重复+Gz暴露后大鼠心室肌的细胞凋亡现象

目的:探讨不同水平的1周重复多次的+Gz暴露后大鼠心室肌凋亡的现象及变化规律。方法:12只雄性SD大鼠随机分为+6Gz组,+10Gz组和对照组,每组4只。+Gz组大鼠分别暴露于+6Gz/3min和+10Gz/3min,1次/天,连续暴露1周;对照组大鼠置于离心机室,但不受加速度作用。大鼠于末次暴露后1d,取左心室,采用透射电镜和末端脱氧核苷酸转移酶介导的dUTP缺口标记技术(TUNEL)观察心肌细胞凋亡情况。结果:电镜下,除+10Gz组可观察到心肌细胞核内异染色质增多、浓缩、边集现象外,各组未见典型的凋亡改变。TUNEL染色可见,+6Gz组、+10Gz组心肌细胞凋亡指数较对照组均显著增高(P0.01);+10Gz组大鼠心肌凋亡指数较+6Gz组显著增多(P0.05)。结论:+Gz重复暴露可引起大鼠心肌细胞凋亡,且随着G值的增大,细胞凋亡指数呈增多趋势。     

重复正加速度暴露对大鼠心肌血管内皮超微结构和ICAM-1表达的影响

目的 :观察重复正加速度 ( Gz)暴露对大鼠心肌血管内皮细胞超微结构的影响及其暴露后细胞间粘附分子 1(ICAM 1)表达的变化情况 ,进一步探讨高 Gz暴露致心肌损伤的机理。方法 :30只雄性Wistar大鼠随机分成 3组 (n =10 ) ,其中对照组不受 Gz作用 ;正加速度组分为 1Gz组 :受 1Gz作用 , 10Gz组 :重复 10Gz暴露 ( 10Gz 30s,5counts/d ,3d/w ,3w)。于末次 Gz作用后次日同时处死大鼠 ,速取左室心肌 ,常规透射电镜制样、观察。另取左室心肌制成石蜡切片 ,行免疫组化检测。结果 :重复 10Gz作用后 ,心肌间质弥漫水肿 ,小血管内皮细胞肿胀 ,吞饮泡增多 ,血管内皮细胞ICAM 1含量也明显增加 (P <0 .0 5 ) ,而 1Gz组心肌血管内皮结构及其I CAM 1含量与对照组之间无明显差别。结论 :重复 Gz暴露后 ,大鼠心肌血管内皮细胞可出现明显损伤 ,其I CAM 1表达增多 ,提示粘附分子诱导的炎症反应参与了高 Gz应激导致的心肌损伤     

反复正加速度暴露后大鼠心肌的细胞凋亡改变

目的：探讨不同水平的1周重复多次的正加速度（＋Gz）暴露后大鼠心室肌凋亡的现象及变化规律。方法：12只雄性SD大鼠随机分为＋6Gz组,＋10Gz组和对照组,每组4只：＋Gz组大鼠分别暴露于＋6Gz／3min和＋10Gz／3min,1次／d,连续暴露1周;对照组大鼠置于离心机室,但不受加速度作用。大鼠于末次暴露后1天,取左心室,采用透射电镜和末端脱氧核苷酸转移酶介导的dUTP缺口标记技术观察心肌细胞凋亡情况。所有实验数据进行方差分析及LSD—t检验。结果：电镜下,除＋10Gz组可观察到心肌细胞核内异染色质增多、浓缩、边集现象外,各组未见典型的凋亡改变。TUNEL染色可见,＋6Gz组、＋10Gz组大鼠心肌细胞凋亡指数较对照组均显著增高（F=42．47,t6G=5．04;t10G=7．43,P〈0．01）;＋10Gz组大鼠心肌凋亡指数较＋6Gz组显著增多（t6G／10G=2．39,P〈0．05）。结论：＋Gz重复暴露可引起大鼠心肌细胞凋亡,且随着G值的增大,细胞凋亡指数呈增多趋势。     

