缺血预适应对缺血脊髓保护作用的实验研究

我们通过阻断腹主动脉建立脊髓缺血模型,观察缺血预适应(IPC)对缺血损伤后脊髓组织中内皮素 1(ET 1)、前列环素(PGI2 )、血栓素A2 (TXA2 )等变化的影响,探讨缺血预处理对脊髓缺血再灌注损伤的保护作用及相关机制。一、材料与方法1.实验动物和模型的建立:健康新西兰大白兔48只,体重2 .5～3 .5kg ,雌雄不拘,随机等分为IPC组和缺血组。左肾动脉下方夹闭腹主动脉,造成脊髓缺血模型[1] 。IPC组夹闭腹主动脉5min ,开放15min ,再次夹闭40min后开放再灌注;缺血组分离出腹主动脉2 0min后,直接夹闭腹主动脉40min后开放再灌注。2 .观察及检测指…     

高氧液预处理对兔脊髓缺血-再灌注损伤的保护作用

目的　探讨高氧液预处理对兔脊髓缺血 再灌注损伤的作用。方法　 2 0只成年雄性新西兰大白兔随机分成对照组 (n =1 0 )及预处理组 (n =1 0 )。预处理组每天静脉给予 1 0ml/kg高氧液 ,2 0分钟匀速泵完 ,连续 5天 ;对照组用同样方法给予等容量生理盐水。最后一次预处理结束后2 4小时 ,夹闭腹主动脉肾下段 2 0分钟 ,制作兔脊髓缺血模型 ;再灌注后 4、8、1 2、2 4和 48小时分别对动物神经功能评分 ;再灌注 48小时后 ,处死动物取脊髓 (L5～ 7) ,制作标本行组织病理学观察。结果　预处理组神经功能评分在各时间点均明显高于对照组 (P <0 0 5) ;与对照组相比 ,预处理组脊髓前角正常神经细胞数明显增多 (P <0 0 5) ,而且神经功能评分与其对应脊髓前角正常神经细胞计数之间有显著相关性 (r=0 894,P <0 0 1 )。结论　高氧液预处理对兔脊髓缺血 再灌注损伤有显著的保护作用。     

脊髓缺血损伤时脑型肌酸激酶与后肢肌电图的变化

目的　观察脊髓缺血损伤时脑型肌酸激酶 (CK BB)和后肢肌电图 (EMG)的变化。方法　 1 6只兔随机分为假手术组和缺血 再灌注组 ,每组 8只。缺血 再灌注组夹闭腹主动脉 4 0min ,检测夹闭前 1 0min、夹闭 4 0min和松夹后 6 0min动脉血中CK BB含量。术后 7d记录后肢神经功能评分和检测肌电活动。结果　与缺血前和假手术组比较 ,缺血 再灌注组CK BB含量明显升高而其神经功能评分显著降低 (P <0 0 5或P <0 0 1 ) ,EMG大量可见自发电位 ,运动单位电位募集类型显著改变 (P <0 0 1 )。结论　监测血清CK BB含量或后肢肌电图变化可反映脊髓缺血性损伤的有无和程度的轻重     

缺血预处理对缺血脊髓微循环影响的实验研究

目的 探讨缺血预处理（IPC）对缺血损伤脊髓的保护作用及其相关机制.方法 48只健康新西兰大白兔随机分为缺血预处理组（IPC组）和缺血组,应用腹主动脉夹闭法建立脊髓缺血模型.观察两组脊髓组织缺血前、缺血40min及再灌注后2、8、24、72 h内皮素-1（ET-1）、血栓素A2（TXA2）与前列环素（PGI2）含量,并观察脊髓组织病理形态学改变及双后肢神经功能评分.结果 IPC组各时间点ET-1含量、TXB2/6-keto-PGF1α比值均显著低于缺血组（P＜0.05）.两个时间点上IPC组后肢神经功能评分明显高于缺血组（P＜0.001、0.01）,病理学累积评分明显低于缺血组（P＜0.001）.结论 IPC对主动脉阻断所致脊髓缺血再灌注损伤有良好的保护作用,抗“无再灌流”作用可能是其保护作用的重要机制之一.     

