红景天对大鼠小肠缺血再灌注损伤的保护作用

目的:利用SD大鼠制备肠缺血再灌注模型,观察红景天对肠缺血再灌注损伤的保护作用及其作用机制。方法:实验于2005-08/2006-05在第四军医大学西京医院胃肠外科实验室完成。雄性SD大鼠30只,体质量200～250g,随机数字表法分为假手术组、缺血再灌注组、红景天处理组,每组10只。红景天液制法参照中药质量标准:取红景天生药102g,加水煎煮2次,第1次1.5h,第2次1h,滤过,滤液合并后加水调至120mL,每只大鼠2mL/d,相当于生药5g/(kg·d)。缺血再灌注模型制备:动物于术前12h禁食,不禁水。以2%盐酸氯胺酮(100mg/kg)腹腔注射麻醉。生理盐水2mL/d,连续灌胃5d后,取正中切口入腹后分离肠系膜上动脉,以无创伤血管夹阻断肠系膜上动脉根部造成小肠完全缺血60min,然后松夹进行再灌注60min。假手术组:生理盐水2mL/d,连续灌胃5d后,只分离肠系膜上动脉,但不作阻断。红景天处理组:红景天按5g/kg生药,溶于2mL水中灌胃给药,连续5d后,分离肠系膜上动脉,夹闭肠系膜上动脉60min后再灌注60min。检测各组大鼠小肠黏膜中肿瘤坏死因子α、白细胞介素-6水平,以及其中的超氧化物歧化酶和丙二醛的含量。结果:30只大鼠均进入结果分析。①缺血再灌注组肿瘤坏死因子α、白细胞介素-6水平均高于假手术组和红景天处理组[肿瘤坏死因子α:(2.57±0.29),(0.32±0.06),(1.06±0.11)μg/L;白细胞介素-6:(965.73±42.01),(122.46±1.74),(385.03±13.50)ng/L,P<0.01]。②缺血再灌注组丙二醛水平高于假手术组和红景天处理组[(0.68±0.11),(0.33±0.10),(0.54±0.12)nmol/g,P<0.01];超氧化物歧化酶水平低于假手术组和红景天处理组[(34.12±5.31),(92.63±3.82),(55.66±5.92)NU/g,P<0.01]。结论:红景天可通过抑制细胞因子表达及清除氧自由基的方式,对肠缺血再灌注损伤起到保护作用。     

红景天对大鼠小肠缺血再灌注损伤的保护作用

目的：利用SD大鼠制备肠缺血再灌注模型，观察红景天对肠缺血再灌注损伤的保护作用及其作用机制。 方法：实验于2005—08／2006—05在第四军医大学西京医院胃肠外科实验室完成。雄性SD大鼠30只，体质量200～250g，随机数字表法分为假手术组、缺血再灌注组、红景天处理组，每组10只。红景天液制法参照中药质量标准：取红景天生药102g，加水煎煮2次。第1次1．5h，第2次1h。滤过，滤液合并后加水调至120mL，每只大鼠2mL／d，相当于生药5g／（kg&;#183;d）。缺血再灌注模型制备：动物于术前12h禁食．不禁水。以2％盐酸氯胺酮（100mg／kg）腹腔注射麻醉。生理盐水2mL／d，连续灌胃5d后，取正中切口入腹后分离肠系膜上动脉，以无创伤血管夹阻断肠系膜上动脉根部造成小肠完全缺血60min。然后松夹进行再灌注60min。假手术组：生理盐水2mL／d，连续灌胃5d后，只分离肠系膜上动脉，但不作阻断。红景天处理组：红景天按5g/kg生药，溶于2mL水中灌胃给药，连续5d后，分离肠系膜上动脉。夹闭肠系膜上动脉60min后再灌注60min。检测各组大鼠小肠黏膜中肿瘤坏死因子α、白细胞介素-6水平，以及其中的超氧化物歧化酶和丙二醛的含量。 结果：30只大鼠均进入结果分析。①缺血再灌注组肿瘤坏死因子α、白细胞介素-6水平均高于假手术组和红景天处理组[肿瘤坏死因子α：（2．57&;#177;0．29），（0．32&;#177;0．06），（1．06&;#177;0．11）μg／L；白细胞介素-6：（965．73&;#177;42．01），（122．46&;#177;1．74），（385．03&;#177;13．50）ng／L。P〈0．01]。②缺血再灌注组丙二醮水平高于假手术组和红景天处理组[（0．68&;#177;0．11），（0．33&;#177;0．10），（0．54&;#177;0．12）nmol／g，P〈0．01]；超氧化物歧化酶水平低于假手术组和红景天处理组[（34．12&;#177;5．31），（92．63&;#177;3．82），（55．66&;#177;5．92）NU／g，P〈0．01]。 结论：红景天可通过抑制细胞因子表达及清除氧自由基的方式，对肠缺血再灌注损伤起到保护作用。     

