The effect of superoxide dismutase overexpression on hepatic gluconeogenesis and whole-body glucose oxidation during resuscitated normotensive murine septic shock

Besides excess cytokine and NO production, enhanced oxygen radical formation was referred to contribute to the impaired hepatic gluconeogenesis during sepsis or endotoxemia. Therefore, we tested the hypothesis that genetic overexpression of the Cu/Zn-superoxide dismutase (SOD-1) may restore the sepsis-related lack of the norepinephrine-induced increase in hepatic gluconeogenesis and whole-body glucose oxidation. Anesthetized, ventilated, and instrumented wild-type control, and heterozygous and homozygous SOD-1-overexpressing mice received hydroxyethyl starch and norepinephrine to maintain normotensive hemodynamics measured at 18, 21, and 24 h after cecal ligation and puncture (CLP) or sham operation. Hepatic gluconeogenesis and whole-body glucose oxidation were calculated from liver tissue isotope and expiratory 13CO2 enrichments during continuous i.v. 1,2,3,4,5,6-13C6-glucose. Superior mesenteric artery and portal vein flows (ultrasound flow probes) and hepatic microcirculatory perfusion (Laser Doppler flowmetry) and O2 saturation (remission spectrophotometry) were comparable in the CLP and sham-operated animals, without any difference related to the mouse strain. Despite continuous i.v. norepinephrine necessary in the CLP mice, both glycemia and hepatic gluconeogenesis were similar, irrespective of the presence of sepsis and the genetic strain. Glucose oxidation rate progressively increased in the CLP groups, again without difference between the genetic strains. The surgery- and CLP-induced increase in liver cell oxidative DNA damage (tail moment in the comet assay) was less pronounced in the homozygous mice. Heterozygous nor homozygous SOD-1 overexpression did not improve the sepsis-related impairment of carbohydrate metabolism, possibly because of the lacking increase of the tissue catalase and the mitochondrial SOD activity, and the ongoing i.v. norepinephrine.     

Effects of polyethylene glycol-linked superoxide dismutase and catalase during in vivo lung ischemia and reperfusion

We have previously demonstrated that reperfusion of a rabbit lung following 24 hours of in vivo pulmonary artery occlusion results in bilateral lung edema and lung inflammation and in systemic leukopenia. We tested whether this in vivo ischemia/reperfusion lung injury in the rabbit could be prevented by the administration of superoxide dismutase (SOD) and catalase (CAT). Polyethylene glycol-linked SOD (PEG-SOD) and CAT (PEG-CAT) were administered to five rabbits, PEG-SOD alone to four rabbits, and neither to nine untreated control rabbits, and the left pulmonary artery was then occluded with a microvascular clamp. Enzyme activity measured at the time of reperfusion 24 hours later demonstrated plasma CAT activity of 1,127 ± 601 U/mL for SOD/CAT-treated rabbits versus 193 ± 25 U / mL for untreated rabbits (P < .05) and SOD activity of 97 ± 25 U/mLfor SOD-treated rabbits versus no measurable activity in untreated rabbits. Following 4 hours of reperfusion, wet to dry ratios were 6.15 ± 0.27 for the reperfused left lungs and 5.55 ± 0.20 for the right lungs. Analysis of variance demonstrated a significant effect of reperfusion on left versus right wet to dry ratios (P < .05) but no effect of enzyme treatment. Lung sections scored by a blinded observer for histologic evidence of lung injury similarly showed a left-to-right difference but no difference between treated and untreated animals in degree of injury to the reperfused left lung. However, the contralateral lung was relatively less injured in treated rabbits. The two groups also differed in that an immediate leukopenia developed following reperfusion in the untreated and PEG-SOD-treated rabbits but not in the rabbits treated with both PEG-SOD and PEG-CAT. We conclude that SOD and CAT prevent the systemic leukopenia that accompanies pulmonary artery reperfusion, but do not prevent the injury to the reperfused lung. The sparing effect on the contralateral lung suggests that the mechanism of injury for that lung differs from the mechanism of injury to the occluded lung.     

