肠淋巴途径对休克大鼠心肌自由基、炎性介质的影响

目的：观察结扎肠系膜淋巴管对重症失血性休克大鼠不同时期心肌自由基、炎症介质的影响。方法：雄性Wistar大鼠78只,分为假手术组、休克组、结扎组。休克组与结扎组复制重症失血性休克模型,结扎组于休克复苏后行肠系膜淋巴管结扎术。于休克后90min、输液复苏后0h、1h、3h、6h、12h、24h等时间点处死大鼠,制备心肌组织匀浆,检测MDA、SOD、TNFα、IL-6、NO、NOS以及MPO水平,RT—PCR方法测定心肌组织iNOS mRNA表达。结果：休克组大鼠输液复苏后多个时间点心肌匀浆MDA、TNFα、IL-6、MPO、NO、NOS和iNOS mRNA表达均有不同程度的升高,3h-12h持续在较高水平,均显著高于假手术组,心肌匀浆SOD活性显著低于假手术组：结扎组多个时间点心肌匀浆MDA、TNFα、IL-6、MPO、NO、NOS以及iNOS mRNA显著低于休克组相应时间点,SOD活性高于休克组相应时间点。结论：肠系膜淋巴管结扎阻断肠淋巴液回流,可减少心肌PMN扣押、降低TNFα、IL-6的释放、抑制NO生成及iNOS mRNA表达、减少自由基释放与SOD消耗。     

失血性休克复苏后肠内给予特殊营养物对肠粘膜血流量的影响

为探讨失血性休克复苏后肠内营养与肠粘膜血流改变的关系 ,从SD大鼠开腹制作空肠袋 ,将激光多谱勒探头和肠粘膜张力计放置在空肠袋两端 ,根据动物分组分别向袋内注射葡萄糖、谷氨酰胺、丙氨酸及甘露醇。复制失血性休克模型 (30mmHg ,维持 6 0min) ,然后用林格氏液复苏 ,恢复灌流 6 0min。分别测定肠粘膜血流量和局部PCO2 张力 (PrCO2 )。结果显示 ,失血性休克和复苏过程中 ,谷氨酰胺和葡萄糖组粘膜血流量比甘露醇和丙氨酸组显著增加 ,PrCO2 显著降低 ;而肠内给予丙氨酸进一步降低肠粘膜血流量 ,升高PrCO2 。提示 :失血性休克复苏后 ,肠内给予丙氨酸减少肠粘膜血流量 ;而给予谷氨酰胺和葡萄糖能增加肠粘膜血流量 ,对缺血再灌流损伤的肠道提供保护作用     

灵光注射液对失血性休克大鼠胃肠粘膜的保护作用

目的　观察灵光注射液 (复方樟柳碱 )对失血性休克再灌注大鼠胃肠粘膜损伤的影响。方法　将 5 6只雄性Wistar大鼠随机分 4组 ,分别设为假休克组 (8只 )、模型组 (16只 )、灵光注射液低剂量组 (16只 )和高剂量组(16只 ) ,除假休克组外 ,大鼠均经历 4kPa ,70min的失血性休克 ,在休克复苏后 6h和 12h各组分别处死半数动物 ,观察大鼠肠道菌移位情况、病理组织学和超微结构变化。结果　灵光注射液对大鼠失血性休克再灌注引起的肠道细菌移位和胃肠粘膜形态损伤有明显的保护作用 ,其治疗机制可能与改善微循环、清除氧自由基作用有关     