脊髓缺血性损伤时脑源性神经营养因子、丝氨酸/苏氨酸蛋白激酶ε蛋白和mRNA含量的变化及远程缺血预处理干预作用

目的探讨远程缺血预处理(RIPC)对兔脊髓缺血再灌注损伤(SCIRI)时脑源性神经营养因子(BDNF)、丝氨酸/苏氨酸蛋白激酶(PKC)ε蛋白和mRNA含量的影响及其意义。方法日本大耳白兔36只,随机均分为假手术组(S组)、缺血性损伤组(IR组)、IR+RIPC组。每组6只动物分别于再灌注第2天和第5天处死。S组不阻断腹主动脉,IR组和IR+RIPC组夹闭腹主动脉30分钟建立SCIRI模型,IR+RIPC组于主动脉阻断前1小时实施RIPC。3组动物在再灌注第2天和第5天行后肢神经功能评分后处死并取脊髓组织L3-L5段,评估病理学变化;用Western blotting和RT-PCR法分别检测脊髓组织BDNF、PKCε蛋白及其mRNA含量。结果同一时间点,与IR组相比,IR+RIPC组后肢神经功能评分和脊髓组织病理切片分级明显改善(P0.05),脊髓组织BDNF、PKCε蛋白及mRNA表达均明显升高(P0.05)。结论 RIPC对兔SCIRI有一定的防治作用,其作用机制与RIPC激活了PKCε/PKC信号通路,进而上调脊髓损伤区域BDNF蛋白的表达有关。     

缺血预处理对犬脊髓损伤及热休克蛋白70表达影响的研究

目的评价缺血预处理对犬脊髓损伤及热休克蛋白70表达的影响。方法41条杂种犬随机分成假手术组6只、预处理组21只、对照组14只。预处理组主动脉阻断6min后开放6min,反复2次,之后阻断35min;对照组主动脉阻断35min。术后进行神经功能评分,检测脊髓组织中热休克蛋白70表达。结果在再灌注后6h、24h预处理组热休克蛋白70于胞质和胞核均有表达,且强于对照组;而且神经功能评分预处理组高于对照组。在再灌注后7d预处理组神经功能评分无明显改变,且仍见热休克蛋白70表达。结论缺血预处理可以增加脊髓的缺血耐受;热休克蛋白70在胞质和胞核中表达可能在缺血耐受中起到一定的作用。     

兔脊髓分级缺血-再灌注损伤对体感诱发电位的影响

目的 了解不同程度脊髓缺血-再灌注损伤与体感诱发电位（SEP）、神经功能评分及脊髓病理改变的关系。方法 将40只新西兰大耳白兔随机均分为4组，假手术组、缺血30min组、缺血45min组和缺血60min组。采用腹主动脉阻断法建立兔脊髓缺血-再灌注损伤模型，分别于缺血前、缺血5、10min、再灌注15、30min、1、2、24和48h监测SEP。于再灌注6、12、24和48h进行神经功能评分，再灌注48h进行脊髓病理学观察。结果 阻断腹主动脉血流30、45和60min后开放分别表现为轻、中、重度缺血-再灌注损伤脊髓的病理学改变特点。脊髓轻度缺血-再灌注损伤中SEP波幅和潜伏期分别于再灌注15和30min时恢复至缺血前水平（P〉0．05）；脊髓中度缺血-再灌注损伤中SEP波幅和潜伏期分别于再灌注30min和再灌注1h恢复至缺血前水平（P〉0．05）；脊髓重度缺血-再灌注损伤中SEP波幅和潜伏期分别明显下降和延长，与其他各组组间比较差异有统计学意义（P〈0.01）。各组神经功能评分组间比较差异均有统计学意义（P〈0. 01）。结论 脊髓缺血-再灌注损伤中SEP波幅较潜伏期恢复迅速。术中SEP监测能够敏感而准确地反映缺血-再灌注损伤中脊髓功能的变化，可为临床应用提供实验依据。     

