色甘酸钠对大鼠肠缺血再灌注损伤的作用

目的 探讨肥大细胞膜稳定剂色甘酸钠对大鼠肠缺血再灌注损伤的作用。方法 32只SD大鼠随机分为4组（n=8）：假手术组（S组）、缺血再灌注组（I/R组）、缺血再灌注＋色甘酸钠25 mg/kg组（C1组）及缺血再灌注＋色甘酸钠50 mg/kg组（C2组）。采用肠缺血45 min再灌注1h制备肠缺血再灌注损伤模型,C1组、C2组再灌注前15min腹腔注射色甘酸钠。再灌注1h后,取小肠组织,光镜下观察小肠粘膜病理学改变,进行Chiu评分,电镜下观察小肠粘膜的超微结构,测定小肠肿瘤坏死因子-α（TNF-α）及组胺含量,进行肠粘膜肥大细胞（IMMC）计数,并测定类胰蛋白酶表达。结果 肠缺血再灌注导致小肠Chiu评分、TNF-α含量、IMMC计数及类胰蛋白酶表达增加,组胺含量降低,IMMC出现胞浆颗粒明显减少,颗粒包膜相互融合形成细胞内空泡等脱颗粒现象;色甘酸钠25、50mg/kg可减弱肠缺血再灌注导致的上述改变,且50mg/kg的作用更明显。Chiu评分与TNF-α、组胺、类胰蛋白酶水平有相关性,相关系数分别为0．532、-0．770（P＜0．05）。结论 色甘酸钠25、50mg/kg可抑制IMMC活性,减少TNF-α的释放,从而减轻了大鼠肠缺血再灌注损伤;色甘酸钠50mg/kg的效果较好。     

地塞米松不同时期给药对小鼠肠缺血再灌注损伤及诱导型一氧化氮合酶活性的影响

目的 评价地塞米松不周时期给药对小鼠肠缺血再灌注损伤及诱导型一氧化氮合酶(iNOS)活性的影响.方法 健康清洁级雄性昆明小鼠35只,体重20～24 g,采用随机数字表法,将其随机分为5组(n=7):假手术组(Ⅰ组)、肠缺血再灌注组(Ⅱ组)、地塞米松缺血前给药组(Ⅲ组)、地塞米松缺血期给药组(Ⅳ组)和地塞米松再灌注即刻给药组(Ⅴ组).采用阻断肠系膜上动脉30 min再灌注的方法制备肠缺血再灌注损伤模型.Ⅰ组只分离肠系膜上动脉,不阻断;Ⅱ组和Ⅲ组分别在缺血前30 min经尾静脉注射生理盐水和地塞米松10 mg/kg;Ⅳ组于缺血5 min时、Ⅴ组于再灌注即刻静脉注射地塞米松10 mg/kg.再灌注3h时处死小鼠,取小肠组织,光镜下观察小肠粘膜病理学结果,采用Chiu评分法对小肠病理损伤进行评分;采用硝酸还原酶法检测一氧化氮(NO)含量,采用比色法检测iNOS的活性.结果 与Ⅰ组比较,Ⅱ组～Ⅴ组肠组织Chiu评分、Ⅱ组、Ⅳ组和Ⅴ组肠组织iNOS活性和NO含量升高(P＜0.05),Ⅲ组肠组织iNOS活性和NO含量差异无统计学意义(P＞0.05);与Ⅱ组比较,Ⅲ组肠组织Chiu评分、iNOS活性和NO含量降低,Ⅴ组肠组织Chiu评分、iNOS活性和NO含量均升高,Ⅳ组上述指标差异无统计学意义(P＞0.05).结论 地塞米松缺血前给药可减轻小鼠肠缺血再灌注损伤,缺血期给药对损伤无明显影响,再灌注即刻给药可加重损伤,可能与地塞米松不同时期用药对iNOS活性影响不同有关.     