心肺复苏后大鼠神经元氧自由基的变化及卡尼汀的干预作用

目的:研究心肺复苏后大鼠脑细胞氧自由基的改变及卡尼汀的干预作用。方法:本实验采用窒息合并冰氯化钾停跳液致大鼠心跳骤停5min后开始心肺复苏的动物模型,SD大鼠88只,随机分为11组:对照组(假手术组)、复苏后3、12、24、48、72h组(每组8只),复苏后卡尼汀干预3、12、24、48、72h组(每组8只)。各组抽静脉血测定血液中丙二醛(MDA)含量及超氧化物歧化酶(SOD)活力。结果:心跳骤停/心肺复苏后各组大鼠血清中MDA含量较对照组显著升高(p<0.05),SOD活力显著降低(P<0.05)。使用卡尼汀干预后,血清MDA含量显著降低(P<0.05),SOD活力基本正常(P<0.05)。结论:心肺复苏后大鼠氧自由基产生增多,清除减少;卡尼汀干预后,氧自由基产生减少。卡尼汀对心肺复苏后大鼠具有保护作用。     

不同时机介入“醒脑开窍”针刺法对脑缺血再灌注大鼠SOD活性和MDA含量的影响

目的:观察不同时机介入“醒脑开窍”针刺法治疗对脑缺血再灌注模型大鼠超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量的影响.方法:将健康成年雄性SD大鼠按随机对照原则分为假手术组、模型组、3h针刺组、6h针刺组、药物组,采用线栓法制备脑缺血再灌注大鼠模型,模型制备成功后,针刺组分别于造模成功后3h、6h予以“醒脑开窍”针法治疗,药物组于在造模成功5h后予香丹注射液腹腔内注射,每日1次,治疗3次.治疗72 h后采集标本检测血清及脑组织中SOD的活性和MDA的含量.结果:与模型组比较,5h药物组血清SOD活性明显降低(P＜0.01),3h针刺组血清MDA的含量明显升高(P＜0.01);6h针刺组血清SOD活性高于3h针刺组和5h药物组(P＜0.01),而6h针刺组血清MDA含量、5h药物组血清SOD活性和MDA含量均显著低于3h针刺组(P＜0.01),6h针刺组血清SOD活性显著高于5h药物组(P＜0.01).3h针刺组脑组织SOD活性和5h药物组脑组织SOD活性及MDA含量均显著高于模型组(P＜0.01);与6h针刺组比较,3h针刺组脑组织SOD活性、5h药物组脑组织内SOD活性和MDA含量均显著升高(P＜0.01).结论:不同时机介入“醒脑开窍”针刺法可不同程度调节血清及脑组织SOD活性水平,增强氧自由基代谢,有效改善脑缺血再灌注引起的缺血性损伤,进而对损伤脑组织起到一定保护作用;且早期介入疗效更佳.     

牛磺酸对失血性休克复苏家兔血浆和心肌NOS活性影响

目的:探讨牛磺酸对失血性休克复苏后血浆和心肌一氧化氮合酶(NOS)活性、一氧化氮(NO)含量变化的影响.方法:新西兰种兔24只随机分为3组(n=8):对照组、休克组、牛磺酸治疗组.采用失血性休克复苏动物模型.连续观察休克前、休克1.5 h、复苏后1 h、2 h、3 h血浆一氧化氮合酶(NOS)活性、一氧化氮代谢产物(NO-2/NO-3)含量、乳酸脱氢酶(LDH)活性的动态变化.测定复苏后3 h心肌一氧化氮合酶(NOS)活性、一氧化氮代谢产物(NO-2/NO-3)含量的变化,并常规留取心肌标本观察形态学改变.结果:①休克组复苏后各时限血浆NOS活性、NO-2/NO-3含量、LDH活性显著高于休克前及休克1.5 h;②休克组复苏后3 h心肌NOS活性、NO-2/NO-3含量显著高于对照组,心肌出现明显水肿和脂肪变性;③牛磺酸(40 mg·kg-1 iv)可显著缓解上述变化.结论:失血性休克复苏后NOS的激活和NO的大量释放,可能介导了休克复苏所致心肌损伤,牛磺酸可减少NO的生成使心肌损伤减轻.     