芦荟多糖对脊髓缺血损伤的神经保护作用

目的:探讨芦荟多糖(aloe polysaccharide,AP)对兔脊髓缺血损伤是否有神经保护作用.方法:32只成年雄性新西兰兔随机分成4组(每组8只 ),即对照组(C 组)、芦荟多糖组(A组)、溶剂对照组( V组 ) 及假手术组(S组).A组在脊髓缺血前30min经耳缘静脉给予50m·kg-1芦荟多糖;V组以同样方式给予等容量生理盐水;C组仅仅制备脊髓缺血损伤模型,不进行其它处理;S组仅仅暴露腹主动脉,而不阻断它,其他处理同C组;兔脊髓缺血模型采用夹闭兔腹主动脉肾下段20min.再灌注后48h,对所有动物神经功能评分,然后处死动物取脊髓(L5-7),制作标本行组织病理学观察.结果:A组的神经功能评分和脊髓前角正常神经细胞数明显多于C组及V组(P<0.01);C组及V组的神经功能评分和脊髓前角正常神经细胞数组间无明显差异(P>0.05);神经功能评分与其对应脊髓前角正常神经细胞计数之间有显著相关性(r=0.804,P<0.01).结论:芦荟多糖对兔脊髓缺血再灌注损伤有明显的神经保护作用.     

缺血再灌注预处理对血浆MDA、SOD及脊髓AQP4 mRNA的表达影响

目的 探讨腹主动脉缺血预处理对再灌注不同时问血浆丙二醛(MDA)、超氧化物歧化酶(SOD)及脊髓组织中水通道蛋白4(AQP4) mRNA表达的影响.方法 将54只体质量189 ～ 207 g雌雄不拘的SD大鼠随机分为假手术组(Sham组)、缺血再灌注组(I/R组)和缺血预处理组(IPC组)3组.采用肾下腹主动脉阻断法,建立脊髓缺血再灌注模型;Sham组6只,手术开始步骤同其他两组,但不作肾下腹主动脉阻断即缝合伤口;I/R组24只,直视下采用动脉夹夹闭腹主动脉段左肾动脉分支起始处下方5 mm处(即肾动脉后型),仅阻断腹主动脉60 min后开放灌注;而IPC组24只,先阻断腹主动脉5min,开放5 min,再阻断60 min后开放灌注.再灌注后12h、1、2、5、10天分别进行神经功能评分,同时观察大鼠血浆MDA、SOD指标的水平,以及预处理对脊髓AQP4 mRNA表达的影响.结果 54只大鼠术后全部存活,I/R组行为学评分降低(P＜0.01),IPC组的神经功能评分在再灌注5天内均高于I/R组(P＜0.01),随着再灌注时间的延长行为学评分逐渐增加.I/R组血浆SOD水平仅在再灌注1天时较Sham组显著下降,随时间延长SOD水平逐渐升高与Sham组无差异,血浆各时间点MDA水平比Sham组低(P ＜0.05);IPC组SOD、MDA水平与Sham组比较没有差异.I/R组再灌注2天时AQP4mRNA表达显著增高(P＜0.01),之后降低至与Sham组无差异;IPC组在再灌注1天时即出现AQP4 mRNA表达明显升高(P＜0.05),之后表达逐渐降低,第5天时与Sham组无差异.IPC AQP4mRNA峰值明显低于I/R组(P＜0.01).结论 大鼠腹主动脉缺血再灌注的预处理IPC可能通过减轻由缺血再灌注造成的全身氧化应激反应和下调AQP4mRNA的表达,进而保护脊髓组织.     

