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。     

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。     

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.     

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。     

Effect of ischemic post-conditioning on spinal cord ischemic-reperfusion injury in rabbits

OBJECTIVES: To investigate the potential protective effect of ischemic post-conditioning (Post-con) on ischemia-reperfusion injury of the rabbit spinal cord, and to determine if there is an additive neuroprotective effect when ischemic preconditioning (IPC) and Post-con are combined. METHODS: Forty New Zealand white rabbits were randomly divided into four groups: group Control (C; n=10), aortic occlusion (AOC; for 30 min; group IPC (n=10) three cycles of three-minute AOC plus three-minute reperfusion before the 30-min AOC; group Post-con (n=10), three cycles of three-minute reperfusion plus three-minute AOC immediately upon reperfusion after 30-min AOC; group IPC+Post-con (n=10), where animals were subjected to both IPC and Post-con. At six hours, 24 hr and 48 hr following reperfusion, neurological function was assessed according to Tarlov scores, and at 48 hr, the spinal cords were procured for the histopathologic evaluation, by comparing the number of intact alpha-motor neurons in the anterior horn. RESULTS: The median count (and quartiles) of intact alpha-motor neurons was greatest in group Post-con 73 (69-76) and group IPC+Post-con 29 (22-42) compared to the numbers of viable alpha-motor neurons in groups C 6 (4-9) and IPC 15 (11-18) (P < 0.001). The numbers of animals who developed paraplegia according to Tarlov criteria were 7/10 in groups Post-con and IPC+Post-con, compared to 9/10 animals in each of groups C and IPC. CONCLUSIONS: This laboratory investigation provides histological evidence that Post-con may protect the spinal cord from moderate to severe ischemia reperfusion injury. Ischemic preconditioning conferred no additional benefits in this rabbit model. The results have potential clinical implications for patients undergoing thoracoabdominal aortic reconstructive surgery.     

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。     

川芎嗪对兔脊髓缺血/再灌注损伤的保护和治疗作用

目的研究川芎嗪(TMP)注射液对兔脊髓缺血/再灌注损伤的保护和治疗作用.方法22只新西兰雄性大白兔,随机分成三组对照组(C组),单纯缺血再灌注;保护组(P组)和治疗组(T组),分别在肾下主动脉阻断前和开放后30min内恒速静脉泵入TMP注射液30mg@kg-1.采用肾下主动脉(IRA)阻断法造成脊髓缺血(20min)/再灌注模型,观察再灌注后4、8、12、24和48h神经功能评分,并于48h处死动物取脊髓(L5～7)制标本行病理组织学观察.结果用TMP干预的P组和T组的神经功能评分在各时间点均明显高于C组(P＜0.05),而P组和T组无统计学差异(P＞0.05);再灌注48h,P组和T组的脊髓前角正常神经元数明显多于C组(P＜0.05),P组和T组之间无统计学差异(P＞0.05),而且神经功能评分与其对应脊髓前角正常神经元计数之间有显著相关性(r=0.776,P＜0.01).结论TMP注射液对脊髓缺血/再灌注损伤有显著的保护和治疗作用.     

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.     

Protective effect of deferoxamine on experimental spinal cord injury in rat

Objective

To observe the protective effect of deferoxamine on experimental spinal cord injury (SCI) in rats.

Methods

Sprague-Dawley rats were randomly divided into the following four groups. Control group: rats were performed laminectomy only; SCI group: rats were performed laminectomy with SCI; DFO group: rats were injected intraperitoneally a bolus of 100 mg/kg deferoxamine after SCI; vehicle group: rats were injected intraperitoneally 0.9% saline after SCI. The SCI of animal model was made by using a modified Allen's method on T₁₀. Six rats of each group were sacrificed at 4 h after injured, and the levels of free iron and malondialdehyde (MDA) of involved spinal cord segments were measured by bleomycin assay and the thiobarbituric acid (TBA) separately. The recovery of function was assessed by Modified Tarlov's scale and inclined plane method at 7, 14, 21 d after SCI. The histologic changes of the damaged spinal cord were also examined at 7 d after SCI.

Results

Following SCI, the levels of free iron and MDA were increased significantly and the Modified Tarlov's score and inclined plane angles decreased in SCI group and vehicle group. In DFO group, the levels of free iron and MDA were not increased, but the Modified Tarlov's score and inclined plane angles decreased, the histological findings were improved as well.

Conclusion

Deferoxamine can reduce the levels of free iron and lipid peroxidation, and improve the hind limb functional status of rats with spinal cord injury.     

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 methylprednisolone on vascular injury in rat spinal cord injury.

