银杏叶提取液抗肢体缺血再灌注损伤

目的 观察银杏叶提取液对肢体缺血再灌注损伤的影响。方法 制作兔肢体缺血再灌注损伤动物模型。并分为对照组，再灌注组和治疗组，检测不同时相点血小板计数，血栓素B2（TXB2）和6-酮-前列腺素F1α（6-Keto-PGF1α）含量，测定骨骼肌丙二醛（MDA），线粒体钙（MitochondrialCa)含量和组织湿/干重量比值（Wet/Dry)。结果 再灌注组与对照组比较，以上各项指标变化明显，银杏叶提取液可抑制血小板活化，降低血浆TXB2和6-Keto-PGF1α水平，减少骨骼肌MDA，线粒体Ca含量和组织湿/干重量比值，治疗组各项测定指标较再灌注组有比较明显改善。结论 银杏叶提取液对肢体缺血再灌注损伤骨骼肌有保护作用。     

重组人促红细胞生成素对骨骼肌缺血再灌注损伤的保护作用

[目的]观察重组人促红细胞生成素（rHuEPO）对肢体骨骼肌缺血再灌注（IZR）损伤的保护作用。[方法]建立大鼠后肢缺血再灌注模型。40只大鼠随机均分为：假手术组（I组），I/R组（Ⅱ组），I/R＋生理盐水组（Ⅲ组），I/R＋rHuEPO组（Ⅳ组）。取血浆测定丙二醛（MDA）、肌酸磷酸激酶（CPK）和乳酸脱氢酶（LDH）含量。取骨骼肌标本测定髓过氧化酶（MP0）活性、湿重／干重比（Wet／dry）。[结果]Ⅱ组与I组比较，血浆和骨骼肌的各项生化指标显著增高（P〈0．01）；IV组血浆及骨骼肌各项测定指标较Ⅱ组相比明显降低（P〈0．01）。Ⅲ组和Ⅱ组之间比较，差异无显著意义。[结论]rHuEPO对肢体骨骼肌缺血再灌注损伤有保护作用。     

冬虫夏草对缺血再灌注肢体能量代谢和线粒体酶活性的影响

目的 观察冬虫草醇提取液对肢体缺血再灌注损伤的影响。方法 制作兔肢体缺血再灌注损伤动物模型，实验分对照组、再灌注组和治疗组。取骨骼肌测定三磷酸腺苷、二磷酸腺苷、一磷酸腺苷、磷酸肌酸含量和线粒体ATP酶活性。结果 再灌注组与对照组比较，骨骼肌能量代谢障碍及其线粒体ATP酶活性降低。使用冬虫夏草后，骨骼肌各项测定指标较再灌注组相比明显改善。结论 冬虫夏草对缺血再灌注损伤骨骼肌有保护作用。     

川芎嗪对肢体缺血再灌注损伤影响的临床实验研究

目的 了解川芎嗪 对肢体组织缺血再灌注损伤的影响。方法 病例选取四肢骨折手术,止血带时间需要1－1.5h的36例,分为A一（川芎嗪组）15例和B组（空白对照组）21例,另设立C组为腰椎或髋部手术病例15例,分别于术前,术后24小时测定血清SOD活性,LPO,GSH和血流流变学指标。结果 A组各项指标相对稳定,术后B组SOD酶活性短暂下降,LPO和GSH升高（P＜0．05）,还原粘度明显升高（P＜0．01）,C组则显示血液流变学指标的降低（P＜0．05）。结论 川芎嗪对肢体组织缺血再灌注损伤有保护作用,其作用机理与川芎嗪活血,化瘀,抗凝,抗癌,改善血液流学特征性,拮抗氧自由基损伤有关。     