山莨菪碱对肝脏缺血再灌注损伤的保护作用

目的 探讨山莨菪碱对肝脏缺血再灌注损伤的保护作用。方法 将雄性Wistar大鼠制成肝脏缺血再灌注模型,随机分为正常对照组、缺血再灌注组、生理盐水组和山莨菪碱组,观察肝脏缺血60min再灌注1、3、6、12及24h后血浆和／或肝组织中内皮素－1（ET－1）、透明质酸（HA）、丙氨酸转氨酶（ALT）、丙二醛（MDA）和再灌注1h后肝细胞内游离Ca^2 ([Ca^2 ]i)、ATP含量变化以及肝组织病理学改变。结果 肝脏缺血再灌注后血浆和／或肝细胞中ET－1、HA、ALT、MDA和肝细胞内[Ca^2 ]u含量均显著升高,而肝组织中ATP含量明显降低;肝脏缺血再灌注前应用山莨菪碱2.0mg/kg者,血浆HA和肝细胞内[Ca^2 ]i含量明显降低,肝组织中MDA也有不同程度的降低,而肝组织中ATP含量明显升高,同时肝酶的漏出减少,肝组织病理学损害明显减轻。结论 山莨菪碱对肝脏缺血再灌注损伤具有保护作用。     

抗坏血酸对肠缺血再灌注大鼠肺损伤的保护作用

目的观察抗坏血酸对肠缺血再灌注(I/R)大鼠肺损伤的保护作用。方法SD大鼠48 只,体重252-335 g,随机分为3组,每组16只,假手术组(A组):开腹仅暴露肠系膜上动脉;缺血再灌注组(B组):肠系膜上动脉阻断2 h后再灌注6 h;抗坏血酸组(C组):缺血再灌注同B组,再灌注前10 min经尾静脉注射抗坏血酸200 mg/kg(用生理盐水稀至1 ml),A、C组则注射等量生理盐水。各组均靶控输注异丙酚维持麻醉。各组分别于再灌注1、6 h处死8只大鼠,取肺组织,测定肺组织丙二醛(MDA)、Na -K -ATP酶活性及含水率,并在光镜下观察肺组织中性粒细胞浸润和间质水肿情况。结果与A组比较,B、C组再灌注1、6 h肺组织MDA含量、含水率均升高,B组再灌注1 h Na -K -ATP 酶活性升高,再灌注6 h Na -K -ATP酶活性降低,C组再灌注1、6 h Na -K -ATP酶活性均升高(P< 0.05);与B组比较,再灌注6h C组肺组织MDA含量及含水率降低,Na -K -ATP酶活性升高(P< 0.05或0.01)。光镜下A组肺组织未见异常改变,B组肺泡壁毛细血管轻度扩张,C组出现轻微充血现象。各组均未见PMN浸润和间质肿胀征象。结论静脉注射200 mg/kg抗坏血酸对小肠缺血再灌注大鼠肺损伤产生一定的保护作用,通过提高Na -K -ATP酶活性,减轻脂质过氧化反应。     

异丙酚对大鼠小肠缺血再灌注时粘膜上皮细胞凋亡的影响

目的 探讨异丙酚对大鼠小肠缺血再灌注时粘膜上皮细胞凋亡的影响及其机制.方法 健康Wistar大鼠24只,随机分为3组(n=8):假手术组(S组)、缺血再灌注组(I/R组)和异丙酚+缺血再灌注组(P+I/R组).夹闭肠系膜上动脉,缺血1 h,再灌注2 h,制备小肠缺血再灌注损伤模型.S组和I/R组缺血前10 min开始经股静脉持续输注生理盐水10 ml·kg-1·h-1,P+I/R组静脉注射异丙酚10 mg/kg,以后持续输注异丙酚10 mg·kg-1·h-1.取空肠组织3 cm,常规制备全层石蜡切片,行HE染色,光镜下观察小肠组织病理学;免疫组化法检测Bcl-2、Bax蛋白的表达;TUNEL法检测小肠粘膜上皮细胞凋亡,计数凋亡细胞及总细胞,计算小肠粘膜上皮细胞凋亡指数.结果 与S组比较,I/R组和P+I/R组Bcl-2和Bax蛋白表达上调,Bcl-2/Bax增加,小肠组织损伤程度增强,小肠粘膜上皮细胞凋亡指数增高(P＜0.01或0.05);与I/R组比较,P+I/R组Bcl-2蛋白表达上调,Bax蛋白表达下调,小肠组织损伤程度减轻,小肠粘膜上皮细胞凋亡指数降低(P＜0.01).结论 异丙酚可减轻大鼠小肠缺血再灌注损伤时粘膜上皮细胞凋亡,其机制与上调Bcl-2基因的表达和下调Bax基因的表达有关.     

