鞘内注射罗哌卡因与布比卡因对大鼠的脊髓神经毒性

目的 评价鞘内注射罗哌卡因与布比卡因对大鼠的脊髓神经毒性.方法 清洁级雌性SD大鼠,体重240～330 g,取鞘内置管成功的大鼠54只,随机分为3组(n=18):NS组鞘内注射生理盐水30μl;Bu组和RO组分别鞘内注射2%布比卡因20μl和2.7%罗哌卡因20μl,随后注射10μl生理盐水冲洗导管.于鞘内注药前、注药后10、20、30、60和120 min时(T1～6)行双后肢运动阻滞评分;于鞘内注药后第4天取腰段脊髓组织,观察病理学结果并行损伤评分.结果 与NS组比较,BU组T2～5时、RO组T2～4时大鼠双后肢运动阻滞评分升高,两组脊髓组织损伤评分升高(P＜0.05),脊髓组织病理学损伤较重;与T2时比较,Bu组和RO组其余各时点双后肢运动阻滞评分降低(P＜0.05),两组T2时差异无统计学意义(P＞0.05);与BU组比较,RO组脊髓组织损伤评分升高(P＜0.05),脊髓组织病理学损伤较重.结论 鞘内注射2.7%罗哌卡因对大鼠的脊髓神经毒性强于2%布比卡因.     

咪唑安定对布比卡因蛛网膜下腔麻醉效果的影响

目的观察咪唑安定加入布比卡因对蛛网膜下腔麻醉维持时间和麻醉效果的影响。方法40例ASAⅠ级子宫切除病人随机分为咪唑安定组（试验组，11=20）和对照组（n=20）。咪唑安定组蛛网膜下腔注入0．5％重比重布比卡因2．5ml加咪唑安定1mg（0．2m1），对照组注入0．5％重比重布比卡因2．5ml加生理盐水0．2ml。观察运动神经阻滞（改良Bromage）、感觉神经阻滞（针刺法）、镇痛时间（VAS）、术者和患者对麻醉的满意率。结果咪唑安定组感觉和运动神经阻滞时间显著延长（P〈0．01），术者和患者对麻醉的满意率提高（P〈0．05）。咪唑安定组有效镇痛时间也显著延长（P〈0．001）。两组血流动力学、不良反应情况差别无显著性。结论咪哗安定加入布比卡因能显著延长麻醉作用时间，麻醉效应增强，而不良反应未见增加。     

Effect of delayed induction of postischemic hypothermia on spinal cord damage induced by transient ischemic insult in rabbits

Objective: This study was performed to determine the effect of delayed induction of mild hypothermia after transient spinal cord ischemia in rabbits. Methods: Abdominal aortic occlusion was performed for 15 minutes to induce spinal cord ischemia at a rectal temperature of 37.3±0.3°C. Four groups of rabbits were investigated: Group 1 (n=8) was subjected to ischemia and reperfused at the same temperature for 7 hours; Group 2 (n=8) was subjected to ischemia and reperfused at the same temperature for 1 hour, followed by 6 hours of systemic hypothermia (32.5±0.5°C); Group 3 (n=8) was subjected to ischemia, reperfusion at the same temperature for 3 hours and then 6 hours of systemic hypothermia (32.5±0.5°C); and Group 4 (n=8) comprised non-ischemic controls. Neurological status of all rabbits in Groups 1– 3 was recorded and animals were sacrificed 1 week after ischemic injury. Spinal cord sections were examined microscopically to determine the extent of ischemic neuronal damage. Results: Mean modified Tarlov’s score at 1 week after ischemic insult was 0.5±0.8 in Group 1, compared to 4.3±1.5 in Group 2 and 2.9±1.8 in Group 3. Mean total number of surviving neurons within examined sections of spinal cord was significantly greater for Groups 2 and 3 compared with Group 1 (Group 1, 81±66.1; Group 2, 293.4±110.9; Group 3,227.1± 105.5; p<0.001). Conclusions: Delayed postischemic hypothermia induced within 3 hours after reperfusion significantly reduces ischemia-induced spinal cord neuronal damage in rabbits.     

