Inhibition of lipid peroxidation by superoxide dismutase following regional intestinal ischemia and reperfusion

In a feline model of regional intestinal ischemia, reoxygenation resulted in a rise in the concentration of oxidized glutathione, from 2.3 +/- 0.7 to 4.1 +/- 0.5% of the total glutathione. Also conjugated diene as an indirect measurement for lipid peroxidation increased after reperfusion from 2.5 +/- 0.5 mumol/g to 5.5 +/- 1.2 micrograms mol/g tissue. These results are in line with the hypothesis that ischemia results in an accumulation of hypoxanthine and a conversion of xanthine dehydrogenase into its O2-dependent form. Upon reoxygenation, hypoxanthine can be oxidized giving yield to a burst of O2-. and its interconversion products. These may initiate peroxidative tissue damage. Pretreatment of the cats with superoxide dismutase inhibited the biochemical alterations and protected the tissue from peroxidation damage.     

局灶性脑缺血再灌注大鼠神经元DNA氧化损伤的研究

目的：研究8－羟基－2′－脱氧鸟苷（8－OHdG)在大鼠局灶性脑缺血－再灌注后的表达情况。方法：采用栓线法制备大脑中动脉再灌注大鼠模型,按再灌注时间不同分为4组,利用免疫组织化学方法显示8－OHdG在脑内的表达,并用寡核苷酸末端核糖核酸转移酶（TdT)介导的dUTP缺口原位末端标记（TUNEL）法标记DNA片段。结果：正常组和假手术组大鼠脑内偶见8－OHdG阳性细胞,缺血2小时再灌注2小时时,缺血区散在8－OHdG阳性细胞;再灌注24小时时,8－OHdG阳性程度达到高峰;48小时时,缺血区内的神经细胞显示中度的8－OHdG阳性,缺血区外的神经细胞为强阳性,此处的细胞TUNEL染色为阴性。结论：脑缺血－再灌注后,DNA氧化损伤比细胞死亡发生范围更加广泛,DNA氧化损伤并不一定导致细胞死亡。抗氧化治疗可能在限制脑缺血－再灌注时氧化应激中起重要作用。     

High-density lipoproteins reduce the intestinal damage associated with ischemia/reperfusion and colitis

High-density lipoproteins (HDLs) have been shown to reduce the organ injury and mortality in animal models of shock by reducing the expression of adhesion molecules and proinflammatory enzymes. However, there is limited evidence that HDL treatment reduces inflammation. As inflammation plays an important role in the development of colitis as well as ischemia/reperfusion (I/R) injury of the intestine, we have investigated the effects of HDL in animal models of associated with gut injury and inflammation (splanchnic artery occlusion [SAO] shock and dinitrobenzene sulfonic acid [DNBS]-induced colitis). We report here for the first time that the administration of reconstituted HDLs (recHDLs; 80 mg/kg i.v. bolus 30 min prior to ischemia in the SAO-shock model or 40 mg/kg i.v. every 24 h in the colitis model) exerts potent anti-inflammatory effects (e.g., reduced inflammatory cell infiltration and histological injury, and delayed the development of the clinical signs) in vivo. Furthermore, recHDL reduced the staining for nitrotyrosine and poly(ADP-ribose) (immunohistochemistry) and the expression of intercellular adhesion molecule-1 in the ileum of SAO-shocked rats and in the colon from DNBS-treated rats. Thus, recHDL reduces the inflammation caused by intestinal I/R and colitis. HDLs may represent a novel therapeutic approach for the therapy of inflammation of the gut.     