Therapeutic effect of lecithinized superoxide dismutase against colitis

Ulcerative colitis (UC) involves intestinal mucosal damage induced by reactive oxygen species (ROS), in particular, superoxide anion. Superoxide dismutase (SOD) catalyzes dismutation of superoxide anion to hydrogen peroxide, which is subsequently detoxified by catalase. Lecithinized SOD (PC-SOD) is a new modified form of SOD that has overcome previous clinical limitations of SOD. In this study, we examined the action of PC-SOD using an animal model of UC, dextran sulfate sodium (DSS)-induced colitis. DSS-induced colitis was ameliorated by daily intravenous administration of PC-SOD. Unmodified SOD produced a similar effect but only at more than 30 times the concentration of PC-SOD. In vivo electron spin resonance analysis confirmed that the increase in the colonic level of ROS associated with development of colitis was suppressed by PC-SOD administration. The dose-response profile of PC-SOD was bell-shaped, but simultaneous administration of catalase restored the ameliorative effect at high doses of PC-SOD. Accumulation of hydrogen peroxide was observed with the administration of high doses of PC-SOD, an effect that was suppressed by the simultaneous administration of catalase. We also found that either a weekly intravenous administration or daily oral administration of PC-SOD conferred protection. These results suggest that PC-SOD achieves its ameliorative effect against colitis through decreasing the colonic level of ROS and that its ineffectiveness at higher doses is because of the accumulation of hydrogen peroxide. Furthermore, we consider that intermittent or oral administration of PC-SOD can be applied clinically to improve the quality of life of UC patients.     

Inhibitory effect of superoxide dismutase on fructosamine assay

The fructosamine assay measures the degree of nonenzymatic protein glycation by virtue of the reducing properties of such proteins in alkaline conditions. We report the marked inhibitory effect of superoxide dismutase (EC 1.15.1.1) on the reducing activity both of protein glycated in vitro and of diabetic sera, indicating superoxide intermediacy in the fructosamine reaction. The free-radical intermediates may be of analytical significance when pathological and physiological changes in serum anti-oxidant activity occur. They may also be of pathological significance in diabetic microangiopathy and protein browning.     

Therapeutic effect of lecithinized superoxide dismutase on pulmonary emphysema

No medication exists that clearly improves the mortality of chronic obstructive pulmonary disease (COPD). Oxidative molecules, in particular superoxide anions, play important roles in the COPD-associated abnormal inflammatory response and pulmonary emphysema, which arises because of an imbalance in proteases and antiproteases and increased apoptosis. Superoxide dismutase (SOD) catalyzes the dismutation of superoxide anions. Lecithinized human Cu/Zn- SOD (PC-SOD) has overcome a number of the clinical limitations of SOD, including low tissue affinity and low stability in plasma. In this study, we examine the effect of PC-SOD on elastase-induced pulmonary emphysema, an animal model of COPD. The severity of the pulmonary inflammatory response and emphysema in mice was assessed by various criteria, such as the number of leukocytes in the bronchoalveolar lavage fluid and the enlargement of airspace. Not only intravenous administration but also inhalation of PC-SOD suppressed elastase-induced pulmonary inflammation, emphysema, and dysfunction. Inhalation of PC-SOD suppressed the elastase-induced increase in the pulmonary level of superoxide anions and apoptosis. Inhalation of PC-SOD also suppressed elastase-induced activation of proteases and decreased in the level of antiproteases and expression of proinflammatory cytokines and chemokines. We also found that inhalation of PC-SOD suppressed cigarette smoke-induced pulmonary inflammation. The results suggest that PC-SOD protects against pulmonary emphysema by decreasing the pulmonary level of superoxide anions, resulting in the inhibition of inflammation and apoptosis and amelioration of the protease/antiprotease imbalance. We propose that inhalation of PC-SOD would be therapeutically beneficial for COPD.     