外源性硫化氢对创伤失血性休克大鼠血浆炎症因子的影响

目的:研究外源性硫化氢(H2S)对创伤失血性休克大鼠炎症反应的影响。方法:选择健康成年雄性SD大鼠随机分为四组:假手术组(Sham),模型组(HTS),生理盐水组(NS),NaHS处理组(NaHS),采用创伤失血性休克模型,Sham组完成所有手术操作,但不放血和复苏,HTS组完成所有手术操作放血后给予Ringer’s液复苏,NS组放血后在Ringer’s液复苏前腹腔注射与NaHS组等容量的生理盐水,NaHS组在复苏前给与NaHS28μmol/kg(生理盐水稀释至0.5ml)腹腔注射。持续监测各组平均动脉压(MAP)及心律(HR),并通过测定血浆中TNF-α、IL-1β、IL-6和IL-10浓度的变化,观察外源性硫化氢对创伤失血性休克大鼠血浆炎症因子的影响。结果:①与HTS组及NS组比较,NaHS组复苏后MAP明显改善(P<0.05)。②与HTS组及NS组比较,复苏后1小时NaHS组血浆TNFα、IL-1β、IL-6浓度明显降低(P<0.05);而IL-10浓度四组间差异不明显(P>0.05)。结论:外源性硫化氢可改善创伤失血性休克大鼠复苏后平均动脉压及抑制复苏后早期炎症反应。     

外源性硫化氢对创伤失血性休克大鼠血浆炎症因子的影响

目的：研究外源性硫化氢（H2S）对创伤失血性休克大鼠炎症反应的影响。方法：选择健康成年雄性SD大鼠随机分为四组：假手术组（Sham）,模型组（HTS）,生理盐水组（NS）,NaHS处理组（NaHS）,采用创伤失血性休克模型,Sham组完成所有手术操作,但不放血和复苏,HTS组完成所有手术操作放血后给予Ringer＇s液复苏,NS组放血后在Ringer＇s液复苏前腹腔注射与NaHS组等容量的生理盐水,NaHS组在复苏前给与NaHS28μmol/kg（生理盐水稀释至0.5ml）腹腔注射。持续监测各组平均动脉压（MAP）及心律（HR）,并通过测定血浆中TNF-α、IL-1β、IL-6和IL-10浓度的变化,观察外源性硫化氢对创伤失血性休克大鼠血浆炎症因子的影响。结果：①与HTS组及NS组比较,NaHS组复苏后MAP明显改善（P〈0.05）。②与HTS组及NS组比较,复苏后1小时NaHS组血浆TNFα、IL-1β、IL-6浓度明显降低（P〈0.05）;而IL-10浓度四组间差异不明显（P〉0.05）。结论：外源性硫化氢可改善创伤失血性休克大鼠复苏后平均动脉压及抑制复苏后早期炎症反应。     

创伤后血二胺氧化酶的变化与肠粘膜损伤

探讨创伤感染对肠道屏障功能的影响。以山羊、大鼠手术+失血再灌注+内毒素(LPS),大鼠肠缺血再灌注和犬低温枪伤多种创伤动物为模型,测定血浆二胺氧化酶(DAO)活性,并测定血乳酶、TNF和LPS含量。观察小肠病理形态改变。结果:失血再灌注后血浆DAO水平显著升高,给予内毒素后山羊血DAO水平再度升高。血浆DAO的变化与血乳酸,TNF和LPS变化呈高度相关(r=0.872,0.842和0.817,p<0.01)。光、电镜检查表明肠粘膜损伤,失血再灌注损伤可致肠粘膜屏障功能损伤,测定血浆DAO活性变化对判断小肠粘膜损伤有帮助     

高灵敏白介素6放射免疫分析的建立及初步应用

用人工重组的白介素6(IL-6)多次免疫兔和豚鼠,获取高效价的IL-6抗体.用氯氨T法制备 ¹²⁵I标记IL-6,经Sephadex G-25纯化,抗原抗体反应采用平衡一步法,4℃温育24 h后经PR试剂分离结合和游离的标记抗原.该法测定范围0.1～3.2 μg/L最低检出量为0.l μg/L,批内和批间误差分别小于6.4％和10％.健康男性115例血清IL-6含量为(0.27±0.13) μg／L.女性101例血清IL-6为(0.26±0.10) μg/L.男女无差异.此外,用该法检测兔失血性休克再灌注损伤后24 h血清IL-6水平明显升高.失血性休克大鼠淋巴液中IL-6水平明显上升,经山莨菪碱（l mg／kg）治疗休克后IL-6又明显下降.内毒素同人牙周纤维细胞共同培养不同时间也促进IL-6释放并明显高于对照水平.     