缺血预处理对兔主动脉阻断后脊髓一氧化氮、后肢神经功能和肌电图的影响

目的　探讨缺血预处理 (IPC)对缺血预处理对兔主动脉阻断后脊髓功能和一氧化氮(NO)的影响。方法　 2 4只日本大白兔随机分为假手术组 (A组 )、缺血再灌注组 (B组 )和IPC保护组 (C组 ) ,每组 8只。分别于首次预处理即刻 (C 40 )、缺血即刻 (I0 )、缺血 45min(I45)、再灌注后 60min(R60 )和术后 7d处死动物前即刻 (R7d)采血检测血清和R7d脊髓组织NO的浓度。术后观察后肢神经功能的评分、后肢针电极肌电图 (EMG)和脊髓组织病理学的改变。结果　缺血再灌注损伤后B组血清NO浓度较缺血前和A、C组对应时点值显著升高 (P <0 .0 1)。C组R7d血清NO浓度明显低于其他时点及A组R7d测定值 (P <0 .0 5或 0 .0 1)。B组脊髓组织NO浓度显著高于A、C组(P <0 .0 1)。B组后肢神经功能和脊髓病理学评分均显著性低于A、C组 (P <0 .0 5或 0 .0 1) ,其后肢EMG亦较C组有显著性病理改变 (P <0 .0 1)。结论　IPC对家兔主动脉阻断后脊髓缺血再灌注损伤有良好的保护作用 ,其保护作用机制与抑制NO的生成有关。     

Evaluation of Rapid Ischemic Preconditioning in a Rabbit Model of Spinal Cord Ischemia

Background: Rapid ischemic preconditioning (IPC) has been shown to reduce cellular injury after subsequent cardiac and cerebral ischemia. However, the data on rapid IPC of the spinal cord is limited. The authors investigated whether pretreatment with sublethal ischemia of spinal cord can attenuate neuronal injury after spinal cord ischemia in rabbits.

Methods: Forty-seven male New Zealand white rabbits were randomly assigned to one of three groups (n = 15 or 16 each). In the IPC(-) group, the infrarenal aorta was occluded for 17 min to produce spinal cord ischemia. In the IPC(+) group, 5 min of aortic occlusion was performed 30 min before 17 min of spinal cord ischemia. In the sham group, the aorta was not occluded. Hind limb motor function was assessed at 3 h, 24 h, 4 days, and 7 days after reperfusion using Tarlov scoring (0 = paraplegia; 4 = normal). Animals were killed for histopathologic evaluation at 24 h or 7 days after reperfusion. The number of normal neurons in the anterior spinal cord (L4-L6) was counted.

Results: Neurologic scores were significantly higher in the IPC(+) group than the IPC(-) group at 3 and 24 h after reperfusion (P < 0.05). However, neurologic scores in the IPC(+) group gradually decreased and became similar to those in the IPC(-) group at 4 and 7 days after reperfusion. At 24 h after reperfusion, the numbers of normal neurons were significantly higher in the IPC (+) group than in the IPC(-) group (P < 0.05) and were similar between the IPC(+) and sham groups. At 7 days after reperfusion, there was no difference in the number of normal neurons between the IPC(+) and IPC(-) groups.     

Ischemic Preconditioning to Prevent Lethal Ischemic Spinal Cord Injury in a Swine Model

