金属硫蛋白对未成熟心肌的保护作用

目的探讨金属硫蛋白(MT)在未成熟心肌中的表达对未成熟心肌的影响。方法采用Langendorff兔离体心脏灌注模型,分为4组:对照组(C),腹腔注射蒸馏水0.3ml,注射后24h取离体心脏,灌注KH液15min转为工作心15min,全心停灌45min,恢复灌注15min改为工作心30min;E12h组、E24h组、E48h组分别腹腔注射3.6%ZnSO412、24和48h后取离体心脏,常规建立Langendorff灌注模型,方法同C组。检测心肌细胞中MT含量、血流动力学指标、生化指标和心肌超微结构。结果MT含量在E24h(49.42±2.63)、E48h组(47.86±2.54)与C(25.76±1.20)、E12h组(28.77±1.45)比较明显增高(P<0.01);E24h、E48h组血流动力学指标恢复优于C组和E12h组(P<0.05),生化指标优于C组和E12h组(P<0.01),心肌超微结构损伤较C组和E12h组明显减轻。结论MT的表达可减轻未成熟心肌的缺血再灌注损伤。     

Protective effect of antioxidants on pulmonary endothelial function after cardiopulmonary bypass

OBJECTIVES: Pulmonary endothelium-dependent vasodilation is impaired after cardiopulmonary bypass. One explanation might be the generation of reactive oxygen species during the period without flow in the pulmonary artery. The aim of the current study was to investigate if treatment with antioxidants could improve pulmonary endothelial function after cardiopulmonary bypass and influence the blood oxidative status. DESIGN: A prospective, randomized, double-blind study. SETTING: The operating room, intensive care unit, and the biochemistry laboratory in University Hospitals. PARTICIPANTS: Patients scheduled for cardiac surgery with cardiopulmonary bypass. INTERVENTIONS: Treatment with vitamin E, vitamin C, allopurinol, and acetylcysteine (n = 12) or placebo (n = 10). MEASUREMENTS AND MAIN RESULTS: The pulmonary reactivity to an infusion of acetylcholine and markers of oxidative stress in blood were measured before and after cardiopulmonary bypass. Sixteen control patients received saline instead of acetylcholine. Before surgery the pulmonary vascular resistance index decreased during infusion of acetylcholine by 24% and 21% in the treatment and placebo groups. After surgery the decrease was 20% and 8%, respectively, (p = 0.422 and p = 0.026) compared with preoperative response. Pulmonary vasodilation induced by acetylcholine was better maintained in the group treated with antioxidants (p = 0.048). In the treatment group, the blood concentrations of early intermediates of lipid peroxidation were higher, but not that of the end products. Glutathione and oxidized glutathione increased after cardiopulmonary bypass in the treatment group. CONCLUSION: The better maintained endothelium-dependent vasodilation after cardiopulmonary bypass in the treatment group indicated that antioxidant therapy reduced endothelial dysfunction.     

Protective effect of aprotinin on ischemic hepatocellular damage

During hepatic resection, occlusion of the hepatoduodenal ligament has been frequently applied to prevent intraoperative bleeding. To reduce hepatocellular ischemic damage in this procedure, we pretreated animals with Aprotinin. Three hours after an intravenous injection of 40,000 KIU Aprotinin in SD rats, we occluded the afferent hepatic vessels for 50-min and 60-min periods. 92% of occluded animals could sustain life after 60 min. Without premedication only 17 of 25 animals (68%) survived the 50-min occlusion, and 18 of 32 (56%) the 60-min occlusion. Biochemical analysis of sera was carried out 12 hr after a 40- and 60-min occlusion of the hepatoduodenal ligament with Aprotinin pretreatment. Furthermore we induced compensatory cirrhosis by application of CCL4 and biochemical analysis of sera was carried out after a 30-min occlusion. The elevation of SGOT and SGPT values was drastically reduced in the animals with Aprotinin medication in comparison with those without treatment. These observations suggest the highly protective effect of Aprotinin in the case of warm ischemic hepatic damage, especially in the cirrhotic liver. After pretreatment of LEW rats with Aprotinin (40,000 KIU i.v.), we perfused the livers with chilled Ringer solution containing 40,000 KIU Aprotinin/20 ml. We transplanted the livers orthotopically into LEW rats. With the application of Aprotinin liver preservation time increased to 10-15 hr. However, without Aprotinin the livers could be successfully preserved for only 4-6 hr. Our results indicated that premedication with high doses of Aprotinin provided highly protective effects against warm and cold ischemic damage of the liver.     