Induction of the activities of antioxidative enzymes and the levels of malondialdehyde in cucumber seedlings as a consequence of Bemisia tabaci (Hemiptera: Aleyrodidae) infestation

The activities of antioxidative enzymes and the concentration of malondialdehyde were assayed in cucumber leaves (Cucumis sativus L.) 0, 6, 12, 24, 48, 72, and 96 h after the cucumber seedlings were infested by Bemisia tabaci (Gennadius). The results indicated that the activities of antioxidative enzymes were increased after herbivore infestation, including superoxide dismutase (SOD), and peroxidase (POD), and the levels of malondialdehyde (MDA), which is a product of membrane lipid peroxidation in the leaves. The enzymes and MDA showed peaks of different activity levels at 24 and 48 h after the infestation. SOD activity reached the highest peak, 10.4% higher than control, at 24 h, POD activity reached the highest peak, 213.2% higher than control, at 6 h, catalase (CAT) activity was not statistically significant compared with the control, and MDA content reached the highest peak, 59.9% higher than control, at 48 h. The results suggested that the enhanced activities of antioxidative enzymes and MDA content may contribute to bioprotection of cucumber plants against B. tabaci infestation. Handling editor: Henryk Czosnek     

Oxidative stress-inducible antioxidant adaptive response during prostaglandin F2alpha-induced luteal cell death in vivo

Oxidative stress-induced antioxidant adaptive response would be particularly important to cells in high reactive oxygen species (ROS) environments. We aimed to determine the dynamic adaptive response of antioxidant enzymatic systems in sheep corpus luteum (CL) during PGF2alpha-induced luteal cell death. Activities of superoxide dismutase (SOD1 and SOD2), catalase (CAT), glutathione peroxidase (GPX) and glutathione reductase (GSR), and in situ DNA fragmentation were determined in CL at day 10 of the estrous cycle (0 h) and at 12, 24 or 48 h after PGF2alpha injection. A decrease in plasma progesterone concentration was first observed at 6 h after treatment (P < 0.05). Apoptotic cells were rarely observed in the CL at 0 h (less than 0.7%), and their incidence increased (P < 0.01) by 12 h post-PGF2alpha (11.7%) and remained thereafter elevated through 48 h. Activities of SOD1, SOD2, GPX and GSR were not changed at any time points after PGF2alpha treatment. CAT activity increased at 12 h (P < 0.01) and at 24 h (P < 0.05) after PGF2alpha treatment as compared to that at 0 h. These findings demonstrate that PGF2alpha induce luteal cell death without depressing the activity of antioxidant enzymes. It is suggested that transient increase in CAT activity is an adaptive response of the CL to oxidative stress induced by PGF2alpha.     

Effects of anthraquinone extract from Rheum officinale Bail on the physiological responses and HSP70 gene expression of Megalobrama amblycephala under Aeromonas hydrophila infection