多普勒组织成像技术对缺血心肌再灌注前后室壁运动的定量研究

目的　利用多普勒组织成像技术 (DTI)观察正常人及冠心病患者心肌运动的特点 ,并了解缺血心肌再灌注前后心肌运动改变情况。方法　 16例健康人及 18例冠心病患者均行DTI检测 ,冠心病患者再灌注后再行DTI ,比较手术前后DTI变化情况。结果　冠心病患者和健康人相比 ,收缩期峰值速度 (VS)明显降低 (室间隔心尖段除外 ) ,舒张早期峰值速度 (VE)也明显减低 (间壁心尖段及下壁心尖段除外 )。再灌注前后比较 ,运动恢复节段VS、VE 均明显提高。结论　DTI能定量分析缺血心肌再灌注前后室壁运动变化情况。     

VEGF antagonism reduces edema formation and tissue damage after ischemia/reperfusion injury in the mouse brain

VEGF is mitogenic, angiogenic, and a potent mediator of vascular permeability. VEGF causes extravasation of plasma protein in skin bioassays and increases hydraulic conductivity in isolated perfused microvessels. Reduced tissue oxygen tension triggers VEGF expression, and increased protein and mRNA levels for VEGF and its receptors (Flt-1, Flk-1/KDR) occur in the ischemic rat brain. Brain edema, provoked in part by enhanced cerebrovascular permeability, is a major complication in central nervous system pathologies, including head trauma and stroke. The role of VEGF in this pathology has remained elusive because of the lack of a suitable experimental antagonist. We used a novel fusion protein, mFlt(1-3)-IgG, which sequesters murine VEGF, to treat mice exposed to transient cortical ischemia followed by reperfusion. Using high-resolution magnetic resonance imaging, we found a significant reduction in volume of the edematous tissue 1 day after onset of ischemia in mice that received mFlt(1-3)-IgG. 8-12 weeks after treatment, measurements of the resultant infarct size revealed a significant sparing of cortical tissue. Regional cerebral blood flow was unaffected by the administration of mFlt(1-3)-IgG. These results demonstrate that antagonism of VEGF reduces ischemia/reperfusion-related brain edema and injury, implicating VEGF in the pathogenesis of stroke and related disorders.     

大鼠局灶性脑缺血再灌注后脑组织的氧化损伤

目的:通过观察大鼠局灶性脑缺血再灌注后脑组织超氧化物歧化酶活性和丙二醛含量的变化,进一步探讨大鼠局灶性脑缺血再灌注后氧化损伤的病理生理改变。方法:实验于2004-09/2005-01在泸州医学院神经生物学教研室进行。将雄性成年Wistar大鼠60只随机分为2组:假手术组30只和缺血再灌注组30只。每组分3个观察时间点,分别为手术后6,12,24h,每个时间点10只。采用线栓法制成大脑中动脉闭塞模型,假手术组手术过程同缺血再灌注组,但未插栓线,不造成脑缺血。测定手术后不同时点脑组织超氧化物歧化酶活性和丙二醛水平。结果:在实验过程中有6只大鼠死亡,缺血再灌注组有8只大鼠手术后模型评价为0级,被排除实验,随机补充14只大鼠,最终进入结果分析仍为60只大鼠。①缺血再灌注组术后6,12,24h超氧化物歧化酶活性均低于假手术组眼(289.72±10.67),(534.77±22.67)μkat/L;(330.57±18.17),(539.11±11.50)μkat/L;(377.58±14.67),(550.78±11.50)μkat/L,P<0.05演。②缺血再灌注组术后6,12,24h丙二醛水平显著高于假手术组眼(15.06±0.59),(6.78±0.25)μmol/L;(13.53±1.11),(6.78±0.26)μmol/L;(11.31±0.97),(6.80±0.26)μmol/L,P<0.05演。结论:脑缺血再灌注后,缺血大鼠脑组织内丙二醛水平升高,超氧化物歧化酶活性降低,说明自由基参与了脑缺血再灌注损伤的病理生理过程。     