内洋地黄素拮抗剂减轻心肌缺血再灌注损伤的实验研究

目的 观察心肌缺血再灌注(myocardial isehemia reperfusion，MIR)时心肌组织内洋地黄素水平的变化和内洋地黄索特异性拮抗剂地高辛抗血清对MIR的影响，证明内洋地黄素是介导MIR损伤的重要介质之一。方法 采用左冠状动脉前降支结扎30min，复灌45min建立在体大鼠MIR、模型。SD大鼠随机分成7组：假手术组，模型组，生理盐水组，维拉帕米组，小剂量、中剂量、大剂量地高辛抗血清组。连续记录Ⅱ导联心电图，于再灌注45min后立即取左室心尖部缺血区心肌，检测心肌匀浆中内洋地黄素含量、心肌细胞膜Na^ -K^ -ATP酶和线粒体内Ca^2 含量。结果MiR损伤时，心肌组织内洋地黄素水平明显升高。心肌细胞膜Na^ -K^ -ATP酶活性显著下降，线粒体内Ca^2 含量升高；心电图ST段显著抬高，再灌注时发生明显的室性心律失常。地高辛抗血清组可显著降低心肌组织内洋地黄素水平，恢复细胞膜Na^ -K^ -ATP酶活性，降低线粒体内Ca^2 含量；显著改善MIR所致ST段抬高和再灌注心律失常的发生率。结论 MIR时，心肌组织内洋地黄素水平显著升高，是介导MIR损伤的重要物质之一。地高辛抗血清通过拮抗内洋地黄素的生物学作用，减轻MIR损伤。     

肠缺血再灌注损伤中钙超载的研究进展

在临床上,各种原因的病理性打击常引起肠道的缺血,而肠缺血再灌注损伤是其常见的病理变化。经相关研究证实肠缺血再灌注损伤在全身性的细菌感染、多器官功能障碍、休克等严重疾病及其进展过程中起着重要作用。而钙超载在肠缺血再灌注损伤的发生、发展中占据重要地位,通过总结、研究钙超载在肠缺血再灌注损伤中的机制及相关作用,可以进行相应的应对措施,从而减少肠缺血中的再灌注损伤,为临床工作提供理论支持,现本文就肠缺血再灌注损伤中钙超载的研究进展作一综述。     

Cyclic arginine-glycine-aspartate attenuates acute lung injury in mice after intestinal ischemia/reperfusion

Introduction

Intestinal ischemia is a critical problem resulting in multiple organ failure and high mortality of 60 to 80%. Acute lung injury (ALI) is a common complication after intestinal ischemia/reperfusion (I/R) injuries and contributes to the high mortality rate. Moreover, activated neutrophil infiltration into the lungs is known to play a significant role in the progression of ALI. Integrin-mediated interaction is involved in neutrophil transmigration. Synthetic peptides containing an arginine-glycine-aspartate sequence compete with adhesive proteins and inhibit integrin-mediated interaction and signaling. Thus, we hypothesized that the administration of a cyclic arginine-glycine-aspartate peptide (cRGD) inhibited neutrophil infiltration and provided protection against ALI induced by intestinal I/R.

Methods

Ischemia in adult male C57BL/6 mice was induced by fastening the superior mesenteric artery with 4-0 suture. Forty-five minutes later, the vascular suture was released to allow reperfusion. cRGD (5 mg/kg body weight) or normal saline (vehicle) was administered by intraperitoneal injection 1 hour prior to ischemia. Blood, gut, and lung tissues were collected 4 hours after reperfusion for various measurements.