银杏叶提取物对糖尿病大鼠心肌损伤的防护作用

目的:研究银杏叶提取物(EGb)对糖尿病大鼠心肌的防护作用.方法:用光镜和透射电镜观察EGb对糖尿病大鼠心肌的形态学改变,并测定心肌组织内超氧化物歧化酶(SOD)、一氧化氮合酶(NOS)、结构型一氧化氮合酶(cNOS)、诱导型一氧化氮合酶(iNOS)的活性及一氧化氮(NO)、丙二醛(MDA)的含量.结果:糖尿病大鼠心肌光镜下主要表现为心肌细胞空泡变性及心肌纤维局灶性溶解;电镜下主要表现为心肌线粒体肿胀,嵴变短,肌原纤维溶解;SOD活性下降,NOS、iNOS活性及MDA、NO含量增高.EGb治疗组病变明显减轻,EGb治疗组心肌组织内SOD活性明显高于糖尿病组,NOS、iNOS活性及MDA、NO含量低于糖尿病组.结论:EGb可能通过抗脂质过氧化作用和降低NO水平而对糖尿病心肌产生保护作用.     

竹节参对大强度耐力训练大鼠心肌线粒体抗氧化能力的研究

目的:探讨竹节参对大强度耐力训练大鼠心肌线粒体抗氧化能力的影响,为该药运用于抗运动疲劳提供理论依据。方法:将大鼠随机分为安静对照组,大强度耐力训练组(训练组),大强度耐力训练+竹节人参组(训练加药组),测定心肌线粒体脂质过氧化产物丙二醛(MDA)和过氧化氢(H2O2)的含量以及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)的活性,研究竹节参对大强度耐力训练大鼠心肌线粒体的保护作用。结果:力竭运动引起大鼠心肌线粒体MDA、H2O2含量显著升高(P0.01),心肌线粒体抗氧化酶CAT、GSH-Px、SOD活性显著下降(P0.01);训练加药组大鼠心肌线粒体MDA、H2O2含量明显低于训练组(P0.01),CAT、GSH-Px、SOD活性明显高于训练组。结论:竹节参可明显提高大强度耐力训练大鼠心肌线粒体的抗氧化能力,保护心肌线粒体的氧化损伤。     

茶多酚对营养性肥胖大鼠肝脏自由基代谢的影响

目的:探讨茶多酚对营养性肥胖大鼠肝脏自由基代谢的影响。方法:采用高脂饲料喂养,体重(200±20)g的雄性SD大鼠32只,随机分为4组(n=8),测定各组大鼠肝脏细胞O自由基和N自由基。结果:高脂饲料组大鼠肝脏超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性显著提高,茶多酚补充组丙二醛(MDA)含量比对照组及高脂饲料组显著下降;高脂饲料组大鼠肝脏TNOS、iNOS活性及NO含量显著升高,茶多酚降低了总-氧化氮合酶(TNOS)、诱导型一氧化氮合酶(iNOS)活性及NO含量。结论:高脂饲料诱导了大鼠肝脏细胞的氧化应激状态,茶多酚提高了营养性肥胖大鼠肝脏的抗氧化能力,对营养性肥胖大鼠肝脏有一定的保护作用。     

核因子κB在精氨酸血管升压素诱导大鼠心肌成纤维细胞一氧化氮合成中的作用

本文探讨了精氨酸血管升压素(AVP)刺激下体外培养的大鼠心肌成纤维细胞(CFs)内一氧化氮(NO)含量、一氧化氮合酶(NOS)活性、诱导型一氧化氮合酶基因表达的变化及其与核因子κB(NF-κB)的关系。用胰酶消化法分离培养Sprague Dawley仔鼠的CFs,分别采用硝酸还原酶法、分光光度法、逆转录-聚合酶链式反应(RT-PCR)、免疫荧光-共聚焦显微镜和蛋白质印迹检测AVP干预下CFs的NO含量、NOS活性、iNOS mRNA表达和NF-κB的活化。结果显示,AVP浓度依赖性(0．001—0．1μmol／L)地增加CFs的NO含量,提高NOS活性,增加iNOS mRNA表达;AVP能够活化NF—κB,使其由细胞浆转位于细胞核;NF-κB特异性抑制剂吡咯啉烷二甲基硫脲(PDTC)能够抑制AVP诱导的CFs NO含量增加、NOS活性提高和iNOS mRNA表达增加。上述结果提示,AVP干预下CFs iNOS mRNA表达增加、NOS活性增高、NO合成增多可能通过NF-κB激活途径,NF-κB激活参与心肌纤维化的发生和发展。     