大鼠局灶性脑缺血再灌注后脑组织的氧化损伤

目的：通过观察大鼠局灶性脑缺血再灌注后脑组织超氧化物歧化酶活性和丙二醛含量的变化，进一步探讨大鼠局灶性脑缺血再灌注后氧化损伤的病理生理改变。方法：实验于2004-09／2005-01在泸州医学院神经生物学教研室进行。将雄性成年Wistar大鼠60只随机分为2组：假手术组30只和缺血再灌注组30只。每组分3个观察时间点，分别为手术后6，12，24h，每个时间点10只。采用线栓法制成大脑中动脉闭塞模型，假手术组手术过程同缺血再灌注组，但未插栓线，不造成脑缺血。测定手术后不同时点脑组织超氧化物歧化酶活性和丙二醛水平。结果：在实验过程中有6只大鼠死亡，缺血再灌注组有8只大鼠手术后模型评价为0级，被排除实验，随机补充14只大鼠，最终进入结果分析仍为60只大鼠。①缺血再灌注组术后6，12，24h超氧化物歧化酶活性均低于假手术组[（289．72&;#177;10．67），（534．77&;#177;22．67）μkat／L；（330．57&;#177;18．17），（539．11&;#177;11．50）μkat／L；（377．58&;#177;14．67），（550．78&;#177;11．50）μkat／L，P〈0．05]。②缺血再灌注组术后6，12，24h丙二醛水平显著高于假手术组[（15．06&;#177;0．59），（6.78&;#177;0．25）μmoL／L；（13．53&;#177;1．11），（6．78&;#177;0．26）μmol／L；（11．31&;#177;0．97），（6．80&;#177;0．26）μmoL／L，P〈0．05]。结论：脑缺血再灌注后，缺血大鼠脑组织内丙二醛水平升高，超氧化物歧化酶活性降低，说明自由基参与了脑缺血再灌注损伤的病理生理过程。     

定量组织速度显像技术评价犬心肌缺血再灌注局部心室壁运动

目的　探讨定量多普勒组织速度显像 (QTVI)评价犬急性心肌缺血再灌注局部心室壁运动异常的可行性 ,为QTVI应用于临床判断心肌缺血部位及再灌注后存活心肌的评估提供实验依据。方法　应用QTVI观察 7条犬冠状动脉结扎前基础状态、结扎后不同时间点及再灌注后的局部室壁每一节段的收缩期峰值流速(Vs)、舒张早期峰值流速 (Ve)。且术后心肌标本经 1%氯代三苯基四氮唑溶液染色及透射电镜超微结构观察以证实心肌细胞有无坏死。结果　结扎犬冠状动脉 5min、10min组局部心肌各节段Vs、Ve较基础状态明显降低(均P <0 .0 5 )。结扎 3 0min后局部心肌收缩速度Vs有一定程度恢复 ,Ve恢复时间晚于Vs。血流再灌注后基本呈恢复趋势 ,但仍低于基础状态。结论　QTVI技术可定量评价缺血再灌注后局部室壁运动异常 ,对临床诊断急性心肌缺血和帮助治疗决策有一定的应用价值。     

犬肠缺血/再灌注时小肠对早期肠内营养耐受能力的实验研究

目的研究肠道低灌注状态下实施早期肠内营养(EEN)时小肠功能指标及耐受能力的变化。方法健康雄性杂种犬24只,夹闭肠系膜上动脉(SM A)1 h后恢复灌注造成肠缺血/再灌注(I/R)损伤,复流后4 h实施EEN,将瑞代营养液(4 m l.k-g 1.-h 1)经肠黏膜张力计管持续滴注3 h,如果动物出现肠道不能耐受症状(如呕吐、腹泻等)则停止,间隔6 h后再次实施EEN,直至动物肠道能够耐受为止。按随机数字表法将动物分成单纯EEN组、单纯I/R组、I/R后EEN组(I/R+EEN组),每组8只。检测小肠黏膜二氧化碳分压(P iCO2)、D木糖吸收量、小肠腔内压力判定小肠灌注和功能变化。结果肠I/R+EEN组肠道不能耐受发生率(87.5%)和严重程度均显著高于单纯EEN组(0)和单纯I/R组(12.5%)。实施EEN后,与单纯I/R组和单纯EEN组相比,I/R+EEN组小肠腔内压力及肠P iCO2均显著升高,而血浆D木糖吸收量显著降低(P均<0.01)。结论肠I/R能显著降低小肠对EEN的耐受能力,肠I/R后过早(<12 h)实施EEN能加重小肠I/R损伤,并进一步抑制小肠吸收和运动功能。     