Objective: Paraplegia is a serious complication of thoracic and thoracoabdominal aortic operations and is the result of ischemic spinal cord injury induced by low perfusion pressure during cross-clamping of the aorta. Ischemic preconditioning (IPC) of the heart or brain with reversible sublethal ischemic injury induces resistance to subsequent lethal ischemia. The aim of this study is to investigate whether ischemic tolerance can be induced by IPC of the spinal cord in a swine model. Study Design: The animals were randomly divided into three groups: the sham group (n = 3), control group (n = 6) and IPC group (n = 8). In the sham group, we performed a left thoracotomy without any ischemic injury. In the IPC group, the swine received a reversible ischemic spinal cord injury by aortic clamping for 20 min, whereas in the control group, no aortic cross-clamping was performed. Forty-eight hours later, the animals in both the IPC and control groups underwent aortic clamping for 30 min. Neurological examination was done 24 h later, and then the animals were euthanized for histopathology and a malonedialdehyde spectrophotometry assay of the spinal cord tissue. Results: A statistically significant difference in neurological outcome was observed between the control and IPC groups at 24 h after ischemic injury. The incidence of paraplegia and severe paresis was 100% in the control group and 62.5% in the IPC group (p =. 028). Between control and IPC groups, there was no statistically significant difference in histopathology and only a borderline statistical difference in the malonedialdehyde assay of the ischemic spinal cord (p =. 0745). Conclusion: In this study, IPC induced protection against a 30-min ischemic insult of the spinal cord, although complete recovery was not achieved (standing up or walking). We expect that combining this IPC with other existing protective methods might lead to a synergistic effect, which warrants further investigation.     

缺血预适应对缺血脊髓保护作用的实验研究

目的：探讨缺血预适应对缺血脊髓的保护作用及其可能机制。方法：48只成年大耳白兔随机分为两组，每组24只，建立脊髓缺血模型。缺血预适应组（IPC组）采用腹主动脉阻断5min，开放15min的预适应方案后，再阻断40min后开放。对照组常规阻断腹主动脉40min后开放。分别于阻断前、阻断40min后、开放后2、8、24和72h，测定脑脊液超氧化物歧化酶（SOD）、脊髓脂质过氧化物酶（LPO）及脊髓组织含水量，并行双后肢神经功能评分。结果：IPC组各时相脑脊液SOD活性及神经功能评分显著优于对照组（P＜0．05），脊髓LPO含量及组织含水量明显低于对照组（P＜0．05）。结论：缺血预适应通过调动与增强脊髓组织内源性抗损害机制对缺血脊髓发挥保护作用。     

Neuroprotective Effect of Epidural Electrical Stimulation against Ischemic Spinal Cord Injury in Rats: Electrical Preconditioning

Background: Electroconvulsion therapy is likely to serve as an effective preconditioning stimulus for inducing tolerance to ischemic brain injury. The current study examines whether electrical stimuli on the spinal cord is also capable of inducing tolerance to ischemic spinal cord injury by transient aortic occlusion.

Methods: Spinal cord ischemia was induced by occlusion of the descending thoracic aorta in combination with maintaining systemic hypotension (40 mmHg) during the procedure. Animals implanted with epidural electrodes were divided into four groups according to electrical stimulation and sham. Two groups consisted of rapid preconditioning (RE group, n = 8) and sham procedure (RC group, n = 8) 30 min before 9 min of spinal cord ischemia. In the two groups that underwent delayed preconditioning, rats were exposed to 9 min of aortic occlusion 24 h after either pretreatment with epidural electrical stimulation (DE group, n = 8) or sham (DC group, n = 8). In addition, rats were exposed to 6-11 min of spinal cord ischemia at 30 min or 24 h after epidural electrical stimulation or sham stimulation. The group P50 represents the duration of spinal cord ischemia associated with 50% probability of resultant paraplegia.

Results: Pretreatment with electrical stimulation in the DE group but not the RE group protected the spinal cord against ischemia, and this stimulation prolonged the P50 by approximately 15.0% in the DE group compared with the DC group.     