High-dose methylprednisolone (MP) given to patients within 8 h of traumatic spinal cord improved neural function at 6 and 12 months, suggesting a probable secondary injury process that may be amenable to therapeutic intervention. Vascular injury plays an important role in the secondary injury process of CNS trauma. We have examined the effect of MP on vascular changes, including tissue edema, vascular permeability, and polymorphonuclear (PMN) cell infiltration in a rat model of spinal cord impact injury. MP significantly reduced extravasation of fluorescein isothiocyanate dextran (FITC-D), a macromolecular tracer, by 64.3% and 50.7% with trauma forces of 20 and 40 g-cm, respectively, when MP was administered IV immediately after trauma at a bolus of 165 mg/kg, with a subsequent continuous MP infusion at 31.5 mg/kg/h for 23 h. MP reduced the water content in the 40 g-cm traumatic cord lesion to 73.0% compared to the traumatic control (74.3%, p < 0.001) at the same schedule of large dose 24-h infusion. The same doses of MP showed a trend to decrease the extent of neutrophil infiltration as determined by myeloperoxidase (MPO) activity, but the change was not significant. MP had little effect in decreasing FITC-D extravasation and cord edema when given at a lower dose (bolus of 30 mg/kg with continued infusion of 1.3 mg/kg/h for 23 h). MP did not reduce extravasation of FITC-D and edema when administered IV as one bolus injection at high (165 mg/kg) or low (30 mg/kg) doses.(ABSTRACT TRUNCATED AT 250 WORDS)     

对大鼠脊髓损伤应用红花注射液的保护作用

[目的]采用重物下降打击法,制备相当于中度大鼠脊髓损伤(spinal cord injury,SCI)的模型,探讨红花注射液对SCI的保护效果。[方法]将72只SD大鼠随机分为假手术组(A组)、脊髓打击损伤组(B组)、甲基强的松龙组(methylprednisolone sodium succinate,MPSS)(C组)、红花溶液组(D组),每组18只。B、C、D组根据改良的重物撞击装置制备脊髓急性打击损伤动物模型,C、D组在脊髓打击损伤后即刻分别腹腔注射MPSS 30 mg/kg和红花溶液100 mg/kg,观察并检测4组大鼠SCI后1、24、48 h 3个不同时间点后肢运动功能评分变化以及脊髓组织病理学、组织含水量、乳酸(lactic acid,LD)含量、乳酸脱氢酶(lactic dehydrogenase,LDH)活性、超氧化物歧化酶(superoxide dismutase,SOD)活性、丙二醛(malondialdehyde,MDA)含量的改变。[结果]术后A组大鼠功能完全恢复;C组或D组与B组相比,大鼠后肢运动功能24、48 h 2个时间点均有所改善,但24 h时已出现明显差异(P<0.05)...     

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.     

The effects of cyclosporin A and insulin on ischemic spinal cord injury in rabbits

We examined the effects of cyclosporin A (CsA), a drug that inhibits mitochondrial permeability transition pore, and insulin on ischemic spinal cord damage in rabbits. We assigned rabbits to 5 groups (n = 6 in each); sham barrier-opened group (sham BO), barrier-opened group (BO), barrier-opened-CsA group (BO-CsA), barrier-opened-insulin group (BO-I), and barrier-opened-CsA-insulin group (BO-CsA-I). The blood-spinal cord barrier was opened to facilitate drug penetration by a mild injury to the lumber spinal cord on day 1. CsA (10 mg/kg per day IV) was administered on day 3 to day 5 (total 30 mg/kg). Insulin was administered 30 min before ischemia. In all groups, spinal cord ischemia was produced on day 5 by occluding the abdominal aorta for 13 min. Neurological and histopathological evaluations were performed 4 days after ischemia. In group BO-CsA, blood glucose concentrations were significantly larger compared with the other four groups, and no protection was observed. In contrast, hindlimb motor function in groups BO-I and Bo-CsA-I and histopathology in group BO-CsA-I were significantly better than in groups sham BO, BO, and BO-CsA. The results indicate that insulin protects against ischemic spinal cord injury, whereas the effect of CsA is, at best, minimal.     

