscitation, followed by 45 minutes of lower torso ischemia and 2 hours of reperfusion, and randomly were selected to receive saline solution or anti-rat CINC monoclonal antibody at the start of hemorrhagic shock. Another group of animals underwent sham operation, and served as a control group. Intestinal and lung permeability, intestinal and lung myeloperoxidase (MPO) activity, intestinal and lung CINC, and tumor necrosis factor-alpha (TNF-alpha) levels, resuscitation fluid requirements, and histologic mucosal injury were evaluated in all groups. RESULTS: The RAAA model resulted in increased lung and intestinal permeability to radiolabeled albumin and lung MPO activity (P <.01), with increases in intestinal TNF-alpha (P <.001) and CINC (P <.01) levels, when compared with sham-operated animals. Treatment with anti-rat CINC monoclonal antibody attenuated the increases in intestinal permeability and histologic mucosal injury (P <.01), gut TNF-alpha level (P <.001), and resuscitation fluid volume required (P <.05), without significantly affecting lung and intestinal MPO activity, lung permeability, and intestinal CINC level (P = NS), compared with animals given saline solution. CONCLUSION: Neutralization of CINC by the anti-rat CINC monoclonal antibody attenuated intestinal injury and induction of intestinal TNF-alpha, but failed to significantly attenuate remote pulmonary injury in this model of RAAA.     

缺血预处理-后处理对大鼠肠缺血再灌注损伤的影响

目的 评价缺血预处理.后处理对大鼠肠缺血再灌注损伤的影响.方法 清洁级成年雄性SD大鼠40只.体重225～275 g,随机分为5组(n=8):假手术组(S组)仅分离肠系膜上动脉(SMA),不夹闭;肠缺血再灌注组(IIR组)采用夹闭SMA 60 min,再灌注60 min的方法制备肠缺血再灌注损伤模型;缺血预处理组(IPr组)夹闭SMA 10 min,再灌注10 min,余同IIR组;缺血后处理组(IPo 组)夹闭SMA 60 min后,再灌注30 s,缺血30 s,反复3次,再灌注60 min;缺血预处理.后处理组(IPr-IPo组)先行缺血预处理,再行缺血后处理,操作过程同IPr组和IPo组.于再灌注60 min时各组取肠粘膜组织,观察肠粘膜形态并行Chiu评分,检测丙二醛(MDA)含量,超氧化物歧化酶(SOD)及髓过氧化物酶(MPO)活性,同时采集动脉血样检测血浆肿瘤坏死因子α(TNF-α)及白细胞介素6(IL-6)浓度.结果 与S组比较,其余各组Chiu评分、MDA含量、MPO活性、血浆TNF-α与IL-6浓度升高,SOD活性降低(P<0.05).与IIR组比较,IPr组、IPo组及IPr-IPo组Chiu评分、MDA含量、MPO活性、血浆TNF-α和IL-6浓度降低.SOD活性升高(P<0.01).与IPr组和IPo组比较,IPr-IPo组Chiu评分和MDA含量降低,SOD活性升高(P<0.05).IPr组与IPo组各指标比较差异无统计学意义(P>0.05).结论 缺血预处理-后处理可减轻大鼠肠缺血再灌注损伤,较单独应用时效果好.     

亚甲蓝预处理对大鼠肝缺血再灌注肺损伤的保护作用

目的研究肝缺血再灌注后肺损伤的机制以及亚甲蓝的保护作用。方法 36只SD大鼠随机分为假手术组（S组,n=12）、缺血再灌注组（I/R组,n=12）和亚甲蓝处理组（MB组,n=12）。阻断肝门30分钟后开放血流,建立大鼠全肝缺血再灌注模型。I/R组与MB组分别于肝门阻断前10分钟腹腔注射亚甲蓝10mg/kg或相应剂量生理盐水,于再灌注1小时取血、处死动物。假手术组不阻断肝门,于上述相应时间点注射生理盐水与取血、处死动物。肝肺病理切片光镜观察、肺干湿重比、肺组织丙二醛（MDA）含量、髓过氧化物酶（MPO）活力、血清TNF-α和IL-8含量。结果病理结果显示,亚甲蓝组缺血再灌注后肺损害程度较缺血再灌注组减轻。缺血再灌注组较假手术组肺组织干湿重比、MDA含量、MPO活性和血清TNF-α和IL-8含量升高（P〈0.01）,而亚甲蓝组较缺血再灌注组肺组织干湿重比和血清TNF-α和IL-8含量（P〈0.01）,MDA含量和MPO活性（P〈0.05）均有下降。结论肝缺血再灌注会导致肺损伤,缺血前给予亚甲蓝对大鼠肝I/R后肺损伤具有有保护作用。