异丙酚对大鼠肠缺血再灌注后肺损伤的影响

目的探讨异丙酚对大鼠肠缺血再灌注后肺损伤的影响。方法32只成年SD大鼠,随机分为4组（n=8）,缺血再灌注组（I/R组）缺血1 h,再灌注2 h;异丙酚1组（P1组）在缺血前10 min、异丙酚2组（P2组）在再灌注前10min静脉注射异丙酚10mg,kg,然后以10mg·kg^-1·h^-1持续输注,余处理同I/R组;假手术组（C组）不行缺血再灌注及异丙酚输注。所有大鼠在再灌注120 min时处死。光镜下观察肺组织形态学及细胞凋亡;测定肺组织超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量及含水量。结果I/R组光镜下可见大量肺泡塌陷、实变,肺实质水肿及中性粒细胞浸润聚集。与C组比较,I/R组及P2组肺组织细胞凋亡计数增加,I/R组肺组织SOD活性降低,MDA含量升高,含水量升高（P＜0．05或0．01）;与I/R组比较,P1组SOD活性升高,MDA含量降低（P＜0．01）。结论细胞凋亡参与了大鼠肠缺血再灌注后肺损伤的发生,肠缺血前给予异丙酚可明显减轻肠缺血再灌注后肺损伤。     

氯喹对全肝缺血再灌注大鼠肺损伤的保护作用

目的 探讨氯喹对全肝缺血再灌注大鼠急性肺损伤（Au）的保护作用及其机制。方法 健康SD大鼠90只，雌雄不拘，体重300～350g，随机分为3组：假手术组（A组）、全肝缺血再灌注组（B组）、全肝缺血再灌注＋氯喹组（C组），每组30只。阻断肝门及肝上、肝下下腔静脉20min时开放血流，建立大鼠全肝缺血再灌注模型。C组于缺血前即刻经股静脉注射氯喹10mg／kg，A、B组给予等量生理盐水。于缺血20min、再灌注4h时每组分别处死10只大鼠，抽取门静脉血，测定血浆D-乳酸、内毒素（ETX）、肿瘤坏死因子-a（TNF-a）浓度，另外10只用于观察再灌注48h时大鼠生存率，并在电镜下观察肺组织超微结构的改变。结果 缺血再灌注可导致大鼠缺血期和再灌注期门静脉血D-乳酸、ETX、TNF-a浓度升高，大鼠生存率降低，肺组织超微结构严重受损，氯喹可减弱全肝缺血再灌注导致的上述改变。结论 氯喹对全肝缺血再灌注大鼠ALI有一定的保护作用，通过抑制磷脂酶A2激活，降低肠粘膜屏障通透性升高，降低肠黏膜内毒素移位。     

舒芬太尼预处理对肠缺血再灌注大鼠急性肺损伤的影响及阿片受体在其中的作用

目的 评价舒芬太尼预处理对肠缺血再灌注大鼠急性肺损伤的影响及阿片受体在其中的作用.方法 成年健康雄性Wistar大鼠48只,体重200 ～ 250 g,采用随机数字表法,将其随机分为6组(n=8):假手术组(S组)、肠缺血再灌注组(I/R组)、舒芬太尼预处理组(SPC组)、COTP+ SPC组、NTD+ SPC组和nor-BNI+ SPC组.I/R组、SPC组、COTP+ SPC组、NTD+ SPC组和nor-BNI+ SPC组采用夹闭肠系膜上动脉45 min,再灌注2h的方法制备肠缺血再灌注模型;S组仅分离肠系膜上动脉,不夹闭.SPC组、COTP+ SPC组、NTD+ SPC组和nor-BNI+ SPC组于缺血前10 min时静脉注射舒芬太尼10μg/kg;COTP+ SPC组、NTD+ SPC组于注射舒芬太尼前10 min时分别静脉注射μ受体拮抗剂COTP 1mg/kg或δ受体拮抗剂NTD 5 mg/kg; nor-BNI+ SPC组于注射舒芬太尼前15 min时静脉注射κ受体拮抗剂nor-BNI 5 mg/kg.于再灌注2h时处死大鼠,取肠组织,观察肠粘膜形态并进行肠粘膜损伤评分;取左肺组织,观察肺组织形态并进行肺损伤评分;采用TUNEL法检测肺组织细胞凋亡情况,计算凋亡指数;采用免疫组化法测定肺组织Bcl-2蛋白和Bax蛋白的表达,计算Bcl-2/Bax比值.结果 与S组比较,I/R组、SPC组、COTP+ SPC组、NTD+ SPC组和nor-BNI+ SPC组肠粘膜损伤评分、肺损伤评分和凋亡指数升高,Bcl-2蛋白和Bax蛋白表达上调,Bcl-2/Bax比值降低(P＜0.01);与I/R组比较,SPC组肠粘膜损伤评分、肺损伤评分和凋亡指数降低,Bcl-2蛋白表达上调,Bax蛋白表达下调,Bcl-2/Bax比值升高(P＜0.01);与SPC组比较,COTP+ SPC组、NTD+ SPC组和nor-BNI+ SPC组肠粘膜损伤评分、肺损伤评分和凋亡指数升高,Bcl-2蛋白表达下调,Bax表达蛋白表达上调,Bcl-2/Bax比值下降(P＜0.01).结论 舒芬太尼预处理可减轻肠缺血再灌注大鼠急性肺损伤,该作用与激活阿片受体有关.     