阿魏酸对家兔脊髓缺血再灌注损伤的防治作用

目的　研究阿魏酸对家兔肾下主动脉阻断所致脊髓损害的防治作用及其机理。方法家兔 2 4只 ,随机分为假手术组 (A组 ) ,缺血再灌注损伤组 (B组 )及阿魏酸组 (C组 ) ,每组 8只。B、C组肾下主动脉阻断 4 0分钟后开放 ,再灌注 7天。C组于阻断前 15分钟一次性静注阿魏酸 5 0mg/kg ,余两组则以同样方法静注等容量生理盐水作对照。测定阻断前 (C0 )、开放前 (C40 )、开放后 6 0分钟(R60 )及 7天 (R7d)血清中MDA、SOD、S10 0蛋白、TNFα、IL 1β的含量 ;术后观察后肢神经功能和脊髓形态学变化。结果　 (1)B组缺血及再灌注后血清MDA、S10 0蛋白、TNFα、IL 1β含量明显高于C0点及A组值 (P <0 0 1) ;C组明显低于B组 (P <0 0 1) ,与A组无显著性差异。 (2 )B组缺血及再灌注后SOD活力明显低于C0 点及A组值 (P <0 0 1) ;C组明显高于B组 (P <0 0 1) ,与A组无显著性差异。 (3)C组瘫痪发生率明显低于B组 (P <0 0 1) ,其后肢神经功能评分显著高于B组 (P <0 0 1)。 (4)B组脊髓病理变化较重 ,可见大量神经元坏死 ;C组偶有神经元坏死。结论　预防性静注阿魏酸对家兔主动脉阻断所致脊髓损害有良好的防治作用。其机理与阿魏酸抗氧化、抗炎及抑制TNFα、IL 1β水平升高有关     

黄连素在脊髓损伤中对线粒体的保护作用及机制

目的探讨黄连素对脊髓损伤(SCI)后线粒体氧化损伤的作用和可能机制。方法将36只C57小鼠随机分为假手术组、SCI组(伤后立即腹腔注射10 mg/kg生理盐水)和黄连素组(SCI后立即腹腔注射10 mg/kg黄连素),每组12只。使用PSI-IH脊髓打击器建立小鼠SCI模型,于损伤后24 h处死小鼠,取脊髓组织。使用全自动酶标仪检测各组小鼠脊髓组织线粒体内丙二醛(MDA)、还原型谷胱甘肽(GSH)和超氧化物歧化酶(SOD)的变化;用蛋白质印迹法检测脊髓组织caspase-3、cleaved caspase-3的表达及细胞质内和线粒体内细胞色素C(Cyt C)的表达;用免疫荧光双标染色法检测脊髓组织中神经细胞凋亡情况。结果与假手术组相比,SCI组小鼠脊髓组织线粒体内MDA水平升高,GSH、SOD水平降低;细胞质内Cyt C和脊髓组织中caspase-3、cleaved caspase-3表达水平增高,线粒体内Cyt C表达水平降低;脊髓组织中神经元凋亡比例增高;差异均有统计学意义(P 0.05)。与SCI组相比,黄连素组小鼠脊髓组织线粒体内MDA水平降低,SOD和GSH水平增高;细胞质内Cyt C和脊髓组织中caspase-3、cleaved caspase-3表达水平降低,线粒体内Cyt C表达水平增高;脊髓组织中神经细胞凋亡比例减少;差异均有统计学意义(P 0.05)。结论黄连素可减轻SCI小鼠脊髓组织中神经细胞凋亡,这可能与其抑制线粒体氧化损伤、减少Cyt C释放、降低凋亡蛋白表达有关。     

Effects of xenon on ischemic spinal cord injury in rabbits: a comparison with propofol

Background: Xenon has been shown to reduce cellular injury after cerebral ischemia. However, the neuroprotective effects of xenon on ischemic spinal cord are unknown. The authors compared the effects of xenon and propofol on spinal cord injury following spinal cord ischemia in rabbits. Methods: Thirty‐two male New Zealand white rabbits were randomly assigned to one of three groups. In the xenon and propofol group, 70% of xenon and 0.8 mg/kg/min of propofol were administered 30 min before an aortic occlusion and maintained until the end of the procedure. The aortic occlusion was performed for 15 min. In the sham group, the aorta was not occluded. After an assessment of the hind limb motor function using the Tarlov score (0=paraplegia, 4=normal) at 48 h after reperfusion, gray and white matter injuries were evaluated based on the number of normal neurons in the anterior spinal cord and the percentage areas of vacuolation in the white matter, respectively. Results: In the xenon and propofol groups, the Tarlov score and the number of normal neurons were significantly lower than those in the sham group, whereas the percentage areas of vacuolation were similar among the three groups. There were no significant differences in Tarlov scores and the number of normal neurons between the xenon and the propofol groups. Conclusion: The results indicated that 70% of xenon has no additional neuroprotective effects on ischemic spinal cord injury in rabbits compared with propofol.