We evaluated the effect of dietary supplementation with anthraquinone extract (from Rheum officinale Bail) on the resistance to Aeromonas hydrophila infection in Megalobrama amblycephala. The fish were randomly divided into two groups: a control group (fed a standard diet) and a treatment group (standard diet supplemented with 0.1% anthraquinone extract) and fed for 10 weeks. We then challenged the fish with A. hydrophila and recorded mortality and changes in serum cortisol, lysozyme, alkaline phosphatase (ALP), total protein, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and hepatic catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA) and the relative expression of heat shock protein 70 (HSP70) mRNA for a period of 5 d. Supplementation with 0.1% anthraquinone extract significantly increased serum lysozyme activity before infection, serum ALP activity at 24 h after infection, serum total protein concentration 12 h after infection, hepatic CAT activity 12 h after infection, hepatic SOD activity before infection, and the relative expression of hepatic HSP70 mRNA both before infection and 6 h after infection. In addition, the supplemented group had decreased levels of serum cortisol 6 h after infection, serum AST and ALT activities 12 h after infection, and hepatic MDA content 12 h after infection. Mortality was significantly lower in the treatment group (86.67%) than the control (100%). Our results suggest that ingestion of a basal diet supplemented with 0.1% anthraquinone extract from R. officinale Bail can enhance resistance against pathogenic infections in M. amblycephala.     

Lipid peroxidation, antioxidant enzymes, and benzo[a]pyrene-quinones in the blood of rats treated with benzo[a]pyrene

The lipid peroxidation (as malondialdehyde, MDA), activities of superoxide dismutase (SOD) and catalase (CAT), and benzo[a]pyrene (BaP) metabolites were investigated in sera and erythrocytes of male Sprague-Dawley rats treated with BaP (20 mg per rat). MDA levels were significantly increased in sera (16.98+/-3.29 nmol/ml serum, P<0.05) 12 h after BaP treatment and persisted up to 96 h (13.80+/-1. 65 nmol/ml serum, P<0.05), but no significant change in NIDA levels was observed in erythrocytes. SOD and CAT activities were significantly increased in erythrocytes shortly after BaP exposure, and they were slightly decreased in sera, indicating an inverse correlation between lipid peroxidation and antioxidant enzyme activity. BaP and BaP-quinones (BaP-1,6-quinone and BaP-3,6-quinone) were measured in sera during the study period. A rapid increase of unmetabolized BaP was observed in sera (41.27+/-4.14 pmol/ml serum) 3 h after BaP treatment, reaching a peak at 6 h (48.56+/-4.62 pmol/ml serum) followed by a sharp decrease. Formation of the BaP-1, 6-quinone and BaP-3,6-quinone started in sera 3 h after BaP treatment, reached a peak at 24 h (7.23+/-1.02 pmol/ml serum) and 12 h (9.20+/-0.98 pmol/ml serum), respectively, and then decreased gradually. The time-dependent pattern of serum lipid peroxidation and the level of erythrocyte antioxidant enzymes were shown to be related to the concentrations of the BaP-quinone metabolites. These results suggest that BaP treatment, probably via the formation of BaP-quinones, oxidatively altered lipids and antioxidant enzymes in the blood, and might be associated with BaP-related vascular toxicity including carcinogenesis.     

The pathogenesis of L-arginine-induced acute necrotizing pancreatitis: inflammatory mediators and endogenous cholecystokinin.