Results

Intestinal I/R caused severe widespread injury to the gut and lungs. Treatment with cRGD improved the integrity of microscopic structures in the gut and lungs, as judged by histological examination. Intestinal I/R induced the expression of β₁, β₂ and β₃ integrins, intercellular adhesion molecule-1, and fibronectin. cRGD significantly inhibited myeloperoxidase activity in the gut and lungs, as well as neutrophils and macrophages infiltrating the lungs. cRGD reduced the levels of TNF-α and IL-6 in serum, in addition to IL-6 and macrophage inflammatory protein-2 in the gut and lungs. Furthermore, the number of TUNEL-staining cells and levels of cleaved caspase-3 in the lungs were significantly lowered in the cRGD-treated mice in comparison with the vehicle mice.

Conclusions

Treatment with cRGD effectively protected ALI and gut injury, lowered neutrophil infiltration, suppressed inflammation, and inhibited lung apoptosis after intestinal I/R. Thus, there is potential for developing cRGD as a treatment for patients suffering from ALI caused by intestinal I/R.     

Anti-inflammatory effects of U74389F in a rat model of intestinal ischemia/reperfusion injury.

OBJECTIVE: To investigate the role of eicosanoid generation and neutrophilic infiltration in the protective effects of U74389F against ischemia/reperfusion injury in the small intestines of rats. DESIGN: Prospective, randomized, controlled study. SETTING: University research laboratory. SUBJECTS: Adult, male Sprague-Dawley rats weighing between 200 and 300 g. INTERVENTIONS: Groups (5-8) of rats treated with U74389F or vehicle were subjected to a sham operation and 30 mins of ischemia by occlusion of the superior mesenteric artery or 30 mins of ischemia followed by 60 or 120 mins of reperfusion. U74389F (2.5 mg/kg i.v.) or vehicle (citrate buffer) were slowly injected 2 mins before ischemia. MEASUREMENTS AND MAIN RESULTS: Ischemia significantly (p < .05) increased mucosal injury (0 [normal] to 5) in both U74389F and untreated rats. In contrast, U74389F significantly (p < .05) attenuated the severity of injury after reperfusion. In vehicle-treated rats, ischemia/reperfusion significantly reduced villus height in both U74389F and untreated groups. However, the surface epithelial layer was intact in the U74389F but not in the vehicle-treated group. In addition, compared with the vehicle-treated group, U74389F significantly reduced neutrophil infiltration and prevented the increase in leukotriene B4 and prostaglandin E2 in response to ischemia and reperfusion. CONCLUSIONS: This study demonstrates that the mechanism of U74389F against mesenteric ischemia/reperfusion includes a delay and reduction of neutrophilic infiltrate, an inhibition of leukotriene B4 production, and a facilitation of mucosal restitution.     

四氢化吡咯二硫代氨基甲酸酯对大鼠肠缺血再灌注损伤的影响响

目的：观察四氢化吡咯二硫代氨基甲酸酯（PTDC）对大鼠肠缺血再灌注后肠组织损伤的影响。方法：36只SD大鼠随机分为3组。每组12只。（1）缺血再灌注组（I／R组），暴露腹腔后夹闭肠系膜上动脉（SMA）60min。开放灌注120min；（2）PTDC组（P组），在肠缺血前5min静脉给予PTDC 100mg／kg；（3）假手术组（S组），仅暴露SMA，不行肠缺血再灌注及PTDC注射。所有动物于再灌注120min时处死，行肠组织苏木精-伊红染色观察肠损伤程度并评分：检测肠组织中丙二醛（MDA）含量及髓过氧化物酶（MPO）、谷胱甘肽过氧化物酶（GSH-PX）活性。结果：与S组相比，I／R组、P组GSH-PX活性明显降低（P〈0．01，P〈0．05），MDA含量、MPO活性及小肠损伤评分明显升高（P〈0．01．P〈0．05）。与I／R组相比，P组小肠损伤评分、MDA含量及MPO活性明显降低．GSH-PX活性明显升高（均P〈0．05）。结论：PDTC对大鼠肠缺血再灌注后的肠道有保护作用，该保护作用与抑制中性粒细胞浸润、减少脂质氧化程度及氧自由基有关。[著者文摘]     