Protective effect of intrathecal ketorolac in spinal cord ischemia in rats: a microdialysis study

BACKGROUND: The prevention of ischemic paraplegia after thoracoabdominal aortic surgery is challenging for both anesthesiologists and surgeons. In a previous study, we showed that intrathecal ketorolac pre-treatment protects rats against ischemic spinal cord injury. In the present study, using a microdialysis method, we investigated whether this neuroprotective effect was related to changes in the spinal cord release of nitric oxide (NO) or the excitatory amino acids (EAAs) aspartate and glutamate. METHODS: Rats were randomized to receive either intrathecal saline or ketorolac 60 microg (10 rats per group), 1 h before spinal cord ischemic injury induced by balloon inflation of a 2F Fogarty catheter in the thoracic aorta with maintenance of the proximal arterial blood pressure at 40 mmHg for 11 min, followed by reperfusion. Another 10 animals were used as the sham-operated control group. Ischemic injury was assessed by hind limb motor function. Cerebrospinal fluid dialysates were collected at baseline (before ischemia) and at 1, 2, 3, 4, 6, 12 and 24 h after the start of reperfusion, and were analyzed for EAAs using high-performance liquid chromatography and for NO metabolites using an NO analyzer. RESULTS: The results showed that intrathecal ketorolac attenuated spinal cord ischemic injury. Dialysate concentrations of NO and EAAs were increased after spinal cord ischemia, and this effect was inhibited by intrathecal administration of ketorolac. CONCLUSIONS: The results of this study suggest that the neuroprotective effect of intrathecal ketorolac in spinal cord ischemia in rats may be caused by a decrease in the spinal cord release of NO and EAAs.     

Effects of intrathecal ketamine added to bupivacaine for spinal anaesthesia

We prospectively studied 30 healthy female patients undergoing intracavitory brachytherapy applicator insertion for carcinoma of the cervix under spinal anaesthesia. Patients were randomly allocated to receive either intrathecal bupivacaine 10 mg alone or bupivacaine 7.5 mg combined with preservative-free ketamine 25 mg. Spinal block onset, maximum sensory level, duration of blockade, haemodynamic variables, postoperative analgesic requirements and adverse events were recorded. Onset of sensory and motor block and duration of spinal analgesia were comparable between groups. Duration of motor blockade was shorter (p = 0.0416) and requirement for intravenous fluids in the peri-operative period was less (p = 0.0159) in the ketamine group. Significantly more patients in the ketamine group had adverse events, such as sedation, dizziness, nystagmus, 'strange feelings' and postoperative nausea and vomiting. Although the addition of ketamine to spinal bupivacaine had local anaesthetic sparing effects, it did not provide extended postoperative analgesia or decrease the postoperative analgesic requirements. Moreover, the central adverse effects of ketamine limit its spinal application.     

亚低温对脊髓损伤后神经细胞凋亡的影响

目的观察大鼠脊髓损伤(SCI)细胞凋亡现象及亚低温对细胞凋亡的影响。方法大鼠SCI后分别于8h、24h、7d取材，采用常规病理HE染色和末端脱氧核苷酸转移酶(TdT)介导的dutp缺口末端标记技术(TNEUL)，研究亚低温对大鼠SCI后神经细胞凋亡的影响。结果SCI后常温组8h灰质区出现较多凋亡细胞，24h时白质和灰质内均有凋亡细胞分布，7d后凋亡细胞多见于白质；亚低温组凋亡细胞明显减少(P＜0．05)。结论亚低温明显减少SCI后细胞凋亡的发生，从病理上为亚低温脊髓保护提供了可靠的依据。     

Effects of adenosine monophosphate-activated kinase in the ventral horn of rabbit spinal cord after transient ischemia

Objective

To investigate the effect compound C, an adenosine monophosphate-activated kinase (AMPK) inhibitor, has on motor neurons of rabbit spinal cord after ischemia/reperfusion.