大蒜素在防治兔肢体缺血再灌注损伤中的疗效观察

目的探讨大蒜素对肢体缺血再灌注损伤的防护作用。方法将32只家兔随机分为再灌注组和治疗组,制备肢体缺血再灌注损伤动物模型。在即将恢复血流灌注前10分钟,再灌注组和治疗组分别自耳缘静脉注射等渗盐水和大蒜素注射液。在再灌注前、后不同时间点上分别测定血清有关生化指标并取胫前肌行光、电镜观察。结果再灌注组再灌注后血清天冬氨酸氨基转移酶（AST）、乳酸脱氢酶（LDH）、肌酸激酶（CK）、丙二醛（MDA）明显升高（P〈0．01）,超氧化物歧化酶（SOD）活力明显下降（P〈0．01）。治疗组再灌注后各指标变化不明显,而与对照组同期相比,差异有非常显著性（P〈0．01）。光、电镜观察可见再灌注组织超微结构改变明显,而治疗组较轻。结论大蒜素可抑制自由基产生并减轻对骨骼肌细胞的损害,对肢体缺血再灌注损伤具有明显的防护作用。     

β-七叶皂甙钠对肢体缺血再灌注损伤的保护作用

目的：观察β－七叶皂甙钠对肢体缺血再灌注损伤的保护作用。方法：用兔造成肢体缺血再灌注损伤动物模型。实验分对照组、缺血再灌注组和β－七叶皂甙钠组。取血浆测定丙二醛、肌酸磷酸激酶、谷草转氨酶和乳酸脱氢酶合量。取骨骼肌标本测定丙二醛、髓过氧化酶活性、肌细胞线粒体钙含量和组织湿／干重比值。结果：缺血再灌注组与对照组比较,血浆和骨骼肌的各项生化指标显著增高（Ｐ〈０．０１）;使用β－七叶皂甙钠后,血浆及骨骼肌     

活络效灵丹加味对兔肢体缺血再灌注损伤的影响

目的：探讨中药方剂活络效灵丹加味在兔肢体缺血再灌注损伤中对骨骼肌的保护作用。方法：健康成年兔32只，随机分为4组，每组8只。应用止血带环扎家兔后肢造成肢体缺血再灌注损伤模型。Ⅰ组（活络效灵丹加味预防和治疗）于造模前活络效灵丹加味灌胃5d，并于恢复血流再灌注始继续活络效灵丹加味灌胃5d；Ⅱ组（活络效灵丹加味治疗）、Ⅲ组（甘露醇治疗）及Ⅳ组（模型对照）于恢复血流再灌注始分别中药灌胃、静推20％甘露醇、蒸馏水灌胃各5d。测定肢体缺血再灌注后2d和5d血清MDA、SOD、NO、LDH的含量；制备肢体缺血再灌注后5d的骨骼肌切片，进行光镜观察并比较各组组织学变化。结果：再灌注2d及5d活络效灵丹加味预防和治疗组、活络效灵丹加味治疗组、甘露醇治疗组血清MDA、LDH值显著低于模型对照组；SOD、NO值显著高于模型对照组（P〈0．05）。光镜下活络效灵丹加味预防治疗组、活络效灵丹加味治疗组、甘露醇治疗组骨骼肌损害轻于空白对照组；活络效灵丹加味预防治疗组、活络效灵丹加味治疗组骨骼肌细胞再生现象较甘露醇治疗组、模型对照组明显，而以活络效灵丹加味预防治疗组为著。结论：活络效灵丹加味在肢体缺血再灌注损伤中对骨骼肌有保护作用且能促进骨骼肌细胞再生。     