The effect of pentoxifylline on intestinal ischemia/reperfusion injury

The small intestine is highly sensitive to oxygen free radical-induced injury. Post-ischemic intestinal tissue damage appears to be due to the formation of oxygen radicals. Free radical initiated lipid peroxidation (LP) following intestinal ischemia/reperfusion (I/R) may disrupt mucosal integrity. Indirectly, the radicals trigger the accumulation of neutrophils within the affected tissue, initiating inflammatory processes that lead to severe mucosal lesions. In the present study we investigated the effect of pentoxifylline (PTX), a potent inhibitor of tumour necrosis factor production, on I/R induced intestinal injury. Wistar albino rats were divided into four groups: (1) Sham operation (S); (2) Sham operation + PTX (50 mg/kg i.v.) (S + PTX); (3) 1 h ischemia + 2 h reperfusion (I/R); and (4) I/R + PTX. Animals were sacrificed at the end of the reperfusion period and ileum samples were obtained. Malondialdehyde (MDA) levels, an end product of LP, glutathione (GSH) levels, a key antioxidant, and myeloperoxidase (MPO) activity (an index of polymorphonuclear neutrophils) stimulation, were determined in ileum homogenates. The results of the present study indicate that ischemia/reperfusion results in a significant increase in MDA content and MPO activity with a significant decrease in GSH content. Treatment with PTX returns these biomarkers to control values. A mechanism of this protective effect may involve inhibition of neutrophil oxidative burst.     

茶多酚对大鼠肠缺血再灌注肺损伤的保护作用

目的:观察茶多酚对大鼠肠缺血再灌注肺损伤的保护作用,并了解这种作用是否有剂量依赖性。方法:实验于2004-03/07在大连医科大学药理教研室实验室进行。①取雄性SD大鼠60只,随机分为模型组、假手术组及茶多酚100.0,50.0,25.0和12.5mg/kg组。②各茶多酚组大鼠舌下静脉注射相应剂量的茶多酚,模型组、假手术组给予等容量生理盐水;20min后通过夹闭肠系膜上动脉60min、再灌注120min,建立肠缺血再灌注损伤模型,假手术组不夹闭肠系膜上动脉。③再灌120min后,各组取血及肺组织,测定血清及肺组织中超氧化物歧化酶、丙二醛和一氧化氮浓度,以及肺灌流液中蛋白质含量,光镜下观察肺组织形态学改变。结果:60只大鼠进入结果分析。①与模型组相比,茶多酚12.5,25.0,50.0和100.0mg/kg组大鼠血清中超氧化物歧化酶活力分别增加38.55%,125.37%,181.58%和185.34%(P<0.05,0.01);丙二醛浓度分别降低55.83%,63.56%,74.20%和80.61%(P<0.01);一氧化氮浓度分别降低11.66%,31.97%,43.24%和84.78%(P<0.05,0.01)。②与模型组相比,茶多酚12.5,25.0,50.0和100.0mg/kg组大鼠肺中超氧化物歧化酶活力分别增加8.12%(P>0.05),116.89%,186.24%和233.59%(P<0.01);丙二醛含量分别降低34.54%(P>0.05),72.69%,75.10%和80.72%(P<0.01);一氧化氮浓度分别降低30.25%,54.61%,92.87%和92.67%(P<0.01)。③与模型组相比,茶多酚12.5,25.0,50.0和100.0mg/kg组大鼠肺灌流液蛋白质含量分别降低55.98%,70.57%,75.03%和82.00%(P<0.01)。④镜检发现模型组肺有明显组织形态学损伤,茶多酚各组较模型组呈剂量依赖性减轻肺部改变。结论:茶多酚对肠缺血再灌注所致肺损伤有剂量依赖性的保护作用,可能与其自由基消除作用,减轻中性粒细胞聚集及活化,抑制大量一氧化氮释放有关。     