Protective effect of ketamine on ischemic spinal cord injury in rabbits

We tested our hypothesis that a commonly used anesthetic, ketamine, may offer benefits to protect animals from spinal cord injury, using the ischemia/reperfusion (I/R) injury rabbit model in a randomized controlled study. We used 24 white adult Japanese rabbits from the animal facility at the Medical College of Wuhan University. The rabbits were randomly assigned to one of three groups, eight rabbits per group: group I, sham-operation group; group II, I/R group; group III, I/R with ketamine treatment group. Spinal cord ischemia was induced by infrarenal aortic cross-clamp for 45 min in group II and group III, and ketamine was intravenously infused at 10 mg/kg in 15 mL 0.9% sodium chloride at a speed of 1.5 mL/min to animals in group III, once at 10 min before aortic clamping and once at the onset of reperfusion. Postoperative neurological function, electromyography of rear limbs, histopathology, malondialdehyde (MDA) levels, and superoxide dismutase (SOD) activity in the spinal cord were assessed in all animals. Compared with the control group I, group II showed significant I/R injury-induced changes in neurological function scores, histopathology, and electromyography (p < 0.01). However, group III with ketamine treatment significantly reversed the changes in all these parameters (p < 0.01). At the same time, the I/R-induced increase in MDA content observed in group II was also significantly reduced in group III (p < 0.01), and the I/R-induced decreases in SOD activity were also significantly prevented in group III (p < 0.01). After ketamine treatment, all parameters examined in group III were not significantly different from those obtained in group I. Ketamine showed potent protective effects against spinal cord I/R injury in the rabbit model and protected loss of antioxidant activity in spinal cord tissues.     

肠缺血后处理对兔缺血再灌注损伤小肠上皮细胞线粒体形态和功能的影响

目的观察缺血后处理对小肠缺血再灌注损伤的保护作用。方法30只大白兔随机分为3组，每组8只：A组，假手术组；B组，肠缺血再灌注损伤模型组；C组，肠缺血再灌注损伤模型肠缺血后处理组，实验结束后取小肠标本进行小肠上皮细胞形态和呼吸功能指标测定。结果A、C两组线粒体的数目、周长均大于B组，A、C两组问比较，A组较大（P〈0．05）。A、C两组线粒体的面积、最大直径、最小直径、等效直径均小于B组（P〈0．05），A、C两组间比较差异无统计学意义（P〉0．05）。B组线粒体的体积密度小于A组，面积密度、比表面和粒子数密度均小于其余两组（P〈0．05）。A、C两组间三维平面形态计量学各参数比较差异无统计学意义（P〉0．05）；B、C组线粒体呼吸控制比率（RCR）低于A组差异有统计学意义（P〈0．05），与C组比较，B组下降更为明显（P〈0．05）。结论小肠缺血后处理对缺血再灌注损伤肠上皮细胞线粒体形态和功能均有保护作用。     

Protective effect of urinastatin on ischemic renal injury in rabbits]

Protective effect of urinastatin on ischemic renal injury in rabbits was investigated by urinary enzymes and renal function tests. Ten rabbits were divided into two groups: the control group and urinastatin group administered 50,000 units/kg of urinastatin. The ischemic renal injury model was made by occluding the left renal artery for 60 minutes. Urinary excretions of N-acetyl-beta-D-glucosaminidase (NAG) and gamma-glutamyl transpeptidase (gamma-GTP) (U-NAG and U-gamma-GTP), creatinine clearance (Ccr), free water clearance (CH2O), fractional excretion of sodium (FENa) and urine volume (UV) were measured before occlusion of the left renal artery and after reflow. There were no significant differences in the values before occlusion (baseline values) for U-NAG, U-gamma-GTP, Ccr, CH2O, FENa, and UV between the two groups. U-NAG after reflow was increased in the two groups compared with baseline values, and the increase was significantly lower in the urinastatin group than control group. U-gamma-GTP after reflow was also increased in the two groups compared with baseline values, but the change was not significant between the two groups. Ccr and CH2O after reflow were significantly decreased, and FENa and UV were increased in the two groups compared with baseline values. However, no significant differences were observed between the two groups in these four parameters. These results suggest that urinastatin is effective for the protection of the kidney against ischemic damage, especially of the renal tubular cells.     