Role of CuZn superoxide dismutase in regulating lymphocyte apoptosis during sepsis

OBJECTIVE: The lymphocyte is a principal mediator of the inflammatory response, and lymphocyte depletion via apoptosis may be an important mechanism of modulating inflammation. Increased oxygen consumption occurs during sepsis and results in the generation of reactive oxygen species. Although reactive oxygen species initiate apoptosis in many biological systems, their role in controlling lymphocyte apoptosis during sepsis is unclear. The objective of this study was to better characterize the role of oxidative stress in precipitating lymphocyte apoptosis during sepsis and to specifically define the role of the CuZn superoxide dismutase (SOD) enzyme complex, a major antioxidant defense, in modulating this process. DESIGN: Prospective, randomized, controlled study. SETTING: Research laboratory at an academic medical center. SUBJECTS: Mice that were either genetically normal or that were deficient in or overexpressed the enzyme CuZn SOD. INTERVENTIONS: Mice from each genetic group were randomized to no manipulation (control), sham surgery, or cecal ligation and puncture. Mice were killed 18-24 hrs after study entry, and the thymi and spleen were removed for analysis of apoptosis. MEASUREMENTS AND MAIN RESULTS: Lymphocyte apoptosis was assessed by three independent methods: light microscopy, fluorescent terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling, and DNA gel electrophoresis. Comparisons were performed using standard parametric statistical tests. Lymphocyte apoptosis was present in mice after CLP but not in control mice or in mice after sham surgery (p < .05). Mice completely lacking CuZn SOD developed significantly more lymphocyte apoptosis than did either partially CuZn SOD-deficient or genetically normal mice (p < .05). This apoptosis was more pronounced in the thymus than the spleen and, within the thymus, more prominent in the cortex than medulla (p < .05 for all). In contrast, mice that overexpressed CuZn SOD did not differ in the amount of apoptosis after CLP compared with genetically normal mice (p = NS for all). CONCLUSIONS: Oxidative stress occurs in sepsis and appears to be one stimulus for the development of lymphocyte apoptosis, a process that is partly regulated by CuZn SOD. However, we were unable to demonstrate that overexpression of this enzyme suppressed lymphocyte apoptosis, suggesting that either other antioxidant defenses or other pathways independent of oxidative stress may mediate lymphocyte elimination in this syndrome.     

重组人超氧化物歧化酶加强一氧化氮吸入治疗幼鼠急性胎粪肺损伤的实验研究

目的　探讨联合应用重组人超氧化物歧化酶 (recombinanthumansuperoxidedismatase ,rhSOD)和一氧化氮吸入 (inhalednitricoxide,iNO)对胎粪诱导幼鼠急性肺损伤的保护作用及可能机制。方法　 32只雄性SD幼年大鼠 ,通过气管置管注入 2 0 %胎粪 1ml/kg建立幼鼠胎粪性肺损伤模型 ,随机分为 :( 1)对照组 (Control,C) :暴露于空气中 ;( 2 )NO吸入组 (iNO) :暴露于 2 0× 10 - 6 NO中 ;( 3)rhSOD组 (SOD) ) :rhSOD 2 0mg/kg·ml气管内注入并暴露于空气中 ;( 4 )联合应用 2 0× 10 - 6 NO和 2 0mg/kgrhSOD组 (iNO/SOD) ,暴露 2 4h后观察支气管肺泡灌洗液 (bronchoalveolarlavagefluid ,BALF)细胞数、肺组织匀浆髓过氧化物酶 (myeloperoxidase ,MPO)活性、丙二醛 (malonyldialdehyde,MDA)、一氧化氮 (nitricoxide,NO)含量和肺损伤病理改变。结果　与对照组比较 ,iNO组、SOD组BALF细胞数、MPO活性、肺损伤病理评分下降(P <0 0 5或 0 0 1)、iNO/SOD组较iNO组BALF细胞数、MPO活性进一步降低 (均P <0 0 5 ) ;但肺损伤病理评分差异无显著牲 ;与对照组比较 ,iNO组肺组织MDA、NO含量略有下降 ,但差异无意义 (均P >0 0 5 ) ,SOD组、iNO/SOD组肺组织MDA、NO含量显著下降 (P <0 0 5或 0 0 1) ,且iNO/SOD组显著低于iNO     