茶多酚对大鼠肠缺血再灌注肺损伤的保护作用

目的：观察茶多酚对大鼠肠缺血再灌注肺损伤的保护作用，并了解这种作用是否有剂量依赖性。 方法：实验于2004—03／07在大连医科大学药理教研室实验室进行。①取雄性SD大鼠60只，随机分为模型组、假手术组及茶多酚100．0，50．0，25．0和12．5mg／kg组。②各茶多酚组大鼠舌下静脉注射相应剂量的茶多酚，模型组、假手术组给予等容量生理盐水；20min后通过夹闭肠系膜上动脉60min、再灌注120min，建立肠缺血再灌注损伤模型，假手术组不夹闭肠系膜上动脉。③再灌120min后，各组取血及肺组织，测定血清及肺组织中超氧化物歧化酶、丙二醛和一氧化氮浓度，以及肺灌流液中蛋白质含量，光镜下观察肺组织形态学改变。 结果：60只大鼠进入结果分析。①与模型组相比，茶多酚12．5，25．0，50．0和100．0mg／kg组大鼠血清中超氧化物歧化酶活力分别增加38．55％，125．37％，181．58％和185．34％（P〈0．05，0．01）；丙二醛浓度分别降低55．83％，63．56％，74．20％和80．61％（P〈0．01）；一氧化氮浓度分别降低11．66％，31．97％，43．24％和84．78％（P〈0．05，0．01）。（参与模型组相比，茶多酚12．5，25．0，50．0和100．0mg／kg组大鼠肺中超氧化物歧化酶活力分别增加8．12％（P〉0．05），116．89％，186．24％和233．59％（P〈0．01）；丙二醛含量分别降低34．54％（P〉0．05），72．69％，75．10％和80．72％（P〈0．01）；一氧化氮浓度分别降低30．25％，54．6l％，92．87％和92．67％（P〈0．01）。③与模型组相比，茶多酚12．5，25.0，50．0和100．0mg／kg组大鼠肺灌流液蛋白质含量分别降低55．98％，70．57％，75．03％和82．00％（P〈0．01）。④镜检发现模型组肺有明显组织形态学损伤，茶多酚各组较模型组呈剂量依赖性减轻肺部改变。 结论：茶多酚对肠缺血再灌注所致肺损伤有剂量依赖性的保护作用，可能与其自由基消除作用，减轻中性粒细胞聚集及活化，抑制大量一氧化氮释放有关。     

大黄素对肠缺血/再灌注损害保护作用的实验研究

目的探讨大鼠肠缺血／再灌注（I／R）损伤致肠黏膜损害的机制及大黄素的保护作用。方法将30只雄性Wistar大鼠随机分成假手术组、肠缺血45min再灌注6h模型组和大黄素预处理组。用无创伤动脉夹夹闭大鼠肠系膜上动脉制备肠I／R模型；假手术组仅开腹不钳夹血管。大黄素预处理组在术前30min经股静脉注入大黄素（2．5mg／kg），假手术组和模型组分别注入等量生理盐水。在缺血45min再灌注6h后，各组分别经下腔静脉采血，然后处死大鼠取肠系膜淋巴组织及小肠组织标本。分别检测各组血清肠脂肪酸结合蛋白（IFABP）、一氧化氮（NO）、肿瘤坏死因子-α（TNF-α）含量；小肠组织丙二醛（MDA）、超氧化物歧化酶（SOD）、髓过氧化物酶（MPO）活性；血液及肠系膜淋巴组织细菌移位率；并进行小肠组织病理学观察。结果与模型组比较，大黄素预处理组IFABP、NO、TNF-α、MDA、MPO水平均明显降低（P均〈0．01），SOD活性明显升高（P〈0．01），肠系膜淋巴组织细菌移位率显著降低（血液2／10只比8／10只，肠系膜淋巴组织3／10只比8／10只，P均〈0．05）；病理损害明显减轻。结论大黄素可减少TNF-α、NO释放，抑制过度炎症反应，减轻中性粒细胞聚集及活化，减少大鼠氧自由基的生成，对大鼠肠I／R损伤具有保护作用。     

丹参预防脊柱外科术后脊髓缺血再灌注损伤的疗效观察

目的 探讨丹参对颈椎管狭窄症术后脊髓缺血再灌注损伤的治疗效果.方法 回顾性分析5年来我院收治的64例颈椎管狭窄症施行颈椎后路单开门术的患者,随机分为丹参组(31例)及对照组(33例).按JOA标准评定疗效.结果 丹参组术前JOA评分平均为(8.8±2.6)分,术后2周JOA评分平均为(13.7±2.4)分,改善率为(61.5±2.9)%.对照组术前JOA评分平均为(9.1±2.2)分,术后2周JOA评分平均为(13.4±2.3)分,改善率为(60.5 ±2.2)%.丹参组JOA评分改善率明显优于对照组(P<0.05).结论 丹参时脊髓缺血再灌注损伤有保护作用,能有效促进术后脊髓功能恢复.     