正加速度重复暴露后大鼠心室肌缝隙连接蛋白43表达及分布的改变

本文旨在探讨不同水平的一周重复多次正加速度( Gz)暴露后大鼠心室肌缝隙连接蛋白43(connexin 43, Cx43)表达及分布的改变.36只雄性Sprague-Dawley大鼠随机分为对照组、 6Gz组和 10Gz组,每组12只. Gz组大鼠分别暴露于 6Gz和 10Gz各3min,1次/d,共1周,分别于末次暴露后即刻、1d、3d、7d(各3只)取心室肌作免疫组织化学染色和Western blot分析,检测Cx43的表达和分布.免疫组织化学结果显示, Gz重复暴露可引起大鼠心室肌Cx43分布方式明显紊乱,Cx43在心肌细胞侧-侧连接处的表达明显增加,在心肌细胞端-端连接处的表达减少.Western Blot结果显示, 6Gz组与 10Gz组的Cx43蛋白表达量于末次暴露后即刻、1d、3d、7d与对照组相应时刻相比均明显减少(P<0.001),以暴露后即刻减少最为明显,且随着 Gz暴露时间的延长,表达逐渐恢复,但在暴露后7d,两组的Cx43表达量仍未恢复至对照组水平.Cx43蛋白表达的上述改变在 10Gz组比 6Gz组更为显著.以上结果提示 Gz重复暴露可引起大鼠心室肌Cx43表达量的一过性减少,分布方式明显紊乱,这种改变很可能是 Gz致心律失常发生的重要原因之一.     

+Gz反复暴露对大鼠主动脉和心脏组织中HO-1、p21及LCAD表达的影响

目的：观察＋Gz反复暴露对大鼠心脏及主动脉组织HO-1、p21和LCAD基因表达的影响。方法：提取＋Gz反复暴露后1h组及对照组大鼠心脏、主动脉组织总RNA,经半定量RT—PCR检测其mRNA水平。结果：＋Gz反复暴露后心脏组织HO-1、p21和LCAD mRNA水平明显升高,主动脉组织中LCAD mRNA水平上调。结论：在＋Gz反复暴露状态下,HO-1是。脏组织中一个早期重要的抗过氧化损伤,维持正常功能的保护性因子。     

甘肃黄芪对阿霉素引起大鼠病变心肌血管紧张素转换酶2mRNA表达的影响

用RT-PCR法探讨甘肃黄芪对阿霉素(DOX)心肌病大鼠模型心肌组织中血管紧张素转换酶2(ACE2)mR-NA、血管紧张素转换酶(ACE)mRNA的表达的影响;并用光镜及透射电镜观察其心肌病理变化。结果显示,DOX组大鼠心肌组织中ACE2 mRNA和ACE mRNA表达均较正常对照组大鼠增高(ACE2:0.94±0.27 vs 0.48±0.21,P=0.001;ACE:3.73±0.59 vs 1.37±0.66,P=0.006);黄芪 DOX组大鼠心肌组织中ACE2 mRNA和ACE mRNA的表达均比DOX组降低(ACE2:0.64±0.23 vs 0.94±0.27,P=0.007;ACE:2.21±0.71 vs 3.73±0.09,P=0.0012)。说明DOX诱导心肌病变大鼠心肌组织中ACE2 mRNA、ACE mRNA表达水平均显著高于正常大鼠;光镜下显示黄芪 DOX组心肌细胞损害程度较DOX组轻;电镜下可见黄芪 DOX组可见心肌细胞核肿胀、线粒体肿胀,肌质中肌丝溶解、中断,但上述变化较DOX组少见。甘肃黄芪对DOX诱导的心肌损害大鼠具有心脏保护作用。     