This study was aimed at an assessment of the role of oxygen-derived free radicals, cytokines and endogenous cholecystokinin (CCK) in the pathogenesis of L-arginine (Arg)-induced acute pancreatitis in rat. We measured the levels of malonyl dialdehyde (MDA), glutathione peroxidase (GPx), catalase and superoxide dismutase (Mn- and Cu, Zn-SOD) in pancreatic tissue, the serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and CCK, and evaluated the protective effect of the xanthine oxidase inhibitor allopurinol and a novel CCK receptor antagonist KSG-504. Acute pancreatitis was induced in male Wistar rats by injecting 2x 250 mg/100 g body weight of Arg intraperitoneally in an 1-h interval, as a 20% solution in 0.15 M NaCl. Control rats received the same quantity of glycine. 200 mg x kg(-1) allopurinol 30 min before the first Arg treatment or 50 mg x kg(-1) KSG-504 30 min before and 6, 18 and 36 h after the first Arg injection was administered subcutaneously. Rats were killed at 6, 12, 24 and 48 h following Arg administration, and acute pancreatitis was confirmed by a serum amylase level elevation and typical inflammatory features observed microscopically. The serum level of amylase reached the peak level at 24 h after the Arg injection (30,800 +/- 3,813 versus 6,382 +/- 184 U x L(-1) in the control) and normalized at 48 h. The tissue concentration of MDA was significantly elevated at 24 h, and reached the peak value at 48 h (5.00 +/- 1.75 versus 0.28 +/- 0.05 nM x mg(-1) protein in the control). The catalase and Mn-SOD activities were significantly decreased throughout the study, while the GPx activity was significantly reduced at 6 and 12 h, and the Cu, Zn-SOD activity was significantly lower at 12 h after the Arg injection as compared with the controls. Both the TNF-alpha and the IL-6 levels were already elevated significantly at 12 h and peak at 24 h versus the controls (19.1 +/- 7.9 U x mL(-1) and 57.6 +/- 11.2 pg x mL(-1) versus 3.1 +/- 0.8 U x mL(-1) and 15.2 +/- 3.1 pg x mL(-1), respectively). No significant changes in plasma CCK levels were observed. Allopurinol treatment markedly reduced the serum amylase elevation (12.631 +/- 2.257 U x L(-1) at 24 h), prevented the increase in tissue MDA concentration (0.55 +/- 0.09 nM x mg(-1) protein at 48 h) and significantly ameliorated the pancreatic edema, necrosis and inflammation at 48 h after Arg administration. KSG-504 administration did not exert any beneficial effect on the development of histopathological changes neither modified the serum amylase or cytokine levels. Oxygen-derived free radicals and cytokines are involved, while endogenous CCK does not seem to play a role in the pathogenesis of Arg-induced acute pancreatitis.     

全氟辛烷磺酰基化合物对剑尾鱼肝脏抗氧化物酶活性的影响

目的研究全氟辛烷磺酰基化合物(PFOS)暴露对剑尾鱼(Xiphophorus helleri Heckel)抗氧化物酶活性的影响,探讨PFOS对鱼类的致毒机理。方法使用浸润法以3.5、7.0、14.0和28.0 mg/L四个PFOS浓度为剑尾鱼染毒,定量测定了96 h内肝脏组织中的超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-PX)活性及丙二醛(MDA)含量的变化。结果 PFOS暴露12 h后,除28.0 mg/L组SOD活性被显著性抑制外,其余各组与对照组均无显著性差异(P>0.05);7.0 mg/L组和14.0 mg/L组在24 h被极显著诱导(P<0.01),并且一直保持至96 h。CAT活性随PFOS浓度的升高而降低,12 h时,除3.5 mg/L组外,其余各组CAT活性被显著或极显著抑制,至24 h时,各组CAT活性有上升趋势,但48 h后,各组呈不断下降趋势持续至96 h,其CAT活性恢复到12 h水平。GSH-PX活性变化与CAT活性变化趋势相似,其中28.0 mg/L组在不同时间均被显著性抑制,并在96 h时抑制率达到最高值64.8%。MDA含量在12 h时呈小幅下降趋势,但随着暴露时间的延长,各处理组MDA含量呈连续上升趋势,并在96 h时达到最高点,诱导率分别为71.2%、70.1%和85.1%。结论结果表明,SOD的高活性是由于机体中超氧阴离子的存在,而高浓度的超氧阴离子能够灭活CAT和GSH-PX活性,因此,CAT和GSH-PX活性始终低于对照组。GSH-PX对PFOS的敏感性高于CAT。MDA含量持续升高反映出细胞组织已经遭受到氧化损伤。剑尾鱼活体的实验表明,PFOS能够诱导肝脏氧化应激反应,氧化损伤是PFOS致毒的主要途径之一。     

Protective Mechanism of Panax notoginseng Saponins on Rat Hemorrhagic Shock Model in Recovery Stage