丹参预防脊柱外科术后脊髓缺血再灌注损伤的疗效观察

Objective To investigate the effect of salvia mihiorrhiza on spinal cord ischemia reperfusion injury after surgical treatment in patients with cervical canal stenosis. Methods Retrospective analysis of 64 cases had cervical canal stenosis in the last 5 years in our hospital. Sixty-four cases were randomly divided into the salvia mihiorrhiza group(31 cases)and the control group(33 cases). The therapeutic effect was assessed using JOA grade system. Results In the salvia mihiorrhiza group,the JOA average score was 8. 8 ±2. 6 before surgical treatment, after two weeks of surgical treatment it was 13. 7 ± 2. 4. The JOA improvement ratio was (61. 5 ± 2. 9) % . In the control group,the JOA average score was 9. 1 ±2. 2 before surgical treatment,after two weeks of surgical treatment it was 13. 4 ± 2. 3. The JOA improvement ratio was (60. 5 ± 2.2)% .The JOA improvement ratio in the salvia mihiorrhiza group was significantly higher than that in the control group (P < 0. 05) . Conclusions Salvia mihiorrhiza has protective effect on spinal cord ischemia reperfusion injury.     

缺血后处理抗大鼠肠缺血-再灌注损伤的蛋白质组学研究

目的 研究缺血后处理(ischemic postconditioning,IPo)抗大鼠肠缺血-再灌注(intestinal ischemic/reperfusion injury,IL/R)损伤后肠黏膜的蛋白质变化,探讨其可能的肠保护机制.方法 16只雄性SD大鼠,随机分为IL/R组和IPo组.IL/R组阻断肠系膜上动脉60 min后再开放60min,IPo组在阻断肠系膜上动脉60 min后行三个循环灌注30 s/,阻断30 s,余同IL/R组.再灌注结束即刻在距回肠末端5 cm处取20 cm小肠刮取肠黏膜,利用高分辨双向电泳对肠黏膜组织进行蛋白质分离,Image Master 2D Elite 5.0图像软件进行分析,应用基质辅助电离解析飞行时间质谱获取肽质量指纹图谱,检索数据库鉴定差异表达的蛋白质,明确其生物学功能.结果 研究发现10个差异表达的蛋白质点,其中6个在IPo组中表达上调,4个表达下调.9个通过鉴定及功能分析,其中醛糖还原酶、醛脱氢酶与抗氧化应激和抑制凋亡相关.结论 建立了重复性较好的IPo与IL/R损伤后肠黏膜组织的双向电泳图谱.IPo的肠保护机制可能与其上调醛糖还原酶和醛脱氢酶的表达,从而抑制氧化损伤及细胞凋亡有关.     

丹参预防脊柱外科术后脊髓缺血再灌注损伤的疗效观察

Objective To investigate the effect of salvia mihiorrhiza on spinal cord ischemia reperfusion injury after surgical treatment in patients with cervical canal stenosis. Methods Retrospective analysis of 64 cases had cervical canal stenosis in the last 5 years in our hospital. Sixty-four cases were randomly divided into the salvia mihiorrhiza group(31 cases)and the control group(33 cases). The therapeutic effect was assessed using JOA grade system. Results In the salvia mihiorrhiza group,the JOA average score was 8. 8 ±2. 6 before surgical treatment, after two weeks of surgical treatment it was 13. 7 ± 2. 4. The JOA improvement ratio was (61. 5 ± 2. 9) % . In the control group,the JOA average score was 9. 1 ±2. 2 before surgical treatment,after two weeks of surgical treatment it was 13. 4 ± 2. 3. The JOA improvement ratio was (60. 5 ± 2.2)% .The JOA improvement ratio in the salvia mihiorrhiza group was significantly higher than that in the control group (P < 0. 05) . Conclusions Salvia mihiorrhiza has protective effect on spinal cord ischemia reperfusion injury.     