异丙酚对大鼠缺血再灌注心肌Toll样受体4、NF-κB及血清IL-6的影响

目的 探讨异丙酚对大鼠缺血再灌注心肌Toll样受体4(TLR4)、核转录因子κB(NF-κB)和血清白细胞介素-6(IL-6)的影响.方法 健康雄性SD大鼠40只,体重200～250 g,随机分为4组,每组10只,假手术组(A组)左冠状动脉前降支只穿线;缺血再灌注组(B组)左冠状动脉前降支穿线结扎30 min后,再灌注120 min;A组和B组在缺血前10 min经股静脉注射生理盐水5 ml/kg后以5 ml·kg-1·h-1持续静脉输注至再灌注120 min;低剂量异丙酚组(C组)缺血前10 min经股静脉注射异丙酚5mg/kg后以5 mg·kg-1·h-1持续静脉输注至再灌注120 min,余处理同B组;高剂量异丙酚组(D组)缺血前10 min经股静脉注射异丙酚10 mg/kg后以10 mg·kg-1·h-1持续静脉输注至再灌注120 min,余处理同B组.再灌注120 min后,测定血清IL-6的浓度及心肌TLR4 mRNA、NF-κB蛋白的表达.结果 与A组比较,B组、C组及D组心肌TLR4 mRNA、NF-κB蛋白表达上调,血清IL-6水平升高;与B组比较,C组和D组心肌TLR4 mRNA、NF-κB蛋白表达下调,血清IL-6水平降低;与C组相比,D组心肌TLR4 mRNA、NF-κB蛋白表达下调,血清IL-6水平降低.结论 静脉注射异丙酚可抑制大鼠缺血再灌注心肌TLR4 mRNA、NF-κB的表达及血清IL-6浓度的升高,呈剂量依赖性.     

L-精氨酸对肝缺血再灌注损伤的保护作用及其机制

目的　探讨L 精氨酸 (L Arg)对肝脏缺血再灌注 (I/R)损伤的保护及其机制。 方法雄性SD大鼠随机分为 :假手术组 (Sham ) :大鼠开腹游离肝十二指肠韧带 ,不阻断 ;对照组 (Con trol) :单纯入肝血流阻断 ;Arg组 :肝缺血前 5min ,从大鼠阴茎背静脉 (PDV )注射L Arg 2 0 0mg/kg体重 ;Arg +L组 :肝缺血前 10和 5min ,依次从大鼠PDV注射L 硝基精氨酸甲酯 (L NAME) 30mg/kg体重和L Arg 2 0 0mg/kg体重 ;fmk组 :肝缺血前 5min ,从大鼠PDV注射N 笨甲基氧化碳酰 缬氨酸 丙氨酸 天冬氨酸 氟化丙酮 (ZVAD fmk) 15mg/kg体重。各组入肝血流阻断时间为 40min ,比较各组的谷丙转氨酶 (ALT)、Caspase 3活性、肝细胞凋亡数和 7d生存率。 结果　肝缺血 40min再灌注 6h ,Arg组的 7d生存率显著高于对照组和Arg +L组 (P <0 .0 5 )。Arg组ALT、Cas pase 3活性和肝细胞凋亡数明显低于对照组和Arg +L组 (P <0 .0 1)。Arg组的Caspase 3活性和肝细胞凋亡数略高于fmk组和假手术组 (P >0 .0 5 )。结论　L Arg对肝脏I/R损伤有良好的保护作用 ,其保护机理可能是通过一氧化氮 (NO)作用于Caspase 3并使其失活 ,从而抑制肝细胞凋亡的发生而实现的。     