川芎嗪联用L-精氨酸对缺血/再灌注损伤兔心肌线粒体功能的影响

探讨川芎嗪联用L-精氨酸对心肌缺血／再灌注损伤（MI／RI）时心肌细胞线粒体功能的影响。方法：选用日本大耳白兔50只,随机分为正常对照组（A组）、心肌缺血／再灌注组（B组）、心肌缺血／再灌注＋川芎嗪治疗组（C组）、心肌缺血／再灌注＋L-精氨酸治疗组（D组）和心肌缺血／再灌注＋川芎嗪＋L-精氨酸治疗组（E组）。观察心肌线粒体呼吸功能、Ca^2＋浓度（[Ca^2＋]m）、丙二醛浓度（MDA）、超氧化物歧化酶活性（SOD）和心肌组织三磷酸腺苷（ATP）、能荷（EC）的变化。结果：C、D、E组与B组比较,线粒体呼吸控制率（RCR）、Ⅲ态呼吸速率（ST3）、SOD明显升高,Ⅳ态呼吸速率（ST4）、[Ca^2＋]m、MDA显著降低,心肌组织ATP、EC均明显增高;且与A组比较,E组上述指标均无明显差异。结论：川芎嗪联用L-精氨酸可通过降低氧自由基水平和减轻钙超载,而改善缺血／再灌注损伤心肌的线粒体功能。     

Increased oxidative stress is correlated with mitochondrial dysfunction in chagasic patients

Previously, we have shown in an experimental model of Trypanosoma cruzi infection that increased oxidative stress and antioxidant insufficiency are associated with myocardial (cellular and mitochondrial) oxidative damage and mitochondrial functional decline and might be of pathological significance in Chagas disease. In the present study, we investigated whether enhanced oxidative stress and mitochondrial functional decline are found in human chagasic patients. Our data show substantially higher plasma (two-four-fold) and mitochondrial (67%) malonylaldehyde (MDA) levels in chagasic (n = 80, group 2) compared to healthy (n = 50, group 1) subjects. Moreover, antioxidant defense was compromised in chagasic patients. Hence, we noted a 50% decline in glutathione content and losses of 31, 60, and 68% in glutathione peroxidase, superoxide dismutase (SOD), and MnSOD activities, respectively, relative to the findings in healthy controls. Further, chagasic subjects exhibited decreased mitochondrial respiratory complex (CI: 72%; CIII: 71%) activities. Nonchagasic cardiomyopathy subjects (n = 20, group 3) exhibited marginally higher plasma MDA levels compared to gp1 subjects and were not compromised in plasma antioxidant defense capacity. These data suggest that human chagasic patients sustain an antioxidant/oxidant imbalance and a mitochondrial decline of respiratory complex activities in the circulatory system. A positive correlation between increased MDA levels, MnSOD decline, and inhibition of respiratory complexes suggests that oxidative stress may contribute to mitochondrial dysfunction in chagasic patients.     

银耳多糖对D-半乳糖致衰老模型小鼠抗氧化能力的影响

研究了银耳多糖对D-半乳糖致衰老模型小鼠抗氧化能力影响。将ICR小鼠腹腔注射D-半乳糖建立衰老模型,同时给予不同剂量的银耳多糖(TP),8周后获取小鼠心、脑,测定超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力以及丙二醛(MDA)含量的差异。结果:TP各剂量组SOD和GSH-Px活力高于对照组(P<0.05),且高剂量组SOD、GSH-Px活力均高于低剂量和中剂量组(P<0.05);中、高剂量TP组MDA含量低于对照组(P<0.05)且高剂量组MDA含量低于低剂量组(P<0.05)。结论:银耳多糖对于衰老模型小鼠抗氧化能力具有一定正性调节作用。     