Propofol improves endothelial dysfunction and attenuates vascular superoxide production in septic rats

OBJECTIVE: To determine the effects of propofol on vascular functions, plasma and endothelium-derived nitric oxide (EDNO), vascular NO, and cyclic guanosine monophosphate (cGMP), as well as vascular production of superoxide anion (O2*-), in septic animals. DESIGN: Prospective, multiexperimental, randomized, controlled studies. SETTING: University research laboratory. SUBJECTS: Male adult Sprague-Dawley rats weighing 350-400 g. INTERVENTIONS: Cecal ligation and puncture (CLP), with and without propofol (25 mg/kg/hr) infusion, after sham or CLP (24 hrs postsurgery). MEASUREMENTS AND MAIN RESULTS: Plasma NOx, basal aortic NOx, and cGMP concentrations all increased, whereas acetylcholine-induced endothelium-dependent relaxation (EDR), contractile response, and EDNO all decreased in CLP vs. sham rats (p < .001). Acetylcholine stimulated aortic NOx and cGMP significantly in sham and CLP-propofol (p < .01) but not CLP rats. Thus, propofol ameliorated the CLP-induced increases in plasma NOx, basal aortic NOx, and cGMP. It restored the CLP-induced impairment of EDR, EDNO, and acetylcholine-stimulated aortic NOx and cGMP levels. More O2*- production (measured by lucigenin-enhanced chemiluminescence) was noted in carotid arteries from CLP vs. sham rats (p < .001). Nicotinamide adenine dinucleotide (NADH; 1 mM) stimulated O2*- production in all rings, with significantly more increase in CLP vs. sham (p < .001). Propofol attenuated the excessive increase in O2*- production of CLP rings. CONCLUSIONS: Propofol treatment attenuated the overproduction of NO and O2*-, thus restoring the acetylcholine-responsive NO-cGMP pathway in CLP-induced sepsis. It also significantly improved the CLP-impaired EDR and EDNO in a parallel manner. These beneficial effects of propofol could be accounted for by improvement of the disturbed NO/O2*- balance in sepsis.     

生长激素对内毒素腹腔感染大鼠中性粒细胞功能的影响

目的研究生长激素对内毒素腹腔感染大鼠中性粒细胞功能的作用,探讨生长激素对感染时机体炎症反应的影响。方法雄性Wistar大鼠随机分为六组(n=7)：对照组,腹腔感染组,腹腔感染 生长激素(0．5 mg/kg)组,腹腔感染 生长激素(1．0mg/kg)组,腹腔感染 生长激素(2．0 mg/kg)组,生长激素对照组(2．0 mg/kg),腹腔感染用内毒素5 mg/kg腹腔注射建立,流式细胞仪分析循环中性粒细胞表面黏附分子CD11b的表达及呼吸爆发水平。结果生长激素增加内毒素腹腔感染大鼠循环中性粒细胞表面CD11b的表达(P＜0．01),增强中性粒细胞的呼吸爆发(P＜0．01),生长激素对照组CD11b表达及呼吸爆发水平与空白对照组没有差异。结论生长激素在机体急性炎症反应过程中起促进作用,可能加重严重感染机体的炎性损伤。     