To explore protective mechanism of Panax notoginseng saponins (PNS) on rat hemorrhagic shock model in recovery stage. 72 Wistar rats were selected and divided into control group, model group and PNS group with 24 rats in each group. 200 mg/kg PNS was injected intravenously at 60 min of hemorrhagic shock stage in PNS groups. Changes of endotoxin, MPO, IL-6, SOD, MDA and TNF α were observed at 30 and 120 min of recovery stage by ELISA; water content of lung and intestine was detected; HE staining was applied to observe morphological change of intestinal mucosa, kidney, liver and lung; western blot was used to detect intercellular adhesion molecule-1 (ICAM-1) level in lung tissue and intestine tissue. At 30 min and 120 min of recovery stage, MDA, MPO, endotoxin, TNF α and IL-6 levels significantly increased in model group compared with control group, however SOD level significantly decreased, the difference was statistically significant (P < 0.05); PNS dose-dependently decreased MDA, MPO, endotoxin, TNF α and IL-6 levels, and increased SOD level, which was statistically significant (P < 0.05); In results of water content detection, water content in lung tissue and intestine tissue was significantly higher than in control group, however, after being treated with PNS, the water content was significantly decreased; HE staining showed the morphologic change of lung tissue cells; Western blot showed that in lung tissue and intestine tissue, ICAM-1 level in model group was significantly higher than in control group, and it was lower in PNS group than in model group. PNS can increase SOD activity, decrease levels of MDA, endotoxin and MPO, decrease expression of TNF α and IL-6, and decrease water content in lung tissue and intestine tissue. Thus, PNS is protective to rat hemorrhagic shock model by anti oxidative stress and anti-inflammatory pathways, and ICAM-1 may play an important role in the mechanism.     

Cardiac depression and cellular injury in hemorrhagic shock and reinfusion: Role of free radicals

We investigated the effects of hemorrhagic shock and reinfusion on the cardiac function and contractility, plasma CK and CK-MB activity and lactate concentration, oxyradical-producing activity of polymorphonuclear leukocytes (PMNL-CL), cardiac chemiluminescence (LV-CL), antioxidant enzyme activity [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-P_X)] and malondialdehyde (MDA) concentration in anesthetized dogs to determine the role of oxyradicals in cardiac depression and cellular injury in hemorrhagic shock and reinfusion. The dogs were assigned into three groups: I (sham), 4 h duration; II (S + R), 2 h of shock followed by reinfusion for 2 h; III (SOD + S + R), as II but pretreated with PEG-SOD. Hemorrhagic shock was produced by withdrawal of blood to maintain the mean arterial pressure at 50 ± 5 mm Hg. Cardiac function and contractility were depressed during hemorrhagic shock. Plasma CK, CK-MB and lactate increased during shock. Following reinfusion after 2 h of shock hemodynamic parameters and plasma lactate tended to return towards control values. Plasma CK and CK-MB, PMNL-CL and cardiac MDA, total-, Mn- and CuZn-SOD activity increased while LV-CL decreased. In spite of the increase in the antioxidant reserve, there was oxidative damage. Pretreatment with SOD attenuated the deleterious effects of shock and reinfusion on the cardiovascular function, plasma CK, and CK-MB, PMNL-CL, cardiac MDA, SOD, and LV-CL. Protection was incomplete for cardiovascular function and plasma CK and CK-MB. These results suggest that oxyradicals may partly be involved in the deterioration of cardiovascular function and cellular injury during hemorrhagic shock and reinfusion.     

The modulation of catecholamines to the immune response against bacteria Vibrio anguillarum challenge in scallop Chlamys farreri