肠缺血后处理对兔缺血再灌注损伤小肠上皮细胞线粒体形态和功能的影响

目的观察缺血后处理对小肠缺血再灌注损伤的保护作用。方法30只大白兔随机分为3组，每组8只：A组，假手术组；B组，肠缺血再灌注损伤模型组；C组，肠缺血再灌注损伤模型肠缺血后处理组，实验结束后取小肠标本进行小肠上皮细胞形态和呼吸功能指标测定。结果A、C两组线粒体的数目、周长均大于B组，A、C两组问比较，A组较大（P〈0．05）。A、C两组线粒体的面积、最大直径、最小直径、等效直径均小于B组（P〈0．05），A、C两组间比较差异无统计学意义（P〉0．05）。B组线粒体的体积密度小于A组，面积密度、比表面和粒子数密度均小于其余两组（P〈0．05）。A、C两组间三维平面形态计量学各参数比较差异无统计学意义（P〉0．05）；B、C组线粒体呼吸控制比率（RCR）低于A组差异有统计学意义（P〈0．05），与C组比较，B组下降更为明显（P〈0．05）。结论小肠缺血后处理对缺血再灌注损伤肠上皮细胞线粒体形态和功能均有保护作用。     

缺血预处理与急性心肌缺血/再灌注细胞凋亡及Bcl-2、BaX蛋白表达的关系

目的：研究缺血预处理对急性心肌缺血／再灌注细胞凋亡的影响及与Bcl-2,Bax蛋白表达的关系。方法：用在体心肌缺血／再灌注模型，将实验动物分为3组：对照组，缺血／再灌注组，缺血预处理组。分别用原末端标记（TUNEL）法测定凋亡细胞和用免疫组化法测定Bcl-2,Bax蛋白的表达。结果：与对照组相比，缺血／再灌注组增加凋亡心肌细胞的百分数（P＜0．01）及Bax蛋白的光密度值（P＜0．01），减小Bcl-2蛋白的光密度值（P＜0．01），与缺血／再灌注组相比，缺血预处理减小凋亡心肌细胞百分数（P＜0．01）及Bax蛋白的光密度值（P＜0．05），增加Bcl-2蛋白的光密度值（P＜0．01）。结论：缺血预处理通过调控Bcl-2/Bax表达而抑制心肌缺血／再灌注细胞凋亡。     

复方丹参对心内直视手术心肌缺血再灌注后血清过氧化脂质及前列环素变化的影响

目的：观察复方丹参对心肺转流（CPB）心内直视手术心肌缺血再灌注后血清过氧化脂质及前列环素（PGI2）变化的影响。方法：20例先天性室间隔缺损或房间隔缺损患者麻醉后随机分为对照组（I组，n=10）及丹参组（Ⅱ组，n=10）。Ⅱ组患者于手术开始前及复温后心脏复跳前分别静注复方丹参200mg/kg，I组给予等容量复方乳酸钠。于手术开始前（T0）、心肌缺血前（T1）、心肌缺血30分钟（T2）、再灌注后10分钟（T3）和30分钟（T4）、停CPB30分钟（T5）及再灌注后24小时（T6）抽中心静脉血测丙二醛（MDA）及前列环素。结果：I组血清MDA于CPB后逐渐升高，再灌注后迅速增加，于T4、T5、T6显著高于其T2时值（P＜0．05或P＜0．01）。Ⅱ组再灌注后未出现显著的血清MDA升高，且缺血及再灌注后各时期Ⅱ组MDA均显著低于I组（P＜0．05）。CPB后再组前列环素均显著上升，而再灌注后迅速下降，但T2及T6时Ⅱ组前列环素均显著低于I组（P＜0．01，P＜0．05）。术后Ⅱ组心功能的恢复优于I组。结论：复方丹参能显著降低心脏缺血及再灌注期脂质过氧化程度，抑制缺血期前列环素的急剧增加，促进术后心肌功能的恢复。     

Lycopene has reduced renal damage histopathologically and biochemically in experimental renal ischemia-reperfusion injury