Study of L—arginine—nitric oxide pathway in ischemiareperfusion injured limbs in rats

OBJECTIVE: To observe the change of nitric oxide (NO) levels in the blood and the morphological change of the muscles in the limbs of rats during the (IR) injury and after being intervened by L-arginine (L-Arg) and L-nitroarginine (L-NNA). METHODS: Sixty-six male Sprague-Dawley (SD) rats were used an d grouped into the normal controls, the sham injury controls, the IR injury group and the intervention groups (L-Arg group and L-NNA group). After 6 hours of ischemia, followed by reperfusion for 3, 12 or 24 hours, the samples in the IR injury group were obtained. The rats in the intervention groups were given L-Ar g (100 mmol/L) and L-NNA (10 mmol/L), respectively, through the abdominal cavity. Then the anterior tibial muscle in the right limb was obtained for histological examination, the anterior tibial muscle in the left limb for ultrastructure observation and the blood for assay of NO in all the rats. NO was assayed by indirect measurement of NO(2)(-)/NO(3)(-) with Griess method. RESULTS: There was no significant difference of NO between the normal controls and the sham injury controls (P>0.05). But NO significantly decreased in the IR injury group (P<0.01), and further decreased with reperfusion (P<0.01) and reached the lowest point at 12 hours after reperfusion. The level of NO in the L-Arg group was significantly higher than that in the IR injury group ( P<0.01), but was not significantly different from that in the controls (P>0.05). In the L-NNA group, NO decreased to the undetectable level (P<0.01). Histological examination and ultrastructure observation showed the muscles were normal in the control groups. After 6 hours of ischemia, the skeletal muscles displayed injuries, and they were most severely injure d after 12 hours of reperfusion. In the L-Arg group, the skeletal muscles were less injured, while in the L-NNA group, the injury was similar to that in the I R injury group. CONCLUSIONS: When the limbs of the rats sustain IR, NO in the blood decreases. Meanwhile, the muscles in the limbs are injured. When L-Arg is given, NO in the blood is restored and the muscles are protected. When L-NNA completely inhibits NO, no protection of the muscles is shown.     

Gangliosides on intestinal microcirculation and animal survival during reperfusion

This study investigated the effect of gangliosides (Gang) on small bowel microcirculation and animal survival after normothermic intestinal ischemia-reperfusion injury. Five adult male EPM-1 Wistar rats in each of three groups received FK506 (0.2 mg/kg), Gang (3 mg/kg), or vehicle (at same volume) either 24 or 12 hours prior to the experiment. The animals were anesthetized intramuscularly with ketamine (60 mg/kg) and xylazine (10 mg/kg) and hydrated with 80 mL/kg of prewarmed saline solution delivered subcutaneously before the ischemic insult and 40 mL/kg at 1 hour after reperfusion. Under anesthesia, they underwent a laparotomy with clamping of the superior mesenteric artery (SMA) at its origin for 75 minutes. Microcirculation was evaluated with a laser Doppler flowmeter, 5 minutes before ischemia (baseline) and reperfusion (ischemia), and 20, 40, and 60 minutes after reperfusion. Animal survival was observed up to 24 hours. Small bowel flow measured before ischemia was considered to be the baseline level (100%). After SMA occlusion a significant reduction in microcirculatory tissue perfusion to about 8% was observed in all groups. At 20, 40, and 60 minutes of reperfusion treatment with Gang (77%, 81%, and 100%) or FK506 (70%, 85%, and 98%) promoted better recovery of the intestinal microcirculation when compared to the control group (45%, 72%, and 75%). Concerning animal survival there was no difference between groups (just one animal from each group, Gang and FK506, survived up to 24 hours). Based on our data we conclude that Gang and FK506 improve intestinal microcirculation in ischemia-reperfusion injury but do not change animal survival after severe ischemia.     