Design

Compound C (30 mg/kg) was administered intraperitoneally to rabbits 30 minutes before ischemia and the animals were sacrificed at 15 minutes after ischemia/reperfusion to measure lactate levels and at 72 hours after ischemia/reperfusion for morphological study.

Results

The administration of compound C did not produce any significant changes in physiological parameters such as pH, arterial blood gas (PaCO₂ and PaO₂), and blood glucose in rabbit either at 10 minutes before ischemia or at 10 minutes after reperfusion. However, the administration of compound C did significantly ameliorate lactate acidosis at 15 minutes after reperfusion. In addition, the administration of compound C significantly improved the neurological scores of the rabbits and reduced the neuronal death seen in the ventral horn of their spinal cords at 72 hours after ischemia/reperfusion.

Conclusions

Inhibition of AMPK can ameliorate the ischemia-induced neuronal death in the spinal cord via the reduction of early lactate acidosis.     

Effects of adenosine monophosphate-activated kinase in the ventral horn of rabbit spinal cord after transient ischemia

Abstract

Objective

To investigate the effect compound C, an adenosine monophosphate-activated kinase (AMPK) inhibitor, has on motor neurons of rabbit spinal cord after ischemia/reperfusion.

Design

Compound C (30 mg/kg) was administered intraperitoneally to rabbits 30 minutes before ischemia and the animals were sacrificed at 15 minutes after ischemia/reperfusion to measure lactate levels and at 72 hours after ischemia/reperfusion for morphological study.

Results

The administration of compound C did not produce any significant changes in physiological parameters such as pH, arterial blood gas (PaCO₂ and PaO₂), and blood glucose in rabbit either at 10 minutes before ischemia or at 10 minutes after reperfusion. However, the administration of compound C did significantly ameliorate lactate acidosis at 15 minutes after reperfusion. In addition, the administration of compound C significantly improved the neurological scores of the rabbits and reduced the neuronal death seen in the ventral horn of their spinal cords at 72 hours after ischemia/reperfusion.

Conclusions

Inhibition of AMPK can ameliorate the ischemia-induced neuronal death in the spinal cord via the reduction of early lactate acidosis.     

Effect of post-ischemic hypothermia on spinal cord damage induced by transient ischemic insult in rabbits

OBJECTIVE: The effect of post-ischemic mild hypothermia applied immediately after induced transient ischemia on the extent of neuronal damage to the spinal cord was investigated in rabbit. SUBJECTS AND METHODS: A 15-minute period of transient abdominal aortic occlusion for spinal cord ischemia at a rectal temperature of 37.3 +/- 0.3 degrees C was performed just below the left renal vein via median laparotomy. Three groups of rabbits were investigated; Group 1 (n = 8) subjected to ischemia and reperfused at the same temperature for 7 hours, Group 2 (n = 8) also subjected to ischemia and then to 6 hours of systemic hypothermia (32.5 +/- 0.5 degrees C), and Group 3 (n = 8) non-ischemic controls. All the rabbits in Group 1 and Group 2 were sacrificed at 1 week after ischemic injury. Spinal cord sections were examined microscopically to determine the extent of ischemic neuronal damage. RESULTS: The mean modified Tarlov's score at 1 week after ischemic injury was 0.5 +/- 0.8 in Group 1, whereas it was 4.4 +/- 1.4 (p < .001) in Group 2. The mean total number of surviving neurons within examined sections of the spinal cord was significantly greater in Group 2 than in Group 1 (Group 1: 81 +/- 66.1 vs Group 2: 300.9 +/- 154.1, p < .001). CONCLUSION: Post-ischemic hypothermia induced immediately after reperfusion significantly reduced ischemia-induced neuronal damage in rabbit.     