乌司他丁对油酸致家兔急性肺损伤的保护作用

目的探讨乌司他丁对油酸致家兔急性肺损伤的保护作用及其可能的机制。方法健康成年新西兰大耳白兔16只随机均分为两组:油酸损伤组(A组),乌司他丁保护组(B组)。A组由颈总静脉缓慢注射分析纯油酸0·12ml/kg;B组先静脉给予乌司他丁50000U/kg,并随之以微量泵5000U·kg-1·h-1持续给予乌司他丁至实验结束,20min后缓慢注射分析纯油酸0·12ml/kg。两组均于给予油酸前(T0)及油酸后30、60、120、180、240min(T1、T2、T3、T4、T5)分别检查血气分析、中性粒细胞蛋白酶活性,实验结束测定肺湿重,计算肺系数。结果A组在注射油酸后PaO2呈进行性下降,B组PaO2保持平稳,各时点PaO2值与B组比较明显降低(P<0·01),A组PaCO2则呈进行性上升,与B组比较明显升高(P<0·01)。两组中性粒细胞弹性蛋白酶水平在注射油酸后均有不同程度升高,各时点比较A组明显高于B组(P<0·01),A组肺系数值明显高于B组(P<0·01),两组心率、pH值比较无显著性差异(P>0·05)。结论乌司他丁能有效地保护油酸致家兔急性肺损伤,可通过抑制血清中中性粒细胞弹性蛋白酶活性而达到肺保护作用。     

奥曲肽对兔肝脏缺血-再灌注损伤的保护作用

目的 研究奥曲肽对兔肝脏缺血再灌注(I-R)损伤的保护作用.方法 24只新西兰大白兔随机均分为肝脏I-R组(R组)、奥曲肽预适应组(T组)和假手术组(C组).观察三组肝门阻断前(T1)、阻断后15 min(T2)、30 min(T3)、再灌注15 min(T4)、30 min(T5)、60 min(T6)、120 min(T7)、240 min(T8)的MAP和HR变化及T1、T3、T5、T6、T7、T8各时点丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH)、内毒素(ET)以及肿瘤坏死因子α(TNF-α)、白细胞介素-1β(IL-1β)的变化.结果 R组T2～T6、T组T2～T4时MAP明显低于、HR明显慢于C组(P<0.05),R组在T2～T6时MAP明显低于、HR明显慢于T组(P<0.05);T3、T5～T8时,R、T两组ALT、AST、LDH、ET均明显高于C组(P<0.05);R组明显高于T组(P<0.05),R组T3、T5～T8、T组T5～T8日血浆TNF-α、IL-1β明显高于C组(P<0.05),且T组T3、T7、T8时血浆TNF-α明显低于R组,T5、T6时明显高于R组(P<0.05).T组T3、T5～T8时血浆IL-1β明显低于R组(P<0.05).结论 奥曲肽对兔肝脏1-R损伤有明显的保护作用,其机制可能与下调TNF-α、IL-1β等炎性介质和降低血浆中ET水平有关.     

The role of lipid peroxidation in endotoxin-induced hepatic damage and the protective effect of antioxidants

Intraperitoneal injection of endotoxin (lipopolysaccharide, [LPS]) to mice at a dose of 15 mg/kg of body weight resulted in a survival rate of 31% 48 hours after administration. Simultaneous intramuscular administration of (10 mg/kg) coenzyme Q10 (CoQ10) increased the survival rates of LPS-administered mice to 69.7%. When LPS administration was increased to 30 mg/kg, no survivors were observed in the placebo group. Simultaneous intravenous injection of CoQ10 (10 mg/kg) or alpha-tocopherol (20 mg/kg) restored the survival rate to 52.9% or 42.9%, respectively. The adenosine triphosphate (ATP) level in the liver, which is the best index of the energy state, decreased gradually to 70% of the control ATP level 24 hours after LPS (15 mg/kg) administration. The lipid peroxide level in the liver increased fivefold 16 hours after LPS administration and then decreased to the control level in 8 hours. Simultaneous treatment of mice with antioxidants, such as CoQ10 or alpha-tocopherol, completely suppressed the lipid peroxide level in the liver and preserved the hepatic ATP level in the normal range. These results indicate that LPS induced hepatic damage in mice because of lipid peroxidation and that antioxidants suppressed lipid peroxidation, preserved energy metabolism in the liver, and enhanced survival of endotoxin-administered mice.     