Evaluation of rapid ischemic preconditioning in a rabbit model of spinal cord ischemia

BACKGROUND: Rapid ischemic preconditioning (IPC) has been shown to reduce cellular injury after subsequent cardiac and cerebral ischemia. However, the data on rapid IPC of the spinal cord is limited. The authors investigated whether pretreatment with sublethal ischemia of spinal cord can attenuate neuronal injury after spinal cord ischemia in rabbits. METHODS: Forty-seven male New Zealand white rabbits were randomly assigned to one of three groups (n = 15 or 16 each). In the IPC(-) group, the infrarenal aorta was occluded for 17 min to produce spinal cord ischemia. In the IPC(+) group, 5 min of aortic occlusion was performed 30 min before 17 min of spinal cord ischemia. In the sham group, the aorta was not occluded. Hind limb motor function was assessed at 3 h, 24 h, 4 days, and 7 days after reperfusion using Tarlov scoring (0 = paraplegia; 4 = normal). Animals were killed for histopathologic evaluation at 24 h or 7 days after reperfusion. The number of normal neurons in the anterior spinal cord (L4-L6) was counted. RESULTS: Neurologic scores were significantly higher in the IPC(+) group than the IPC(-) group at 3 and 24 h after reperfusion (P < 0.05). However, neurologic scores in the IPC(+) group gradually decreased and became similar to those in the IPC(-) group at 4 and 7 days after reperfusion. At 24 h after reperfusion, the numbers of normal neurons were significantly higher in the IPC (+) group than in the IPC(-) group (P < 0.05) and were similar between the IPC(+) and sham groups. At 7 days after reperfusion, there was no difference in the number of normal neurons between the IPC(+) and IPC(-) groups. CONCLUSION: The results indicate that rapid IPC protects the spinal cord against neuronal damage 24 h but not 7 days after reperfusion in a rabbit model of spinal cord ischemia, suggesting that the efficacy of rapid IPC may be transient.     

Ischemic preconditioning reduces neurologic injury in a rat model of spinal cord ischemia.

BACKGROUND: Ischemic preconditioning (IPC) is an endogenous cellular protective mechanism whereby brief, noninjurious periods of ischemia render a tissue more resistant to a subsequent, more prolonged ischemic insult. We hypothesized that IPC of the spinal cord would reduce neurologic injury after experimental aortic occlusion in rats and that this improved neurologic benefit could be induced acutely after a short reperfusion interval separating the IPC and the ischemic insult. METHODS: Forty male Sprague-Dawley rats under general anesthesia were randomly assigned to one of two groups. The IPC group (n = 20) had 3 minutes of aortic occlusion to induce spinal cord ischemia 30 minutes of reperfusion, and 12 minutes of ischemia, whereas the controls (n = 20) had only 12 minutes of ischemia. Neurologic function was evaluated 24 and 48 hours later. Some animals from these groups were perfusion-fixed for hematoxylin and eosin staining of the spinal cord for histologic evaluation. RESULTS: Survival was significantly better at 48 hours in the IPC group. Sensory and motor neurologic function were significantly different between groups at 24 and 48 hours. Histologic evaluation at 48 hours showed severe neurologic damage in rats with poor neurologic test scores. CONCLUSIONS: Ischemic preconditioning reduces neurologic injury and improves survival in a rat model of spinal cord ischemia. The protective benefit of IPC is acutely invoked after a 30-minute reperfusion interval between the preconditioning and the ischemic event.     

Neuroprotective effect of epidural electrical stimulation against ischemic spinal cord injury in rats: electrical preconditioning