Abstract

Background: The present study aimed to investigate whether the inflammatory and antioxidant lycopene has a therapeutic effect against renal ischemia/reperfusion (I/R) injury. Materials and methods: In this study, 24 Wistar-Albino rats, weighing from 200 to 250?g, were divided into four groups. All rats underwent median laparotomy under anesthesia. No procedures were performed in the control group (Group C), whereas 100?mg/kg lycopene was administered by gavage in the lycopene group (Group L). The arteries of both kidneys were clamped for 45?min in the ischemia group (Group I), whereas 100?mg/kg lycopene was administered by gavage 30?min before clamping renal arteries, and ischemia was performed in the treatment group (Group T) rats. For all rats, blood samples and renal tissues were collected at 6?h of reperfusion. Samples were used to examine serum BUN, creatinine, MDA and GSH levels, and the renal tissues were used to examine MDA and GSH levels, and renal histopathologies. Results: The treatment group had statistically significant lower serum MDA levels, histopathological tubular vacuolization, loss of brush border and tubular dilatation (p?<?0.05), whereas serum BUN, creatinine, tissue MDA, and tissue and serum GSH levels were improved in favor of the treatment group, even though it was not statistically significant (p?>?0.05). Conclusion: The present study demonstrated that lycopene, which was administered prior to renal I/R injury, prevented renal damage through biochemical and histopathological parameters.     

Gpx1-Klk1转基因对肾缺血再灌注损伤保护作用的研究

目的 制备人谷胱甘肽过氧化物酶（Gpx1）、 组织激肽释放酶（Klk1）共转基因小鼠,在此基础上制作肾缺血再灌注损伤小鼠模型。观察转基因小鼠对缺血再灌注损伤的耐受能力。在体研究Gpx1-Klk1转基因对肾缺血再灌注的保护作用。 方法 应用基因工程技术制备pKsp-Gpx1-IRES-Klk1质粒,酶切后回收转基因片段并纯化,通过外源基因受精卵雄原核显微注射法制备Gpx1-Klk1共转基因小鼠。采用丝线悬吊控制法制备转基因小鼠肾缺血再灌注模型。设立C57BL野生型小鼠同法制备的肾缺血再灌注损伤为对照。在肾缺血再灌注实验前后,测定血尿素氮、血肌酐、肾组织中超氧化物歧化酶（SOD）、丙二醛（MDA）、总一氧化氮合酶（tNOS）及诱导型一氧化氮合酶（iNOS）。留取肾脏组织制备病理切片,观察Gpx1-Klk1转基因小鼠抗肾缺血再灌注损伤的能力。 结果 获得全长为6.585 kb的pKsp-Gpx1-IRES-Klk1重组质粒,并证明了该克隆的正确性。在转基因小鼠制备过程中,共获得525枚注射卵,移植成功率为81.0%,小鼠出生总数109只。经基因组DNA的PCR检测,确认10只为转基因阳性小鼠,阳性率为9.2%。Western印迹法检测证实了阳性转基因小鼠肾脏组织有Gpx1和Klk1蛋白强表达。转基因小鼠（实验组）和野生型小鼠（对照组）肾缺血再灌注损伤模型建立后,实验组血样中尿素氮及肌酐水平显著低于对照组（P < 0.01）;肾脏组织中SOD显著高于对照组 （P < 0.01）,MDA显著低于对照组（P < 0.01）;两组肾组织中tNOS较缺血再灌注前均显著升高,且实验组显著高于对照组（P = 0.025）,实验组肾组织中iNOS显著低于对照组（P < 0.01）。缺血再灌注后,实验组肾组织间质轻度水肿,肾小管上皮坏死细胞较少,对标本损伤程度采用半定量评分后显示,实验组损伤程度显著轻于对照组（1.58±1.05比3.95±0.80,P < 0.05）。 结论成功制备Gpx1-Klk1转基因小鼠。Gpx1-Klk1过表达对肾缺血再灌注损伤的保护作用。     