胸部硬膜外神经阻滞对高脂血症家兔冠状动脉粥样硬化形成的影响

目的 探讨胸部硬膜外神经阻滞（ＴＥＡ）对实验性高脂血症家兔冠状动脉粥样硬化形成的影响。方法 健康纯种新西兰雄兔２１只，随机分为三组，每组７只，对照组：普通饲料喂养；高脂组：普通饲料＋１．５ｇ胆固醇／ｄ；ＴＥＡ组：普通饲料＋１．５ｇ胆固醇／ｄ＋ＴＥＡ（０．１２５％布比卡因０．３ｍｌ，２次／日），实验前和实验第２、４、６、８周分别从耳中央动脉抽血２ｍｌ，测定血清中总胆固醇（ＴＣ）、甘油三脂（ＴＧ）、高密度脂蛋白（ＨＤＬ－Ｃ）、低密度脂蛋白（ＬＤＬ－Ｃ）的水平，实验第８周末，气栓法处死全部动物，立那开胸取出心脏，固定后在心室乳头肌水平横断心室，切片染色后，用ＢＨＥＣ显微微机图像处理系统测定横断面每根肌间小动脉截面的硬化程度。结果 实验前三组血清血脂水平无显著性差异（Ｐ〉０．０５）；与对照组比较，高脂组及ＴＥＡ组血清Ｔ     

高压氧对家兔肝脏缺血再灌注损伤的保护作用

目的　探索高压氧 (HBO)对肝缺血再灌注损伤 (I/R )的作用及其干预时相。方法　阻断兔入肝血流 2 0min后再灌注。术后分为对照组和不同时期HBO处理组 ,观察动物苏醒时间、不同时相谷丙转氨酶 (ALT) ,超氧化物歧化酶 (SOD )和丙二醛 (MDA)的变化 ,于第 11天取活体肝脏组织行电镜观察。结果　HBO立即组的ALT恢复较快 ,与对照组差异有显著性 (P <0 .0 5 )。高压氧处理组的SOD水平高于对照组 (P <0 .0 5 )。各高压氧处理组的MDA水平与对照组比较无显著性差异 (P >0 .0 5 )。电镜观察结果 :HBO立即组 ,HBO 2 4h组 ,HBO 72h组和对照组的肝细胞凋亡数分别为 :偶见/片 ,2个 /片 ,5个 /片和 10个 /片 ;细胞水肿程度以立即组最轻 ,对照组最重。结论　HBO对肝I/R具有保护作用 ,处理越早作用越明显。     

Protective effect of hypothermia on contractile force in skeletal muscle

The clinical success of limb replantation and tissue transfer is partly dependent on the duration of ischemia experienced by the amputated part. This study focused primarily on the damage that occurs during this ischemic period. An experimental system was implemented that allowed the observation of contractile function in totally isolated skeletal muscle after ischemia. Contractile function was selected as an indicator of ischemic damage because normal function is the ultimate goal of replantation. All experiments were performed on the rat extensor digitorum longus. The muscles were subjected to ischemic periods of 1.5, 3.0, and 5.0 hours and were stored in either a hypothermic (4°C) or a room-temperature (23°C) environment during the ischemic interval. After the ischemic period, all muscles were transferred to a tissue bath and were subjected to contractility testing, followed by fatigue testing. In both groups, muscle function decreased as the ischemic interval was increased. A significant difference in function between the normal control and the muscles of both ischemic group implied that ischemic injury had occurred in the hypothermic and room-temperature muscles, even with the relatively short 1.5-hour ischemic interval. After each ischemic interval, however, the hypothermic muscles produced significantly greater contractile force than the room-temperature muscles in both the contractility and the fatigue tests. After 1.5 hours of ischemia, the contractile force in the hypothenic group was about three times as great as that observed in the room-temperature group. These results indicated that muscle function after a period of totally isolated ischemia is protected by hypothermic preservation. They also support the advisability of storage of amputated parts and free muscle flaps in hypothermic environments before replantation, even after relatively brief intervals of ischemia.     