BACKGROUND: Electroconvulsion therapy is likely to serve as an effective preconditioning stimulus for inducing tolerance to ischemic brain injury. The current study examines whether electrical stimuli on the spinal cord is also capable of inducing tolerance to ischemic spinal cord injury by transient aortic occlusion. METHODS: Spinal cord ischemia was induced by occlusion of the descending thoracic aorta in combination with maintaining systemic hypotension (40 mmHg) during the procedure. Animals implanted with epidural electrodes were divided into four groups according to electrical stimulation and sham. Two groups consisted of rapid preconditioning (RE group, n = 8) and sham procedure (RC group, n = 8) 30 min before 9 min of spinal cord ischemia. In the two groups that underwent delayed preconditioning, rats were exposed to 9 min of aortic occlusion 24 h after either pretreatment with epidural electrical stimulation (DE group, n = 8) or sham (DC group, n = 8). In addition, rats were exposed to 6-11 min of spinal cord ischemia at 30 min or 24 h after epidural electrical stimulation or sham stimulation. The group P50 represents the duration of spinal cord ischemia associated with 50% probability of resultant paraplegia. RESULTS: Pretreatment with electrical stimulation in the DE group but not the RE group protected the spinal cord against ischemia, and this stimulation prolonged the P50 by approximately 15.0% in the DE group compared with the DC group. CONCLUSIONS: Although the optimal setting for this electrical preconditioning should be determined in future studies, the results suggest that epidural electrical stimulation will be a useful approach to provide spinal protection against ischemia.     

Anesthetic preconditioning with sevoflurane does not protect the spinal cord after an ischemic-reperfusion injury in the rat

Anesthetic preconditioning (APC) is a protective mechanism, whereby exposure to a volatile anesthetic renders a tissue resistant to a subsequent ischemic insult. We hypothesized that APC of the rat spinal cord with sevoflurane would reduce neurologic deficit after an ischemic-reperfusion injury. Rats were randomly assigned to 1 of 5 groups. The ischemic preconditioning (IPC) group (n = 14) had 3 min of IPC, 30 min of reperfusion, and 12 min of ischemia. The chronic APC (cSEVO) group (n = 14) had 1 h of APC with 3.5% sevoflurane on each of 2 days before ischemia. The acute APC (aSEVO) group (n = 14) had 1 h of APC with 3.5% sevoflurane followed by a 1-h washout period before the induction of ischemia. The controls (n = 14) underwent no preconditioning before ischemia. IPC attenuated the ischemia-reperfusion injury, whereas aSEVO and cSEVO groups were no better than control animals. Histologic evaluation of the spinal cord showed severe neurologic damage in all groups except for the IPC group and sham-operated rats. APC with sevoflurane did not reduce neurologic injury in a rat model of spinal cord ischemia. Traditional ischemic preconditioning had a strong protective benefit on neurologic outcome.     

Is remote preconditioning as effective as direct ischemic preconditioning in preventing spinal cord ischemic injury?

BACKGROUND: Spinal cord injury remains a devastating complication of thoracic and thoracoabdominal aortic operations. The aim of this study was to assess the affectivity of direct ischemic preconditioning (PC) and remote PC in preventing spinal cord ischemic injury in an experimental model. MATERIALS AND METHODS: Thirty-eight New Zealand white rabbits were divided into five groups: One group served as Sham group (n = 7). Rabbits in other groups had their abdominal aorta cross-clamped for 40 min. Before aortic occlusion, aorta was clamped twice at the same site of aortic occlusion for 5 min followed by 15 min of reperfusion after each ischemic episode in one group (Direct PC, n = 8), left renal artery was clamped twice for 5 min followed by 15 min of reperfusion after each renal ischemic episode in one group (Remote PC, n = 8), left renal artery was first clamped for 5 min followed by 15 min of reperfusion and then aorta was clamped for 5 min followed by 15 min of reperfusion in one group (Remote + Direct PC, n = 8), and no PC method was used in Control group (n = 7). RESULTS: In all PC groups, neurological status of rabbits (Tarlov score) at post-ischemia 24th and 48th hours was better than the control group (P < 0.05), but worse than Sham group (P < 0.05). Mean viability index values in PC groups were higher than control group (P < 0.01). Post-ischemia serum NSE and MDA levels obtained in all three PC groups were significantly lower than control group (P < 0.05 and P < 0.01). CONCLUSIONS: The use of direct ischemic PC and/or remote PC is an effective way of reducing spinal cord ischemic injury because of aortic occlusion, while direct PC is more effective. The combined use of direct PC and remote PC did not provide better protection.