川芎嗪对心肺复苏后脑缺血-再灌注损伤的保护作用

目的 :观察川芎嗪对心肺复苏后对脑损伤的保护作用及其机制。方法 :将 4 2例需行心肺复苏患者按随机数表法分为治疗组 (A组 )与对照组 (B组 )。 A组 2 2例在心肺复苏开始同时给予川芎嗪 2 4 0 mg加质量分数为 5 %的葡萄糖 2 5 0 ml中静脉滴注 ,1h滴完 ,其后按上述剂量每日 1次 ,连用 7d。B组除不用川芎嗪外 ,其他治疗同 A组。检测两种治疗方法对患者血中超氧化物歧化酶 (SOD)、丙二醛 (MDA)、血栓素 B2 (TXB2 )的影响 ;并以意识恢复为主要指标评定临床疗效。结果 :A组显效 16例 (72 .72 % ) ,有效 3例 (13.6 4 % ) ,无效 3例(13.6 4 % ) ;B组显效 8例 (40 .0 0 % ) ,有效 3例 (15 .0 0 % ) ,无效 9例 (45 .0 0 % ) ,两组之间差异显著 (P<0 .0 5 )。两组治疗后静脉血 SOD、MDA和 TXB2 均有改善 ,但 A组改善程度明显优于 B组 (P均 <0 .0 1)。结论 :川芎嗪能对抗脂质过氧化 ,提高 SOD活性 ,抑制血小板活化 ,对心肺复苏后脑缺血再灌注损伤有一定的保护作用 ,早期应用可提高脑复苏成功率。     

改构型和野生型aFGF对肠缺血-再灌注损伤后肝肾功能的影响

目的　观察肠缺血再灌注损伤后的肝、肾功能的变化 ,并探讨不同类型酸性成纤维细胞生长因子 (a FGF)对肠缺血再灌注损伤后的肝、肾功能的保护作用。方法　将 78只 Wistar大鼠分成假手术组 (C)、生理盐水治疗组 (R)、改构型 a FGF治疗组 (rh F)和野生型 a FGF治疗组 (wt F) ,后 3组根据再灌注时间又分为 2、6、12和 2 4 h4个时间点。阻断肠系膜上动脉 4 5 m in后松夹制备肠缺血再灌注模型。于不同时间点腹主动脉抽血 5 ml,检测肝、肾功能的变化。结果　与 C组比较 ,R组、rh F组和 wt F组肝、肾功能都有明显下降 ,以 R组下降更明显 ,rh F组次之 ,wt F组肝、肾功能恢复得最好。组织病理学检查发现 ,3组动物均有小肠绒毛脱落、黏膜下层炎细胞浸润等改变 ,其严重程度与肝、肾功能指标水平一致。结论　肠缺血再灌注损伤导致多脏器功能损伤 ,野生型、改构型 a FGF对脏器功能有明显的保护作用。     

雌激素抑制脑缺血再灌注损伤后炎症反应

背景：炎性细胞因子的释放、粘附分子上调导致的白细胞浸润与脑梗死灶的形成有密切关系，哪些因素对其能产生影响已得到人们的广泛关注。 目的：探讨雌激素对大鼠局灶性脑缺血再灌注操作后炎症反应的影响。 设计：随机对照实验。 单位：解放军南京军区南京总医院。 材料：实验在解放军南京军区南京总医院神经内科和病理科完成。成年雌性SD大鼠，制作脑缺血模型时体质量控制在280～350g。 方法：大鼠分3组：对照组、卵巢切除组、雌激素治疗组（雌二醇，200μg/kg，皮下注射，每周1次，共4周）。4周后线栓法建立右侧大脑中动脉闭塞1h、2h再灌注0、1、3、6、22、70h模型。在苏木精-伊红染色缺血半球选取10个高倍视野计算脑组织内浸润的中性粒细胞均数，免疫组化检测核因子κB表达。 主要观察指标：脑实质内中性粒细胞浸润程度和核因子κB表达水平。 结果：①核因子-κB表达：卵巢切除组缺血1h即有表达，对照组及雌激素治疗组在缺血2h才有阳性细胞，3组均在缺血2h再灌注3h时相表达最强，后逐渐降低，卵巢切除组在再灌注70h仍有少量表达，对照组及雌激素治疗组再灌注22h后未见核因子κB阳性细胞。②在缺血2h再灌注22h时，卵巢切除组动物脑缺血区中性粒细胞浸润数量明显增多，此雌激素治疗组相比，差异有显著性差异（P=0.045），在缺血2h再灌注70h时，卵巢切除组仍多于对照组和雌激素治疗组，但仅和对照组的差异有显著性意义。 结论：雌激素能抑制脑缺血再灌注操作后炎症反应。     