酸性成纤维细胞生长因子对大鼠肠缺血再灌注损伤影响的研究

目的　观察外源性酸性成纤维细胞生长因子 ( a FGF)对肠缺血再灌注损伤肠道保护效应及与组织损伤修复的关系。方法　采用肠系膜上动脉 ( SMA)夹闭 4 5 m in后松夹方法制备肠缺血再灌注损伤动物模型。将 Wistar大鼠随机分为假手术组、单纯肠缺血再灌注组及 a FGF治疗组。假手术组分离 SMA但不夹闭 ,4 5 min后取血并活杀动物 ;其余两组分别松夹形成血流再灌注 ,缺血再灌注组从尾静脉注射 0 .15 ml生理盐水 ,a FGF治疗组则从尾静脉给予 0 .15 m l( 4 g) a FGF。于再灌注后 0 .5、1、2、6、12和 2 4 h取血检测血浆D乳酸水平 ;活杀动物后取小肠组织行苏木素伊红 ( HE)染色 ,光镜下观察组织病理形态学改变 ;观察两组大鼠肠缺血再灌注损伤后不同时间点的存活率。结果　与肠缺血再灌注组各时间点比较 ,a FGF治疗组动物存活率均高于对照组 ,以 2 4 h最为显著 ,有统计学意义 ( P<0 .0 5 ) ;血浆 D 乳酸水平于再灌注后 1h则明显低于缺血再灌注组 ,至 2 4 h仍呈降低趋势 ( P均 <0 .0 5 ) ;小肠黏膜病理形态学改变较缺血再灌注组轻。结论　外源性 a FGF对肠缺血再灌注损伤有保护作用 ,其机制可能与体内诱导细胞促分裂效应与非促分裂激素样活性有关     

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。     

亚低温复合缺血预处理对大鼠肠缺血再灌注肝损伤的保护作用

目的:观察复合预处理对肠缺血再灌注大鼠模型肝组织细胞凋亡相关基因Bcl-2和Bax蛋白表达的影响,分析复合预处理防治缺血再灌注肝损伤的作用途径。方法:实验于2002-05/12在咸宁学院医学院中心实验室完成。选用Wistar健康雄性大鼠30只,由咸宁学院医学院动物室提供[实验动物机构许可证号:SCXK(鄂)2004-007]。将30只大鼠按随机数字表法分为3组,即假手术组、缺血再灌注组、复合预处理组,每组10只。肠缺血再灌注模型制备:麻醉后暴露大鼠肠系膜上动脉用无损伤动脉夹夹闭其根部导致缺血,松夹即为再灌注。①假手术组:仅暴露肠系膜上动脉而不夹闭,共2h结束实验后取材。②缺血再灌注组:夹闭肠系膜上动脉60min后,松夹60min再取材。③复合预处理组:在小肠周围充填碎冰造成小肠亚低温(33～35℃),再夹闭肠系膜上动脉5min和松夹5min作为预处理,余同缺血再灌注组。动物模型制备后,在各时段处死大鼠,同时取少许肝左中叶组织,一部分常规切片,采用SABC法进行免疫组化染色,胞浆出现棕黄色颗粒为Bcl-2,Bax蛋白染色阳性细胞,计算Bcl-2,Bax蛋白的阳性表达指数;另一部分行光、电镜观察,观察各组大鼠的肝脏组织学改变。结果:30只大鼠全部进入结果分析,无脱失。①各组大鼠肝组织Bcl-2,Bax蛋白的阳性表达指数比较:缺血再灌注组大鼠肝组织Bcl-2,Bax蛋白的阳性表达指数显著高于假手术组(5.31±1.15)%,(15.16±1.35)%;(1.01±0.09)%,(0.98±0.07)%(P<0.01);复合预处理组大鼠的肝组织Bcl-2蛋白阳性表达指数(12.21±1.17)%显著高于缺血再灌注组(P<0.01),Bax蛋白的阳性表达指数(7.45±1.61)%显著低于缺血再灌注组(P<0.01)。②各组大鼠肝脏组织学改变:光镜下缺血再灌注组肝细胞水肿,肝窦淤血变窄;复合预处理组肝细胞索及肝窦排列整齐,未见肝细胞水肿。电镜下缺血再灌注组肝细胞有空泡形成,线粒体肿胀,胞浆疏松化,部分肝细胞核固缩、变小;复合预处理组肝细胞损伤减轻,内未见空泡,线粒体稍肿胀。结论:亚低温复合缺血预处理可通过上调Bcl-2蛋白与下调Bax蛋白表达以保护缺血再灌注肝损伤,这可能是复合预处理保护肠缺血再灌注肝损伤的作用途径之一。     