阻塞性黄疸时L-精氨酸对肾功能的保护作用

目的：研究阻塞性黄疸（OJ）时，L－精氨酸（L－Arg)对肾功能的保护作用。方法：胆总管结扎大鼠30只，随机分成生理盐水对照（NS）组、L－精氨酸（L－Arg)组和L－硝基精氨酸（L－NNA）组，每组10只。胆总管结扎后第2天起分别腹腔注射1ml NS、1ml L-Arg(500mg/kg)、1ml L-NNA(10mg/kg)，连用9d；假手术（SO）组用1ml NS腹腔注射。观察各组肾功能的变化，同时测定血和肾组织内皮素（ET）、一氧化氮（NO）水平、一氧化氮合酶（NOS）活性和丙二醛（MDA）的含量。并用图像分析检测ET1 mRNA和NOS mRNA表达的部位及量的变化。结果：用L－Arg后，血和肾组织NOS活性增加，肾组织ET1 mRNA表达减少，血和肾组织ET下降，NO升高；同时伴有内生肌酐清除率（Ccr)、肾皮质平均血流（RCBF）的升高，肾组织MDA含量降低。结论：L－Arg通过增强血和肾组织NOS活性来增加体内NO水平、抑制ET1 mRNA表达、降低体内ET水平，从而提高Ccr与RCBF，减轻阻塞性黄疸时的肾功能损伤。     

Prolonged survival and decreased mucosal injury after low-dose enteral allopurinol prophylaxis in mesenteric ischemia

Previous studies demonstrating protective effects of allopurinol in intestinal ischemia have evaluated intravenous allopurinol (presently unavailable for human use) or enteral allopurinol at supranormal doses and, therefore, have questionable clinical relevance. To address this problem, we evaluated the protective effects of clinically used doses of enteral allopurinol in rats with intestinal ischemia. Forty male Sprague-Dawley rats (weighing 300 to 400 g) received enteral allopurinol (10 mg/kg) or water daily for 1 week. Rats were then subjected to superior mesenteric artery occlusion with interruption of collateral flow for 20 minutes to produce ischemic injury to the intestine. Segmental small bowel resections were performed in 10 control rats and 10 allopurinol-treated rats before and after reperfusion to identify histopathologic evidence of reperfusion injury. Mucosal injury was quantitated using a grading scale of 0 to 5 (5 being most severe). The remaining 20 rats (10 in each group) were observed for mortality (death within 7 days) after reperfusion. Mucosal injury after reperfusion was graded at 4.4 +/- 0.20 in controls versus 2.3 +/- 0.23 in the treated group (P less than .001). In addition, there was a significant increase in mucosal damage in the control group when postreperfusion specimens were compared with specimens taken before reperfusion (2.8 +/- 0.19 before and 4.4 +/- 0.20 after reperfusion, P less than .001). Injury score for the allopurinol-treated group did not significantly increase after reperfusion. Survival was 50% in the water-fed control group compared with 100% survival in allopurinol-treated rats (P = .016). We conclude that enteral allopurinol in the presently available form and dose is effective in reducing mesenteric reperfusion injury.     

大鼠肝缺血／再灌注后肝组织一氧化氮和不同亚型一氧化氮合酶的变化

目的探讨一氧化氮（NO）和一氧化氮合成酶（NOS）在肝缺血／再灌注（I／R）过程中的变化和作用。方法健康雄性SD大鼠24只，随机分为3组（每组8只）：①正常对照组，术中只分离肝周围韧带，不做肝门阻断及再灌注。②I/R组，进行45min的部分肝门阻断及60min的再灌注。③L-精氨酸（L—Arg）组，缺血前20min经阴茎背静脉注射L—Arg（300mg／kg），余同②组。实验结束后，取下腔静脉血2ml，并迅速切取缺血肝组织。检测血清丙氨酸转氨酶（ALT）、门冬氨酸转氨酶（AST）、乳酸脱氢酶（LDH）；测定肝组织中超氧化物歧化酶（SOD）、丙二醛（MDA）、黄嘌呤氧化酶（XOD）、一氧化氮（NO）和一氧化氯合成酶（NOS）等指标；观察光镜和电镜下肝组织学变化。结果与正常对照组相比，I／R组iNOS升高，NO降低；L-Arg组NO、eNOS均高于I／R组。2、3组比1组大鼠的肝组织病理损害重、肝功能差，L—Arg组病理损害较I／R组明显减轻、肝功能改善。结论NO对大鼠肝I／R损伤具有保护作用．不同亚型NOS的变化参与其中。     

The role of alpha-tocopherol and allopurinol in lipid peroxidation and mitochondrial respiration in the ischemic rat liver