intermedin对大鼠肾脏缺血再灌注损伤的保护作用及其机制

目的 观察intermedin（IMD）对大鼠肾脏缺血再灌注损伤（IRI）的保护作用并探讨其机制。 方法 健康雄性Wistar大鼠24只随机分为对照组、IRI组、转空质粒组、转IMD质粒组。动物右肾切除后,用超声微泡技术将质粒转染入肾脏,1周后制作肾脏IRI模型。PAS染色观察肾脏病理损伤,比色法检测肾组织超氧化物岐化酶（SOD）、髓过氧化物酶（MPO）和天冬氨酸半胱氨酸蛋白酶3（caspase-3）,以及脂质过氧化物丙二醛（MDA）含量。免疫组织化学方法检测细胞间黏附分子1（ICAM-1）、P选择素及内皮素1（ET-1）表达。TUNEL染色检测肾组织细胞凋亡。 结果 PAS染色结果显示,IRI组肾小管及间质病理损伤显著重于对照组（P < 0.01）;转IMD组肾组织病理损伤则显著轻于IRI组（P < 0.01）。IRI组肾组织SOD活性显著低于对照组（P < 0.05）,MPO活性、活性caspase-3、MDA含量及ICAM-1、P选择素和 ET-1表达均显著高于对照组（均P < 0.01）;转IMD组SOD活性显著高于IRI组（P < 0.05）,MPO活性、活性caspase-3、MDA含量及ICAM-1、P选择素和ET-1表达均显著低于IRI组（均P < 0.01）。TUNEL染色显示,IRI组肾组织凋亡细胞数显著高于对照组（34.83%±8.75%比3.33%±0.47%,P < 0.01）;转IMD组肾组织凋亡细胞数（20.67%±7.71%）则较IRI组显著减轻（P < 0.01）。转空质粒组和IRI组以上指标差异均无统计学意义。 结论 IMD能减轻肾脏IRI,其机制至少部分与抑制氧自由基生成、炎细胞浸润及炎性因子ICAM-1、P选择素生成、ET-1生成、细胞凋亡有关,从而减轻肾组织局部氧化应激反应产生的活性氧。     

姜黄素对骨骼肌缺血再灌注损伤的保护作用及其机制研究

目的:观察姜黄素对肢体骨骼肌缺血再灌注损伤中血浆肌酸磷酸激酶(CPK)、乳酸脱氢酶(LDH)、丙二醛(MDA)含量及骨骼肌99m锝亚甲基二磷酸钠(99mTcMDP)吸收量的影响,探讨姜黄素对肢体骨骼肌缺血再灌注损伤的保护作用及其机制。方法:制作大鼠后肢缺血再灌注损伤模型,30只大鼠随机分为假手术组、对照组、干预组。分别于再灌注1 h后测定血浆CPK、LDH、MDA含量和腓肠肌99mTcMDP吸收量变化,透射电镜观察腓肠肌超微结构变化。结果:缺血再灌注对照组和姜黄素干预组与假手术组相比,血浆CPK(7296.18±1086.53,5168.49±975.39,3014.26±963.78)、LDH(1203.66±282.53,726.56±203.65,463.85±75.32)、MDA(10.36±2.65,6.78±2.12,3.54±1.89)含量明显增高(P<0.01),99mTcMDP吸收量(16.69±3.14,11.45±2.35,9.12±1.96)明显升高(P<0.01);腓肠肌超微结构损伤明显加重;姜黄素组血浆和骨骼肌的各项指标与缺血再灌注对照组相比显著降低(P<0.01),腓肠肌超微结构损伤明显减轻。结论:姜黄素能有效降低血浆CPK、LDH、MDA含量,减少骨骼肌99mTcMDP吸收量,减轻缺血再灌注骨骼肌坏死程度和坏死范围,改善骨骼肌再灌注损伤的超微结构,说明姜黄素对骨骼肌缺血再灌注损伤具有明显的保护作用。     

Renoprotective effect of berberine via intonation on apoptosis and mitochondrial-dependent pathway in renal ischemia reperfusion-induced mutilation