一氧化氮、内皮素-1对大鼠肢体缺血/再灌注后脑损伤的影响

目的: 研究一氧化氮(NO)和内皮素-1(ET-1)在大鼠肢体缺血/再灌注(LI/R)后脑损伤中的作用,探讨NO/ET-1平衡关系的变化对脑损伤的影响.方法: 在大鼠LI/R损伤模型上,应用NO合成前体物质L-精氨酸(L-Arg)、一氧化氮合酶(NOS)抑制剂氨基胍(AG)、ETA受体阻断剂BQl23进行干预,观察血浆 NO、ET-1、MDA、XOD、SOD、LDH及脑组织tNOS、iNOS、cNOS、NO、ET-1、MDA、XOD、MPO、 SOD的变化.结果: 与对照组比较,I/R组血浆MDA、XOD、LDH及脑组织MDA、XOD、MPO升高,SOD活性降低(P<0.01),脑组织tNOS和iNOS明显升高,而cNOS明显降低(P<0.01),I/R组血浆及脑组织NO、ET-1增加,NO/ET-1比值降低,脑损伤加重.应用L-Arg及BQ123后,血浆及脑组织NO/ET-1比值较I/R组升高,脑损伤减轻,应用AG后,NO/ET-1比值降低,脑损伤进一步加重.结论: 肢体缺血/再灌注后,一氧化氮与内皮素-l的比值降低时脑损伤加重.     

Influence of Selenium on Hepatic Mitochondrial Antioxidant Capacity in Ducklings Intoxicated with Aflatoxin B<Subscript>1</Subscript>

The aim of the study was to investigate the effect of selenium on hepatic mitochondrial antioxidant capacity in ducklings administrated with aflatoxin B₁ (AFB₁). Ninety 7-day-old ducklings were randomly divided into three groups (groups I–III). Group I was used as a blank control. Group II was administered with AFB₁ (0.1 mg/kg body weight). Group III was administered with AFB₁ (0.1 mg/kg body weight) plus selenium (sodium selenite, 1 mg/kg body weight). All treatments were given once daily for 21 days. The results showed that the activities of mitochondrial superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GR) in group II ducklings significantly decreased when compared with group I (P < 0.01). Furthermore, the content of hepatic mitochondrial malondialdehyde (MDA) significantly increased (P < 0.01). However, the activities of hepatic mitochondrial SOD, CAT, GSH-Px, and GR in group III ducklings significantly increased when compared with group II (P < 0.05). In addition, the content of hepatic mitochondrial MDA significantly decreased (P < 0.01). These results revealed that AFB₁ significantly induced hepatic mitochondrial antioxidant dysfunction. However, sodium selenite could significantly ameliorate the negative effect induced by AFB₁.     

饲料脂肪水平对芙蓉鲤鲫幼鱼血清生化指标、免疫反应及抗氧化能力的影响

为研究饲料脂肪水平对芙蓉鲤鲫(Furong crucian carp)幼鱼[初始体重, (2.040.01) g]血清生化指标、免疫指标及抗氧化能力的影响, 以鱼油为主要脂肪源, 配制五种脂肪水平分别为2.50%、4.39%、6.61%、8.42%和10.81%的等氮实验饲料。实验在室内循环水养殖系统中进行, 每种饲料3个重复, 每个重复随机放养30尾芙蓉鲤鲫, 养殖周期为60d。结果显示: 随着饲料中脂肪水平的升高, 芙蓉鲤鲫增重率和蛋白质效率呈现先显著升高后显著降低的趋势(P0.05), 而饲料系数呈现相反的趋势。饲料脂肪水平升高显著提高了芙蓉鲤鲫血清中总胆固醇(CHO)和球蛋白(GLB)含量, 而显著降低总蛋白(TP)和白蛋白(ALB)含量。饲料脂肪水平未对鱼体血清高密度脂蛋白胆固醇(HDL-C)和甘油三酯(TG)含量造成显著影响(P0.05)。芙蓉鲤鲫血清免疫球蛋白M (IgM)含量、血清和肝胰脏超氧化物歧化酶(SOD)活力、肝胰脏总抗氧化能力(T-AOC)随脂肪水平增加先升高后下降(P0.05)。血清中过氧化氢酶(CAT)活力10.81%组显著高于其他各组(P0.05)。肝胰脏CAT和丙二醛(MDA)活力在各处理组组间差异不显著(P0.05)。研究结果表明, 在饲料中适宜的脂肪添加有助于改善芙蓉鲤鲫健康状况, 但过高的脂肪水平加重了芙蓉鲤鲫的代谢压力和氧化速率。增重率与饲料脂肪水平作二次回归分析显示, 芙蓉鲤鲫获得最大增长所需饲料脂肪最佳水平为6.94%。     