In the present study, the effects of alpha-tocopherol and allopurinol in liver ischemia and reperfusion injury on lipid peroxidation and mitochondrial respiratory function were investigated in rats. Ischemia was induced in the left and median liver lobes clamping the vessels for 90 minutes. After declamping reperfusion was continued for 60 minutes. Liver tissue was taken before and 90 minutes after ischemia and 60 minutes after reperfusion to measure lipid peroxides and mitochondrial respiratory function. In one group of rats alpha-tocopherol (10mg/kg) was given intraperitoneally for three consecutive days preoperatively and in the other group allopurinol (50mg/kg) was given intravenously 10 minutes before ischemia. alpha-Tocopherol caused inhibition of increase in lipid peroxides at reperfusion and improvement in lowering of mitochondrial respiratory function. This improvement was less than previously reported, probably due to not only reperfusion injury but also ischemic injury. Allopurinol, on the other hand, caused neither such inhibition nor such improvement, suggesting the other source of oxygen-derived free radicals than xanthine oxidase system.     

Comparison of the protective effect of dipyridamole and acetylsalicylic acid on long-term histologic damage in a rat model of testicular ischemia-reperfusion injury

PurposeIschemia reperfusion injury arising from testicular torsion results in a loss of spermatogenesis and a significant increase in germ cell apoptosis. We investigated the effects of dipyridamole and acetylsalicylic acid (ASA), 2 well-known platelet inhibitors, on testicular ischemia reperfusion injury.MethodsThirty adult male Sprague-Dawley rats were randomly divided into 5 groups (n = 6 for each group): control, sham-operated, torsion/detorsion (T/D), T/D + dipyridamole, and T/D + ASA. Testicular ischemia was achieved by rotating the left testis 720° clockwise for 2 hours. Thirty minutes before torsion, 10 mg/kg dipyridamole was injected transperitoneally in the T/D + dipyridamole group, and 100 mg/kg ASA was injected transperitoneally in the T/D + ASA group. Sixty days after the initial surgical procedure, ipsilateral orchiectomies were performed for histopathologic examination to determine Johnsen's mean testicular biopsy score (MTBS), mean seminiferous tubular diameter (MSTD), and apoptotic index (AI) in all groups.ResultsUnilateral testicular torsion-detorsion led to a significant decrease in Johnsen's MTBS and MSTD values in the ipsilateral testis and a significant increase in AI values of the T/D group. There were no significant differences between the T/D + dipyridamole and control groups in terms of MSTD and MTBS values. Although an amount of improvement exits in T/D + ASA group, there were significant differences between the T/D + ASA and control group MSTD and MTBS values. There was no significant difference between the T/D + dipyridamole and control groups in terms of AI values (P > .05), but the differences between the T/D + ASA and control groups were significant despite a slight decline in AI values of the T/D + ASA group.ConclusionsOur findings show that the use of dipyridamole before testicular reperfusion has a potentially protective effect against long-term injury in testicular ischemia reperfusion injury.     

异氟醚预处理对兔局灶性脑缺血再灌注时降钙素基因相关肽和NF-κB的影响

目的 探讨异氟醚预处理对兔局灶性脑缺血再灌注时降钙素基因相关肽( CGPP)和NF-κB水平的影响.方法 新西兰纯系家兔54只,雌雄不拘,体重2.0～2.5 kg,采用随机数字表法,将其随机分为3组(n＝18):假手术组(S组)、脑缺血再灌注组(I/R组)和异氟醚预处理(I组).麻醉下气管内插管,机械通气,S组和I/R组静脉输注咪达唑仑维持麻醉;I组吸人1.4％异氟醚30 min后洗脱10 min进行异氟醚预处理,然后制备脑缺血再灌注损伤模型,在脑缺血再灌注损伤过程中静脉输注咪达唑仑,3组静脉输注芬太尼和维库溴铵.I/R组和I组采用线栓法制备局灶性脑缺血再灌注损伤模型,于缺血2h时进行再灌注.分别于麻醉前和再灌注即刻、1h、2h、3h、4h、5h时取耳中央动脉血样,测定血浆CGRP浓度,各时点取完血样后立即处死动物,测定脑组织神经元NF-κB活性及其表达.结果 与S组比较,I/R组血浆CGRP浓度、脑组织神经元NF-κB活性升高,脑组织NF-κB表达上调(P<0.05);与I/R组比较,I组血浆CGRP浓度升高,脑组织神经元NF-κB活性降低,脑组织NF-κB表达下调(P<0.05).结论 异氟醚预处理减轻兔脑缺血再灌注损伤的机制与促进CGRP释放及抑制神经元NF-κB功能有关.