氯胺酮对感染性休克大鼠保护作用的研究

目的　观察氯胺酮对感染性休克大鼠血流动力学、血浆肿瘤坏死因子α( TNFα)和白细胞介素 6 ( IL 6 )水平的影响 ,探讨其可能的抗休克机制。方法　取健康成年雄性 ( SD)大鼠 2 0只 ,采用盲肠结扎加穿孔 ( CL P)法复制败血症或感染性休克模型。随机分为假 CL P组、CL P组、氯胺酮 组和氯胺酮 组。假CL P和 CL P组术前 30 m in经股静脉持续输注生理盐水 5 ml· kg- 1· h- 1 ,氯胺酮 和氯胺酮 组分别输注氯胺酮 5 m g· kg- 1· h- 1和 10 m g· kg- 1· h- 1。经股动脉穿刺置管 ,持续监测平均动脉压 ( MAP)、心率 ( HR)及采集血样 ,应用酶联免疫吸附试验 ( EL ISA)检测血浆 TNFα和 IL 6水平。结果　 CL P组术后 MAP进行性下降 ,HR则先加快后减慢 ;血浆 TNFα和 IL 6水平明显升高。两种剂量的氯胺酮处理均能逆转 MAP和 HR下降 ,同时抑制血浆 TNFα和 IL 6水平升高 ,尤以氯胺酮 组作用更加明显。结论　氯胺酮对败血症或感染性休克大鼠具有明显的保护效应 ,其机制可能主要是拮抗促炎性细胞因子的产生     

Amelioration of antigen-induced arthritis in rats by transfer of extracellular superoxide dismutase and catalase genes

Reactive oxygen species (ROS) have been implicated in the pathogenesis of rheumatoid arthritis (RA), while antioxidant enzymes, such as extracellular superoxide dismutase (EC-SOD) and catalase, block radical-induced events. The present study tested if the ex vivo transfer of EC-SOD and catalase genes alone or in combination in the knee joint of rats with monoarticular antigen-induced arthritis (AIA) was anti-inflammatory, and examined the potential mechanisms involved. Synoviocytes isolated from female Wistar rats were immortalized with a retroviral vector SUV19.5. These cells were permanently transfected with an EC-SOD expression plasmid (pEC-SODZeo) or a catalase expression plasmid (pCatalaseZeo) to create cells overexpressing EC-SOD or catalase, as measured by RT-PCR and Western blots. The cells were engrafted in knee joints of animals at the time of the induction of AIA. Three gene transfer groups, an EC-SOD group, a catalase group and a combined therapy group (EC-SOD and catalase) were included in these experiments. Animals in the control group were engrafted with synoviocytes transfected with the plasmid pZeoSV2 without an insert. Clinical and histological assessments were performed, as well as tissue measurements of SOD, catalase and gelatinase activities. Ex vivo gene transfer of EC-SOD and catalase into rat knee joints produced about a six- to seven-fold increase in EC-SOD activity and a two- to three-fold increase in catalase activity compared with the control animals. Rats treated with cells overexpressing EC-SOD, catalase or a combination of EC-SOD and catalase showed significant suppression of knee joint swelling, decreased infiltration of inflammatory cells within the synovial membrane and reduced gelatinase activity in knee joints, compared with animals receiving cells transfected with the plasmid alone. No statistically significant difference was found between the groups treated with cells overexpressing EC-SOD, catalase or a combination of both. Gene therapy involving the local intra-articular overexpression of two antioxidant enzymes, EC-SOD and catalase, was anti-inflammatory in AIA. One mechanism appears to be the suppression of gelatinase activities by both EC-SOD and catalase.     