丙泊酚对大鼠肠缺血-再灌注后肺细胞间黏附分子-1蛋白表达的影响

目的 研究丙泊酚对大鼠肠缺血-再灌注(I／R)后肺细胞间黏附分子-1(ICAM-1)蛋白表达的 影响。方法 SD大鼠随机分为4组(n=8):①I／R组:暴露腹腔后夹闭肠系膜上动脉(SMA)1 h,开放再灌注 2 h;②丙泊酚预处理组(P1组):肠缺血前10 min给予丙泊酚;③丙泊酚治疗组(P2组):肠再灌注前10 min给 予丙泊酚;④假手术组:仅暴露SMA,不行肠I／R及丙泊酚输注。丙泊酚剂量为首剂10 mg／kg,然后以 10 mg·kg-1·h-1持续输注。所有动物于再灌注2 h处死,检测血浆和肺组织肿瘤坏死因子-α(TNF-α) 及肺组织MPO含量,免疫组化染色检测肺组织ICAM-1蛋白的表达。结果 肠I／R后动物血浆和肺组织 TNF-α含量及肺组织MPO含量、ICAM-1蛋白表达均增加。丙泊酚可以抑制上述改变,以P1组效果最明 显,其中血浆TNF-α及肺组织ICAM-1表达在I／R组和P1组间存在显著性差异(P均<0.05),而P2组上 述各指标显著高于假手术组。结论 ICAM-1在肠I／R后肺损伤的发生中发挥重要作用。肠I／R早期应用丙 泊酚可减少肺组织ICAM-1表达,在一定程度上减轻肺损伤。     

Lisofylline ameliorates intestinal mucosal barrier dysfunction caused by ischemia and ischemia/reperfusion

In an effort to determine whether treatment with lisofylline (LSF) ameliorates intestinal barrier dysfunction in rats subjected to mesenteric ischemia and reperfusion (I/R), regional mesenteric vessels were occluded for 60 min and then unclamped for 60 min more. In Protocol 1, intravenous LSF (15 mg/kg bolus then 10 mg/kg/h) was administered 5 min before ischemia. In Protocol 2, LSF (same dose) was given 1 min before reperfusion. Controls received an equivalent volume of Ringer's lactate solution. Permeability was assessed by determining the mucosal-to-serosal clearance of fluorescein isothiocyanate-conjugated dextran (4 kDa) in everted ileal gut sacs incubated ex vivo. In Protocol 1, LSF treatment during ischemia ameliorated mucosal barrier dysfunction; mean +/- SEM clearances for the LSF and Ringer's lactate solution groups after 60 min of ischemia were 34.4+/-6.1 and 64+/-7.1 nL/min/cm2, respectively; p = .007. Clearances after reperfusion were the same in the two groups. In Protocol 2, LSF treatment just before reperfusion ameliorated barrier dysfunction measured 60 min after the restoration of blood flow; clearances for the LSF and Ringer's lactate solution groups were 23.1+/-3.8 and 40.2+/-4.5 nL/min/cm2, respectively; p = .012. Treatment with LSF did not affect intestinal levels of reduced glutathione or adenosine triphosphate or the extent of histological damage to the mucosa after I/R. Nevertheless, villus height was greater in animals treated with LSF than RLS prior to ischemia in Protocol 1 (250+/-37 and 160+/-15 microm, respectively; p = .04) and during reperfusion in Protocol 2 (170+/-21 and 82+/-7 microm, respectively; p = .002). We conclude that LSF is effective in reducing both ischemia- and I/R-induced gut barrier dysfunction, possibly due to a mechanism related to preservation of villus height.     