Abstract

Ischemic acute renal failure is a condition that extends subsequent to sudden and momentary fall in overall or regional blood flow to the kidney. The present investigation was deliberated to scrutinize the renoprotective potential of berberine in animal model of renal ischemia reperfusion (RIR) induced dent via assessment of various biochemical and molecular biomarkers. Male Wistar rats were anesthetized and the right kidney was removed through a small flank incision. Renal ischemia reperfusion was persuaded in uni-nephrectomized rats by occlusion of left renal artery for 45?min and reperfusion for 4 weeks. After 4 weeks of treatment of berberine (10, 20, and 40?mg/kg, p.o.), hemodynamic and left ventricular function were evaluated. Induction of ischemia reperfusion resulted callous mutilation in kidney which was confirmed by alterations in oxidative stress (SOD, GSH, and MDA), membrane bound enzymes, kidney function markers (serum creatinine and BUN), and mitochondrial dysfunction. Moreover, RIR injury exhibited incredible alterations in mRNA expression of KIM-1, NGAL, Caspase-3, Bax, Bcl-2, and TNF-α levels. Conversely treatment of berberine (20 and 40?mg/kg) significantly (p?<?0.01 and p?<?0.001) restored ischemia reperfusion induced marring via intonation of biochemical and molecular biomarkers. To sum up, berberine demonstrated compelling renoprotective effect in RIR injury via caspase-mitochondria-dependent pathway.     

Pyrrolidine Dithiocarbamate Reduces Lung Injury Caused by Mesenteric Ischemia/Reperfusion in a Rat Model

Background Pyrrolidine dithiocarbamate (PDTC) is a low-molecular thiol antioxidant and potent inhibitor of nuclear factor-κB (NF-κB) activation. It has been shown to attenuate local harmful effects of ischemia/reperfusion (I/R) injury in many organs. In this study, we aimed to study the effect of PDTC on lung reperfusion injury induced by superior mesenteric occlusion. Methods Male Wistar-albino rats randomized into three groups: (1) sham-operated control group (n = 12), laparotomy without I/R injury; (2) intestinal ischemia/reperfusion (I/R) group (n = 12), 60 min of ischemia by superior mesenteric occlusion followed by 2 h of reperfusion; and (3) I/R+PDTC-treated group (n = 12), 100 mg/kg injection of PDTC intravenously, 30 min after the commencement of reperfusion. Evans blue dye was injected to half of rats in all groups before the induction of I/R. We assessed the degree of pulmonary tissue injury biochemically by measuring malondialdehyde (MDA), glutathione (GSH), and nitric oxide (NO) levels, and histopathologically by establishing pulmonary neutrophil sequestration and acute lung injury scoring. Pulmonary edema was evaluated by Evans blue dye extravasation, as well as lung tissue wet/dry weight ratios. Results Pyrrolidine dithiocarbamate treatment significantly reduced the MDA and NO levels, and increased the GSH levels in the lung parenchyma, biochemically (p < 0.05), and atteneuated the pulmonary parenchymal damage, histopathologically (p < 0.05). However, pulmonary neutrophil sequestration was not affected by postischemic treatment with PDTC (p > 0.05). Pyrrolidine dithiocarbamate administration also significantly alleviated the formation of pulmonary edema, as evidenced by the decreased Evans blue dye extravasation and organ wet/dry weight ratios (p < 0.05). Conclusions This study showed that postischemic treatment with PDTC significantly attenuated the lung reperfusion injury. Further clinical studies are needed for better understanding of the specific mechanisms of PDTC protection against I/R-related organ injury and to clarify whether PDTC may be a useful therapeutic agent during particular operations where remote organ I/R injury occurs.     