Potential Prevention and Treatment of Maifanite for Alzheimer's Disease Based on Behavior Test, Oxidative Stress Assay, and Trace Element Analysis in Hippocampus of Aβ(25–35)-Induced AD Rats

This study aimed to assess whether maifanite can improve the learning and memory, and antioxidant abilities of Alzheimer’s disease (AD) rats. The 70 rats were divided into seven groups: [A] normal control group, [B] AD model group, [C] sham group, [D] positive control group (donepezil), [E] low-dose maifanite group, [F] middle-dose maifanite group, [G] high-dose maifanite group. For [B], [D], [E], [F], and [G] groups, Aβ_(25–35) ventricle injection was carried out, then respective medicine were administered once a day for 60 consecutive days. The step-down and step-through test were used to measure learning and memory ability. The hippocampus levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) were assayed. The hippocampus contents of Al, Fe, Cu, Zn, Se, and Mn were analyzed by inductively coupled plasma–atomic emission spectrometer. Maifanite decreased the acquisition errors and the retention errors while prolonging the step-down latency, and decreased the number of electric shocks while prolonging the first latency of AD rats. Aβ_(25–35) ventricle injection initiated the decrease of SOD and GSH-Px activities and the increase of MDA content, and triggered the rise of Al, Fe, and Cu levels and the decline of Mn, Zn, and Se levels. The SOD and GSH-Px activities were enhanced followed by reduced MDA level, and the levels of Mn, Zn, and Se increased accompanied by Al, Fe, and Cu decreased in the maifanite treat groups. Maifanite could improve the learning and memory, and the antioxidant abilities of AD rats. Maifanite had the potential prevention and treatment for AD.     

Preventive Effects of Tocotrienol on Stress-Induced Gastric Mucosal Lesions and Its Relation to Oxidative and Inflammatory Biomarkers

This study aimed to investigate the possible gastroprotective effect of tocotrienol against water-immersion restraint stress (WIRS) induced gastric ulcers in rats by measuring its effect on gastric mucosal nitric oxide (NO), oxidative stress, and inflammatory biomarkers. Twenty-eight male Wistar rats were randomly assigned to four groups of seven rats. The two control groups were administered vitamin-free palm oil (vehicle) and the two treatment groups were given omeprazole (20 mg/kg) or tocotrienol (60 mg/kg) orally. After 28 days, rats from one control group and both treated groups were subjected to WIRS for 3.5 hours once. Malondialdehyde (MDA), NO content, and superoxide dismutase (SOD) activity were assayed in gastric tissue homogenates. Gastric tissue SOD, iNOS, TNF-α and IL1-β expression were measured. WIRS increased the gastric MDA, NO, and pro-inflammatory cytokines levels significantly when compared to the non-stressed control group. Administration of tocotrienol and omeprazole displayed significant protection against gastric ulcers induced by exposure to WIRS by correction of both ulcer score and MDA content. Tissue content of TNF-α and SOD activity were markedly reduced by the treatment with tocotrienol but not omeprazole. Tocotrienol significantly corrected nitrite to near normal levels and attenuated iNOS gene expression, which was upregulated in this ulcer model. In conclusion, oral supplementation with tocotrienol provides a gastroprotective effect in WIRS-induced ulcers. Gastroprotection is mediated through 1) free radical scavenging activity, 2) the increase in gastric mucosal antioxidant enzyme activity, 3) normalisation of gastric mucosal NO through reduction of iNOS expression, and 4) attenuation of inflammatory cytokines. In comparison to omeprazole, it exerts similar effectiveness but has a more diverse mechanism of protection, particularly through its effect on NO, SOD activity, and TNF-α.     

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.