缺血后处理对兔脊髓缺血-再灌注损伤的保护作用

目的研究缺血后处理是否可以减轻兔脊髓缺血再灌注的损伤。方法雄性新西兰大白兔30只,随机分为五组,每组6只。假手术组(N1组)仅行单纯手术操作但不阻闭腹主动脉;对照组(N2组)行单纯缺血再灌注;缺血后处理15s/30s/60s(PA/PB/PC组)分别于阻闭腹主动脉15min后,再灌注15s/30s/60s,缺血15s/30s/60s,反复3次。再灌注48h时对所有动物的后肢运动功能进行评分并行脊髓前角正常神经元计数。结果PB组再灌注48h后肢运动功能评分[3.5(2～4)分],明显高于N2组[2(1～3)分](P<0.05),其他各组与N2组相比差异无显著意义。脊髓前角正常神经元计数PB组为36.7±7.0,明显多于N2组25.7±4.3(P<0.01),而PA组18.2±2.2和PC组8.0±4.1则明显少于N2组(P<0.05)。结论缺血后处理对兔脊髓缺血再灌注损伤的作用取决于后处理时间,缺血后处理30s/30s对脊髓缺血再灌注损伤具有保护作用,而缺血后处理15s/15s和60s/60s会加重脊髓损伤。     

Protective effect of trapidil against oxidative organ damage in burn injury

Animal models of thermal injury indicate reactive oxygen species and inflammatory cytokines as causative agents in tissue injury on various organs distant from the original wound. Trapidil has various properties, such as inhibition of platelet aggregation and lipid peroxidation as well as reduction of the inflammatory response to injury. This study was designed to determine the possible protective effect of trapidil treatment against oxidative organ damage in lung, intestine and kidney induced by cutaneous thermal injury. Thirty Wistar rats were randomly divided into five groups. Sham group (n=6) was exposed to 21 degrees C water while burn-3 h group (n=6) and burn+trap-3h group (n=6), burn-24 h (n=6) and burn+trap-24 h groups were exposed to boiling water for 12s to produce a full thickness burn in 35-40% of total body surface area. In both burn+trap-3 h and burn-trap-24 h group, 8 mg/kg trapidil was given intravenously immediately after thermal injury. Three and 24 h later, tissue samples were taken for biochemical analysis from lung, intestine and kidney and blood samples were obtained to determinate serum TNF-alpha levels. Cutaneous thermal injury caused a significant increase in myeloperoxidase (MPO) activity and malondialdehyde (MDA) and 3-nitrotyrozine (3-NT) levels in all tissues and elevated serum TNF-alpha levels at post-burn 3 and 24 h. Trapidil treatment significantly reduced in biochemical parameters, as well as serum TNF-alpha levels. These data suggest that trapidil has a protective effect against oxidative organ damage in burn injury.     

缺血对兔血管平滑肌的损伤作用

研究兔断肢血管平滑肌组织中钙、镁离子含量及线粒体形态的变化与术后血循环危象的关系。方法:用原子吸收光谱分光光度计测定血管平滑肌组织中钙、镁离子的含量。用图像分析仪定量分析线粒体的结构变化。结果:缺血时间超过8小时,血管平滑肌组织中钙离子含量明显升高(P<0.01);线粒体明显受损。结论:血管平滑肌组织中钙离子增高在血循危象的发生中起着重要作用。     

大蒜素在防治兔肢体缺血再灌注损伤中的疗效观察

目的探讨大蒜素对肢体缺血再灌注损伤的防护作用。方法将32只家兔随机分为再灌注组和治疗组,制备肢体缺血再灌注损伤动物模型。在即将恢复血流灌注前10分钟,再灌注组和治疗组分别自耳缘静脉注射等渗盐水和大蒜素注射液。在再灌注前、后不同时间点上分别测定血清有关生化指标并取胫前肌行光、电镜观察。结果再灌注组再灌注后血清天冬氨酸氨基转移酶（AST）、乳酸脱氢酶（LDH）、肌酸激酶（CK）、丙二醛（MDA）明显升高（P〈0．01）,超氧化物歧化酶（SOD）活力明显下降（P〈0．01）。治疗组再灌注后各指标变化不明显,而与对照组同期相比,差异有非常显著性（P〈0．01）。光、电镜观察可见再灌注组织超微结构改变明显,而治疗组较轻。结论大蒜素可抑制自由基产生并减轻对骨骼肌细胞的损害,对肢体缺血再灌注损伤具有明显的防护作用。     

Protective effect of low-grade hypothermia in experimental skeletal muscle ischemia.