脓毒症早期大鼠肾上腺皮质功能变化及地塞米松的干预作用

目的 探讨脓毒症早期是否存在相对肾上腺皮质功能不全及其可能的发病机制,以及地塞米松替代治疗的时机.方法 雄性Wistar大鼠260只,随机均分为正常对照组、假手术组、模型组[行盲肠结扎穿孔术(CLP)制备脓毒症模型]、激素预处理组(CLP前腹腔注射10 mg/kg地塞米松)、激素治疗组(CLP后7 h腹腔注射10 ml/kg地塞米松),各组再分为2、4、6、8、12 h时间点.于8 h和12 h给予促肾上腺皮质激素(ACTH)刺激实验,于刺激前及刺激后30 min用放射免疫分析法测定血清皮质醇浓度;用半定量逆转录-聚合酶链反应(RT-PCR)测定肾上腺Toll样受体4(TLR4)、肿瘤坏死因子-α(TNF-α)的mRNA表达;透射电镜下观察肾上腺皮质束状带超微结构;其余大鼠观察12 h存活情况.结果 ①模型组、激素预处理组和治疗组刺激前血清皮质醇浓度显著高于正常对照组和假手术组,且预处理组明显高于模型组和治疗组(P均＜0.05),但ACTH刺激前后血清皮质醇浓度均无明显变化.②模型组肾上腺TLR4、TNF-α的mRNA表达较假手术组明显升高(P＜0.05或P＜0.01),激素预处理组和治疗组肾上腺TLR4、TNF-α的mRNA表达较模型组明显下降,且预处理组可降至假手术组水平.⑧模型组、激素预处理组和治疗组肾上腺皮质超微结构发生代谢性改变,其中以模型组为重.④激素预处理组、治疗组大鼠12 h生存率均明显高于模型组(76.92%、40.00%比33.33%,P＜0.01和P＜0.05),且激素预处理组高于治疗组(P＜0.05).结论 ①脓毒症早期即存在相对肾上腺皮质功能不全;②肾上腺TLR4、TNF-α mRNA的表达和超微结构变化可能参与了相对肾上腺皮质功能不全的发生;③地塞米松可以降低肾上腺TLR4、TNF-α mRNA的表达,减轻超微结构变化,提高生存率,改善预后,且早期应用效果更理想.     

短期运动对大鼠心肌组织超氧化物歧化酶活性的影响

[目的]研究短期中等强度运动对大鼠心肌组织超氧化物歧化酶(SOD)活性的影响.探讨运动时心脏的保护作用的机制.[方法]将16只Wistar大鼠随机分为运动组和对照组.对运动组大鼠进行游泳训练,对照组正常饲养.训练结束后,取大鼠左心室心肌样品测定SOD活性.[结果]运动组心肌组织锰一SOD活性显著高于对照组(P＜0.01),两组总SOD和铜锌-SOD活性差异无统计学意义(P＞0.05).[结论]短期中等强度运动通过升高心肌组织锰-SOD活性发挥保护心脏作用.     

Natural killer cells participate in bacterial clearance during septic peritonitis through interactions with macrophages

Natural killer (NK) cells have a well-established role in host defense against viral infections and malignancies. However, their function in bacterial infection and sepsis is poorly defined. We hypothesized that NK cells, as a major producer of interferon-gamma during sepsis, would be important in host defense against bacterial infections. Cecal ligation and puncture (CLP) was performed on Swiss Webster mice depleted of NK cells by pretreatment with anti-asialo GM1 and control mice given immunoglobulin G (IgG) antibody. NK cell-depleted mice had significantly higher anaerobic bacterial counts in the liver and peritoneal lavage fluid, as well as higher aerobic counts in the liver and blood 4 h after CLP. Macrophage phagocytosis, nitric oxide production, and interleukin (IL)-6 levels at 4 h were also decreased in mice depleted of NK cells compared with controls. Greater neutrophil influx into the peritoneum, indicated by higher myeloperoxidase levels, was also seen in NK cell-depleted mice. At 8 and 18 h after CLP, bacterial counts were similar between groups, and overall survival rates were not significantly different. Peritoneal IL-12 levels significantly increased by 18 h in normal mice, but not in NK cell-depleted animals. Our data suggest that NK cells participate in the early local and systemic eradication of bacteria and regulation of IL-12 during polymicrobial sepsis. These effects are likely due to their interactions with macrophages.     