Catecholamines are pivotal signal molecules in the neuroendocrine-immune regulatory network, and implicated in the modulation of immune response. In the present study, the activities of some immune-related enzymes and the concentration of catecholamines were determined in circulating haemolymph of scallops Chlamys farreri after bacteria Vibrio anguillarum challenge. The activities of superoxide dismutase (SOD), catalase (CAT) and lysozyme (LYZ) increased significantly and reached 610 U mg(-1) at 12 h, 37.6 U mg(-1) at 6 h and 261.5 U mg(-1) at 6 h after bacteria challenge, respectively. The concentration of norepinephrine, epinephrine and dopamine also increased significantly and reached 114.9 ng mL(-1) at 12 h, 86.9 ng mL(-1) at 24 h and 480.4 pg mL(-1) at 12 h after bacteria challenge, respectively. Meanwhile, the activities of these immune-related enzymes in haemolymph were monitored in those scallops which were challenged by bacteria V. anguillarum and stimulated simultaneously with norepinephrine, epinephrine and adrenoceptor antagonist. The injection of norepinephrine and epinephrine repressed significantly the induction of bacteria challenge on the activities of immune-related enzymes, and they were reduced to about half of that in the control groups. The blocking of α and β-adrenoceptor by antagonist only repressed the increase of CAT and LYZ activities significantly, while no significant effect was observed on the increase of SOD activities. The collective results indicated that scallop catecholaminergic neuroendocrine system could be activated by bacteria challenge to release catecholamines after the immune response had been triggered, and the immune response against bacteria challenge could been negatively modulated by norepinephrine, epinephrine, and adrenoceptor antagonist. This information is helpful to further understand the immunomodulation of catecholamines in scallops.     

非体外循环与并行循环不停跳冠脉搭桥术炎性因子的比较

目的:通过对比非体外循环与并行循环下不停跳冠脉搭桥术炎性因子的变化,观察不同方法对机体全身炎性反应程度的影响.方法:选择2009年6月～2010年1月在我院行冠脉搭桥术患者30例,其中选取采用并行循环下不停跳冠脉搭桥术(OnP-BH CABG)和非体外循环冠脉搭桥术(OPCABG)患者各15例,即A组和B组.检测T1(术前)、T2(手术结束时)、T3(术后6小时)、T4(术后12小时)、T5(术后24小时)不同时间点血浆肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)、白介素-8(IL-8)、肌钙蛋白I(cTnI)含量,并记录桥血管数量、精神状况、引流量及ICU入住时间.结果:两组血浆TNF-α、IL-6、IL-8、cTnI舍量T1时无统计学意义(P>0.05),T2、T3、T4、T5均呈升高趋势.A组较B组T2、T3、T4、T5各时间点TNF-α、IL-6、IL-8指标升高差异显著(P<0.01);cTnI升高幅度略缓,T4、T5差异无统计学意义.比较患者术后精神状况及ICU入住时间,B组均优于A组(P>0.05).术中搭桥血管支数无统计学差异、A组引流量较B组多,有统计学意义(p=0.02).结论:并行循环下不停跳冠脉搭桥术与非体外循环冠脉搭桥术相比,心肌损伤略重;体外循环可加重机体全身炎性反应程度.

Abstract：

Objective: The aim of this study was to compare the differences of inflammatory cytokines level and inflammatory reaction in patients between on-pump beating heart CABG and off-pump CABG. Methods: Select the patients from June 2009 to Jan 2010 who underwent the CABG in our hospital with on-pump beating heart CABG and off-pump CABG and each group was 15 patients. That was named Group A and group B. Serial blood samples were collected at the following intervals respectively: before operation and Oh, 6h, 12h, 24h after the operation to evaluate the concentration of TNF-α , IL-6, IL-8 and cTn I. Recorded and compared the grafts, mental status、bleeding and the time of intensive care unit. Results: There was no significant difference between two groups in plasma TNF -α , IL - 6, IL - 8 and cTn I level at T1. The level of TNF -α , IL - 6 and IL - 8 was significantly increased at T2 - T5 compared with that before operation (T1) in both groups. However, the plasma concentrations of TNF -α , IL - 6, IL - 8 were significantly lower in group B than group A. The level of cTnI was significantly increased at T2-T3 compared with T1, and no significantly difference at T4, T5. The general condition of the patients in group B was better than group A. The bleeding was significantly fewer in groups B. Conclusions: Myocardial injury was slightly heavier in patients with on pump beating heart CABG than off pump CABG. Cardiopulmonary bypass can aggravate inflammatory reaction.