Pretreatment with bone morphogenetic protein-7 (BMP-7) mimics ischemia preconditioning following intestinal ischemia/reperfusion injury in the intestine and liver

Intestinal ischemia/reperfusion (I/R) injury has been shown to cause intestinal mucosal injury and adversely affect function. Ischemic preconditioning (IPC) has been shown to protect against intestinal I/R injury by reducing polymorphonuclear leukocyte infiltration, intestinal mucosal injury, and liver injury, and preserve intestinal transit. Bone morphogenetic protein 7 (BMP-7) has been shown to protect against I/R injury in the kidney and brain. Recently, microarray analysis has been used to examine the possible IPC candidate pathways. This work revealed that IPC may work through upregulation of BMP-7. The purpose of this study was to examine if pretreatment with BMP-7 would replicate the effects seen with IPC in the intestine and liver after intestinal I/R. Rats were randomized to six groups: sham, I/R (30 min of superior mesenteric artery occlusion and 6 h of R), IPC+R (three cycles of superior mesenteric artery occlusion for 4 min and R for 10 min), IPC+I/R, BMP-7+R (100 microm/kg recombinant human BMP-7), or BMP-7+I/R. A duodenal catheter was placed, and 30 min before sacrifice, fluorescein isothiocyanate-Dextran was injected. At sacrifice, dye concentrations were measured to determine intestinal transit. Ileal mucosal injury was determined by histology and myeloperoxidase activity was used as a marker of polymorphonuclear leukocyte infiltration. Serum levels of aspartate aminotransferase were measured at sacrifice to determine liver injury. Pretreatment with BMP-7 significantly improved intestinal transit and significantly decreased intestinal mucosal injury and serum aspartate aminotransferase levels, comparable to animals undergoing IPC. In conclusion, BMP-7 protected against intestinal I/R-induced intestinal and liver injury. Bone morphogenetic protein 7 may be a more logical surrogate to IPC in the prevention of injury in the setting of intestinal I/R.     

肢体缺血-再灌注后大鼠心肌中的氧化应激及HO-1 mRNA表达

目的 探讨肢体缺血-再灌注损伤后心肌的氧化损伤机制及HO-1的保护作用,为研究肢体缺血-再灌注损伤所致的心肌损伤的预防提供实验依据.方法 应用止血带构造SD大鼠双后肢IR模型,实验动物随机(随机数字法)分为正常对照组和缺血4 h再灌注2 h,4 h,6 h,8 h,16 h,24 h共7组,分别取心肌和血液标本检测MDA,SOD,MPO,心肌形态学及心肌组织中HO-1 mRNA的表达.方差分析方法进行统计学处理.结果 (1)血浆及心肌IR各组MDA均较对照组明显升高(P<0.05),且于IR 4 h达高峰.血浆及心肌IR各组SOD均较对照组明显降低(P<0.05),且血清SOD于IR4 h达最低值,心肌SOD于IR 8 h达最低值.血浆及心肌IR各组MPO均较对照组明显升高(P<0.05),且血清MPO于IR 4 h达高峰,心肌MPO于IR 6 h达高峰.(2)在肢体缺血4 h再灌注4-6 h组,心肌形态学损伤最重.(3)与对照组比较,IR2 h组HO-1 mRNA表达差异无统计学意义(P>0.05),其余各组HO-1 mRNA表达均显著上调(P<0.05)且于IR 16 h达高峰.结论 心肌局部组织的自由基和中性粒细胞聚集活化是LIR心肌损伤的机制且能上调HO-1 mRNA的表达,HO-I在心肌组织的高表达能减轻心肌组织的损伤.     

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]     

全脑缺血再灌注损伤早期脑皮质超微结构的变化

目的探讨全脑缺血再灌注损伤大鼠早期脑皮质神经元、胶质细胞和血脑屏障的变化。方法将6只Wistar大鼠随机分为缺血再灌注组（n=3）和假手术对照组（n=3）。制备大鼠全脑缺血再灌注模型。缺血再灌注组于缺血再灌注1h、假手术组于手术后1h取脑，电镜观察皮质超微结构的变化。结果缺血再灌注早期（1h）皮质神经细胞发生不同程度的固缩，胶质细胞肿胀，核内染色质溶解，核膜不清；血管周围足突轻度肿胀，与基膜分离；微管有部分溶解。结论再灌注损伤早期皮质神经元、胶质细胞、细胞骨架和血脑屏障即发生变化。     