In the present study, a rat hindlimb tourniquet model was used to investigate the effect of moderate hypothermia on ischemic muscle necrosis. Complete circulatory arrest was maintained for 4.5 h. During the ischemic period the animals were kept in an infant incubator at different temperatures. After 72 h survival the percentage of necrosis in the anterior tibial muscle was measured morphometrically on histological slides. At an ambient temperature of 24 degrees C there was 80% necrosis in the anterior tibial muscle. At 22 degrees C the necrosis was reduced to 29%. This reduction corresponds to more than 30 min shortening of the ischemia time. Differences in tissue temperature may explain some of the discrepancies reported in tolerance limits for muscle ischemia. To achieve consistent results in experimental muscle ischemia, it is necessary to control the ambient temperature.     

Protective effect of rutin on mercuric chloride-induced reproductive damage in male rats

This study investigated the effects of rutin against reproductive damage caused by toxic mercury in male rats. Thirty-five Sprague Dawley rats were used. Control group was injected with saline for 7 days. The rutin-100 group received 100 mg/kg/b.w. rutin for 7 days. Mercuric chloride (HgCl₂) group received 1.23 mg/kg/b.w. of HgCl₂ for 7 days. Mercury chloride + rutin-50 group received 50 mg/kg/b.w. rutin and HgCl₂ 1.23 mg/kg/b.w. for 7 days. HgCl₂ + rutin-100 group received 100 mg/kg/b.w. rutin and HgCl₂ 1.23 mg/kg/b.w. for 7 days. It was detected that HgCl₂ treatment increased malondialdehyde (MDA) levels, tumour necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2) expressions, necrosis and degeneration of spermatogonium, dead and abnormal sperm percentages; tubular walls thinning; and decreased antioxidant enzyme activities and sperm motility. It was determined that rutin application reduced testicular damage caused by HgCl₂. In conclusion, rutin administration may treat HgCl₂ toxicity in testes.     

依那普利拉减轻大鼠烧伤早期脏器损害的研究

目的 探讨依那普利拉对烧伤早期内脏损害保护作用的量效关系.方法 随机将54只SD大鼠分为烫伤组(B组)和烫伤后小剂量、中剂量和大剂量依那普利拉治疗组(E1、E2、E3组),每组12只大鼠,另取6只大鼠不致伤作为正常对照组.检测烫伤前及伤后6 h和12 h动脉血压、血管紧张素Ⅱ、尿素氮(Bun)、肌酐(Cr)和肌酸激酶(CK)、丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST),以及主要脏器组织病理变化.结果 B组血管紧张素Ⅱ明显升高,治疗组均明显低于B组(P均＜0.05),E2和E3组明显低于E1组;B组大鼠CK、Bun、Cr、ALT、AST均显著高于正常参考值(P均＜0.05),治疗组较B组不同程度降低,E1组下降明显(P＜0.05),各时相点基本与正常值接近;E2和E3组下降不明显,明显高于E1组;烫伤后各组动脉收缩压和舒张压均有不同程度下降,其中E2、E3组较E1组更明显,E1组较B组明显升高.结论 小剂量依那普利拉能够显著减轻严重烧伤后脏器损害的程度,但对动脉收缩压和舒张压无显著影响.     

氢饱和生理盐水对兔脊髓缺血再灌注损伤的神经保护作用

目的 研究氢气对脊髓缺血再灌注损伤的保护作用及其潜在机制。方法 新西兰兔随机分为3组：对照组、脊髓缺血再灌注损伤组和氢水治疗组。对照组仅接受暴露,无脊髓缺血再灌注损伤;缺血再灌注组动物采用ZIVIN法建立脊髓缺血再灌注损伤模型,造成脊髓腰骶段缺血35 min 后行再灌注;氢水治疗组动物在再灌注前5 min腹腔注射饱和氢盐水（5 mL/kg）,再灌注后8 h重复注射。不同时间点检测后肢运动功能。术后72 h取脊髓进行HE染色、TUNEL染色、氧化-抗氧化指标检测及ELISA检测细胞因子。结果 含氢生理盐水治疗能显著改善动物神经功能、抑制脊髓神经元凋亡、抑制氧化应激、改善抗氧化能力,同时降低炎症相关细胞因子,从而发挥脊髓保护作用。结论 腹腔注射含氢生理盐水通过抗氧化和抗炎对脊髓缺血再灌注损伤发挥保护作用。