雌激素抑制脑缺血再灌注损伤后炎症反应

背景:炎性细胞因子的释放、粘附分子上调导致的白细胞浸润与脑梗死灶的形成有密切关系,哪些因素对其能产生影响已得到人们的广泛关注。目的:探讨雌激素对大鼠局灶性脑缺血再灌注损伤后炎症反应的影响。设计:随机对照实验。单位:解放军南京军区南京总医院。材料:实验在解放军南京军区南京总医院神经内科和病理科完成。成年雌性SD大鼠,制作脑缺血模型时体质量控制在280～350g。方法:大鼠分3组:对照组、卵巢切除组、雌激素治疗组(雌二醇,200μg/kg,皮下注射,每周1次,共4周)。4周后线栓法建立右侧大脑中动脉闭塞1h、2h再灌注0、1、3、6、22、70h模型。在苏木精-伊红染色缺血半球选取10个高倍视野计算脑组织内浸润的中性粒细胞均数,免疫组化检测核因子κB表达。主要观察指标:脑实质内中性粒细胞浸润程度和核因子κB表达水平。结果:①核因子-κB表达:卵巢切除组缺血1h即有表达,对照组及雌激素治疗组在缺血2h才有阳性细胞,3组均在缺血2h再灌注3h时相表达最强,后逐渐降低,卵巢切除组在再灌注70h仍有少量表达,对照组及雌激素治疗组再灌注22h后未见核因子κB阳性细胞。②在缺血2h再灌注22h时,卵巢切除组动物脑缺血区中性粒细胞浸润数量明显增多,与雌激素治疗组相比,差异有显著性差异(P=0.045)熏在缺血2h再灌注70h时,卵巢切除组仍多于对照组和雌激素治疗组,但仅和对照组的差异有显著性意义。结论:雌激素能抑制脑缺血再灌注损伤后炎症反应。     

Lymphatic system as a path underlying the spread of lung and gut injury after intestinal ischemia/reperfusion in rats

We investigated in rats the influence of the lymphatic system and of tumor necrosis factor (TNF) on the lung inflammation resulting from intestinal ischemia/reperfusion (I/R) performed by 45-min occlusion of the superior mesenteric artery followed by 2 h of reperfusion. A group of rats had the thoracic lymph duct ligated before I/R. In lungs, intestinal I/R evoked a significant neutrophil recruitment, and enhanced microvascular permeability, in addition to generation of TNF in serum. In the gut, there was lowered lactate dehydrogenase (LDH) activity and increased microvascular permeability. Upon lymph duct ligation, I/R rats had a significant reduction of pulmonary neutrophil recruitment and plasma extravasation, in addition to high amounts of TNF in the lymph, contrasting with undetectable levels in the serum. In addition, LDH gut levels in these animals were close to basal values; there was also some (yet significant) reduction of microvascular permeability, suggesting that the ligation of the lymphatic duct exerted some degree of protection against the intestinal injury caused by I/R. In I/R rats, the treatment with pentoxifylline (PTX) reduced TNF in serum and blunted other lung alterations. The gut alterations caused by intestinal I/R were largely blocked by PTX. On the other hand, in I/R rats with lymph duct ligation, PTX exacerbated the reduction of pulmonary neutrophil recruitment, but did not affect pulmonary and intestinal microvascular permeabilities. Similarly, intestinal LDH activity and serum TNF levels were unaffected. Overall, our data show that the pulmonary and gut injuries induced by intestinal I/R are partially dependent on TNF, which is conceivably generated in the injured gut tissue due to intestinal I/R and carried by the lymphatic system. Thus, the mesenteric lymphatic drainage seems to play a role as a path modulator of the pulmonary and intestinal dysfunctions that follow a gut trauma.