Myocardial ischemia in intestinal postischemic shock: the effect of hypoxemic reperfusion

OBJECTIVE: The circulatory shock following intestinal ischemia-reperfusion injury has been attributed to hypovolemia. The purpose of the current study is to clarify the pathophysiology of this type of shock and to test the hypothesis that hypoxemic compared with normoxemic reperfusion improves hemodynamics. DESIGN: Randomized animal study. SETTING: Medical school laboratory. SUBJECTS: Twenty-one pigs. INTERVENTIONS: Pigs were subjected to 120 mins of intestinal ischemia by clamping the superior mesenteric artery. Upon declamping, the animals were randomized into two groups: a group that received hypoxemic reperfusion (HR group, n = 8) with a PaO2 = 30-35 and a control group reperfused with PaO2 = 100 mm Hg (control group, n = 13). MEASUREMENTS AND MAIN RESULTS: Measurements included mean arterial pressure, cardiac index, pulmonary artery occlusion pressure, and requirements for fluids and epinephrine. Biopsies from the terminal ileal mucosa were taken for malondialdehyde measurements at baseline, at 120 mins of ischemia, and at 30 and 60 mins of reperfusion. A piece of left ventricle was obtained after 120 mins of reperfusion for histologic studies. Five of 13 animals of the control group died in intractable shock; no animal of the HR group died (p =.11). The decrease in the mean arterial pressure during reperfusion was more pronounced in the control group (p <.008) despite the larger doses of epinephrine administered, compared with the HR group (p <.02). During reperfusion, both groups exhibited a decrease in cardiac index; this was more pronounced in the control group (p =.0007). Pulmonary artery occlusion pressure increased during reperfusion in both groups and was more pronounced in the control group (p =.04 at 60 mins). Although mixed venous blood oxygen saturation of the control animals was higher at 30 mins of reperfusion (p =.005), it declined after 60 mins and became lower than that of HR animals at the end of reperfusion (p <.02). The myocardial histopathologic injury score was higher in the control group (2.0 +/- 0.69 and 3.4 +/- 0.89 for the HR and control groups, respectively; p <.03). The concentrations of intestinal mucosa malondialdehyde were significantly higher in the control group at 60 mins of reperfusion (p <.03). CONCLUSIONS: Acute myocardial ischemia and left heart failure significantly contribute to the circulatory shock that follows intestinal ischemia/reperfusion injury and are attenuated by hypoxemic reperfusion.     

Emulsified isoflurane protects rat heart in situ after regional ischemia and reperfusion

Volatile anesthetic postconditioning reduces myocardial infarct size against ischemia/reperfusion (I/R) injury. We tested the hypothesis that emulsified isoflurane (EIso) administrated after ischemia exerts cardioprotection in a rat model of myocardial I/R. Male SD rats underwent 30‐min coronary occlusion followed by 3‐h reperfusion except for sham rats. All vehicles were administrated intravenously at reperfusion onset for 30 min. In the first study, 56 rats were given saline (CON), 30% intralipid (IL) and 1, 2, 4, 8 or 16 mL/kg EIso for infarct size measurement. In a second study, 32 rats were randomized to four groups and administrated saline in sham (sham) and control (CON) groups, 30% intralipid in IL group and 2 mL/kg emulsified isoflurane in EIso group. Cardiomyocytic enzyme activity was determined. Myocardial mitochondria and cytosol were isolated to determine mitochondrial energy metabolism, cytochrome c release, mitochondrial membrane potential (ΔΨm) and opening of the mitochondrial permeability transition pore (mPTP). Morphologic changes in mitochondria were observed by transmission electron microscopy. Compared with CON and IL, 2, 4 and 8 mL/kg EIso limited infarct size (P < 0.01). Serum levels of cardiac enzyme leakage were reduced in EIso‐treated hearts compared with CON (P < 0.01 or P < 0.05). EIso preserved the ultrastructure of mitochondria, protected against mPTP opening, decreased cytochrome c release and preserved ATP production and ΔΨ_m. In conclusion, EIso is effective in reducing infarct size and in preserving mitochondrial function after ischemia and reperfusion injury.