脑缺血状态下超氧化物歧化酶的保护功能

目的超氧化物歧化酶是机体内广泛存在的酶家族,可有效催化超氧阴离子的歧化反应.人脑中有3种超氧化物歧化酶,在缺血损伤时均发挥了有益作用.近年来以基因工程鼠作为工具研究脑缺血时超氧化物歧化酶的保护作用.资料来源应用计算机检索Medline数据库1991-01/2003-12期间的相关文章,检索词为"Chan PH and superoxide dismutase and cerebral ischemia",限定文章语言种类为英文.资料选择对资料进行初审,选取实验包括上述干预组(转基因组)和对照组的文献,筛除非随机的实验,对剩余的文献开始查找全文,以随机对照实验作为纳入标准.资料提炼共收集到38篇关于脑缺血与超氧化物歧化酶关系的随机和非随机实验,13个实验符合纳入标准,排除的25篇实验中,15篇为重复实验,10篇与本文无相关性.资料综合研究表明,活性氧参与了缺血中枢神经系统的氧化还原信号传导通路,并直接造成生物大分子如脂类,蛋白质,核酸的损伤.在缺血性脑损伤中,氧自由基产生过多及超氧化物歧化酶的消耗导致了组织细胞的损伤.铜锌超氧化物歧化酶,锰超氧化物歧化酶,细胞外超氧化物歧化酶的功能相同,可将超氧阴离子自由基分解成过氧化氢而进一步分解.从而改善脑水肿,缩小脑梗死灶及减少神经元死亡,改善缺血时的功能障碍.结论氧自由基增加是脑缺血损伤的重要机制,3种超氧化物歧化酶均可改善脑缺血时的功能损伤,这种保护作用与其对核酸修复酶、转录因子、凋亡相关蛋白和信号转导通路等作用相关.     

心肺复苏中血浆内皮素和超氧化物歧化酶水平的动态观察与分析

目的　探讨血浆内皮素 (endothelin ,ET)及超氧化物歧化酶 (superoxidedismutase,SOD)水平与心肺复苏 (cardiopulmonayresuscitation ,CPR)患者预后的关系。方法　 2 5例心搏骤停和心肺复苏患者 ,依复苏效果分为A组 (9例 ) ,心肺复苏 30min无效死亡 ;B组 (11例 ) ,复苏成功 ,自主循环建立 >2h ,但经抢救 2 4h后死亡 ;C组 (5例 ) ,复苏成功存活出院。三组患者于复苏即刻、 30min、 2h、 4h分别测定血中ET、SOD的浓度 ,比较三组患者上述指标的动态变化。结果　B、C两组随着CPR的进展ET、SOD的浓度逐渐降低 ,于CPR 2 4h差异具有显著性意义。C组ET水平下降速度比B组慢 ,而SOD水平下降速度比B组快。结论　在CPR过程中 ,ET功能衰竭是预后不良的指标 ,ET下降速度快提示预后较差。动态监测血中SOD浓度对评估心肺复苏期间患者再灌流损伤程度及代偿能力有参考价值 ,对预测抢救效果有一定的临床意义     

Absence of pulmonary edema during peritonitis and shock in rats

We evaluated the development of pulmonary edema early in the course of peritonitis and shock in rats. Peritonitis was established by cecal ligation and perforation. In a preliminary experiment, sepsis was induced in five animals and five animals served as sham-operated controls. Lungs harvested for gravimetric analysis at 6 hours revealed no significant difference in wet-dry/dry (W-D/D) ratios. In a second experiment, 15 rats were randomized to three groups: septic animals, septic animals infused with 5% albumin, and sham-operated animals. Thermodilution cardiac output and arterial blood gases were sequentially measured over a 6-hour interval. At 6 hours, the lungs were harvested for gravimetric analysis. Lung W-D/D and arterial oxygenation were not significantly different between the three groups. The W-D/D was 3.46 +/- 0.10 in sham-operated rats, 3.37 +/- 0.12 in septic rats, and 3.88 +/- 0.27 in albumin-infused septic rats. The alveolar-arterial oxygen difference at 6 hours was 10 +/- 2 mm Hg in sham-operated rats, 7 +/- 1 mm Hg in septic rats, and 13 +/- 6 mm Hg in albumin-infused septic rats. These data suggest that overt pulmonary edema and arterial hypoxemia may not occur early in septic shock when fluid infusion is not excessive.