Effects of selenium on ischaemia–reperfusion injury in a rat testis model

Selenium is shown to have beneficial effects on ischaemia–reperfusion (IR) injury. Our aim was to assess the effects of selenium on IR‐induced testicular damage in terms of biochemical and histopathological evaluation. A total of 32 rats were randomised into four groups: control, IR, IR + selenium (IR + S) and S. Detorsion was applied after 3 h of torsion. Testicular tissue superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), total antioxidant capacity (TAC) and DNA fragmentation levels were determined. Testicular tissue samples were examined by histopathological examination and terminal deoxynucleotidyl transferase dUTP nick end‐labelling staining. The control, IR and IR + S groups had higher SOD values compared with the S group; SOD levels of the control and IR + S groups were higher than those of the IR group (P < 0.05). Further, MDA levels of the IR group were higher than those in the other three groups (P < 0.05). The IR group revealed lower TAC levels than the three groups (P < 0.05 for all). GSH levels of the IR group were significantly lower than those in the other three groups (P < 0.05 for all). In contrast, GSH levels of the IR + S group increased compared with those of the S group. The IR group had more DNA fragmentation than the control and S groups (P < 0.05). It is concluded that selenium possibly reduces oxidative stress and apoptosis caused by testicular IR injury in rats. The testicular protective effect of selenium appears to be mediated through its anti‐apoptotic and antioxidative effects. However, selenium does not affect DNA fragmentation.     

敲除诱导性一氧化氮合成酶治疗骨骼肌缺血再灌注损伤的实验研究

目的研究敲除诱导性一氧化氮合成酶治疗骨骼肌缺血再灌注损伤的机制和作用.方法本实验采用敲除一氧化氮合成酶的小鼠(治疗组)及正常小鼠(对照组)各21只,造成去神经游离提睾肌皮瓣完全缺血3小时,在荧光显微镜下,活体动态观察该肌肉在恢复血液灌注前后90分钟过程中平均微动脉管径的一系列变化,测量灌注前后肌肉的血恢复率,重量比率,并观察其病理变化.结果 (1)在灌注后10和90分钟,对照组小鼠肌肉的再灌注率分别为(38.7±18)%和(63.8±50.3)%;而治疗组已达(92.9±17.2)%和(108.7±25.0)%(P＜0.001).(2)再灌注10分钟时,对照组的平均微动脉管径始终维持在未缺血时的51.5%至57.5%之间,90分钟后分别达到(71.6±10.9)%(10～20um),(71.2±15.1)%(21～40um),(63.4±11.2)%(41～70um).而治疗组再灌注10分钟时的平均微动脉的管径即为缺血前的72%,90分钟以后,分别达到(91.8±7.8)%(10～20um),(88.2±7.6)%(21～40um),(85.4±6.6)%(41～70um)(P＜0.001).(3)缺血3小时再灌注90分钟后,左、右两侧提睾肌的重量比,对照组为(173.3±44.5)%,而治疗组为(116.2±7.7)%(P＜0.01).结论诱导型一氧化氮合成酶的敲除能有效地改善骨骼肌的缺血再灌注损伤,其作用机理可能主要是通过调节血管张力,骨骼肌的血流量,抑制白细胞粘附于内皮细胞表面从而抑制血管壁内皮下细胞增殖及调控缺血后的代谢产物.     

Mortality following Lower Limb Ischemia-Reperfusion: A Systemic Inflammatory Response?

n = 10); and (2) animals subjected to 3 hours of bilateral hind limb ischemia followed by reperfusion ( n = 10). Both groups were observed under standard conditions for 4 days. In a second experiment three groups of animals were studied: (I) control ( n = 12); (II) 3 hours of bilateral hind limb ischemia alone ( n = 12); and (III) 3 hours of bilateral hind limb ischemia followed by 2 hours of reperfusion ( n = 12). Animals subjected to bilateral hind limb ischemia followed by reperfusion had a significantly higher mortality rate (70%) than controls (0%) ( p < 0.005). Morphometric assessment of the small bowel showed a significant decrease in mean mucosal thickness in the ischemia-reperfusion group compared with that in the group of controls and the ischemia-alone group ( p < 0.05). Bilateral hind limb ischemia followed by reperfusion was associated with significantly increased plasma concentrations of endotoxin ( p < 0.05) and interleukin-6 ( p < 0.0001) compared with that of controls and ischemia alone. These results indicate that reperfusion of the acutely ischemic lower limb is accompanied by structural changes in the gut mucosa associated with increased systemic endotoxin concentrations and cytokine activation. Mortality following reperfusion of the acutely ischemic limb may be related to a systemic inflammatory response triggered by endotoxin of gut origin.