Effects of delta-opioid agonist SNC80 on white matter injury following spinal cord ischemia in normothermic and mildly hypothermic rats

Purpose Although the delta-opioid agonist SNC80 has been shown to attenuate hind-limb motor function and gray matter injury in normothermic rats subjected to spinal cord ischemia (SCI), its effects on white matter injury remain undetermined. In the present study, we investigated whether SNC80 could attenuate white matter injury in normothermic and mildly hypothermic rats. Methods Forty rats were randomly allocated to one of following five groups: vehicle or SNC80 with 10 min of SCI at 38°C (V-38-10m or SNC-38-10m, respectively), vehicle or SNC80 with 22 min of SCI at 35°C (V-35-22m or SNC-35-22m, respectively), or sham. SNC80 or vehicle was intrathecally administered 15 min before SCI. Forty-eight hours after reperfusion, the white matter injury was evaluated by the extent of vacuolation. Results The percent area of vacuolation in the ventral white matter was significantly lower in the SNC-38-10m and SNC-35-22m groups compared with that in the V-38-10m and V-35-22m groups, respectively (P < 0.05). Conclusion The results indicate that intrathecal treatment with the delta-opioid agonist SNC80 can attenuate the ventral white matter injury following SCI in rats under normothermic and mildly hypothermic conditions.     

Epidural cooling for regional spinal cord hypothermia during most or all of descending thoracic or thoracoabdominal aneurysm repair

Purpose: Hypothermia has some protective effect against ischemia of the spinal cord in thoracoabdominal aneurysm repair. Its method is divided into systemic or regional cooling. Several experimental studies of the regional cooling of the spinal cord have been performed, however, clinical reports are few. The purpose of this study is to evaluate the effect and safety of perfusion cooling of the epidural space during thoracic or thoracoabdominal aortic replacement. Methods: Between January 1998 to June 2001 37 patients (True aneurysm: 18 patients, type B aortic dissection: 19 patients) underwent thoracic or thoracoabdominal aortic replacement with an aid of epidural perfusion cooling. The age ranged from 23 to 78 years old with a mean age of 61 years old. Separate perfusion of upper and lower body was used in all cases. Temperature was lowered to around a 31°C or 32°C. In cases where proximal cross-clamping was danger, deep hypothermic circulatory arrest was used.

Results: Ten patients underwent most or all of descending thoracic aneurysm repair with no spinal cord injury and hospital death. Number of patients of the Crawford type I, type II, and type III were 14, 8 and 5 patients, respectively. One Crawford type II patient was complicated with postoperative spinal cord injury (2.7%). There was one hospital death (2.7%) in Crawford type III. The mean epidural cooling time was 150 minutes, and mean infusion volume of cold saline was 981 cc. The mean lowest cerebrospinal fluid (CSF) temperature was 24.3°C, and mean temperature differences between nasopharynx and CSF was 6.3°C.

Conclusion: Perfusion cooling of the epidural space during most or all of the descending thoracic or thoracoabdominal aneurysm repair was effective in reducing postoperative spinal cord injury and a safe method in clinical situations.     

An experimental study on spinal cord ischemia during cross-clamping of the thoracic aorta: The monitoring of spinal cord ischemia with motor evoked potential by transcranial stimulation of the cerebral cortex in dogs

The usefulness of spinal motor evoked potential by transcranial stimulation of the motor cortex (MEPt) in detecting spinal ischemia and predicting postoperative neurological dysfunction was evaluated using a model of spinal ischemia. Group 1 was comprised of 11 dogs used for measuring the basic wave form of spinal MEPt. The normal spinal MEPt response curve consists of two major peaks: peak I and peak II. The latency of peak I and peak II at T13–L1 was 6.0±0.6 and 7.1±0.6 msec, and the amplitude, 3.3±1.6 and 6.1±2.6 V, respectively. Group 2 was comprised of six animals subjected to spinal ischemia, in which a time-related deterioration of the MEPt as well as evoked spinal cord potential (ESP) was demonstrated. The time taken until the loss of peak I and peak II was 19.2±5.3 and 21.7±6.2 min, respectively, while the time taken until the loss of ESP was 36.7±14.0 min. In group 3, comprised of seven animals, the aorta was unclamped and the animals were allowed to recover when the spinal MEPt had disappeared. Four had paraparesis immediately after the operation, two had a normal gait, one died, and one developed spastic paraplegia after 24h. We concluded that the change in spinal MEPt during spinal ischemia occurred earlier than the change in ESP, and that the loss of MEPt suggested irreversible spinal cord damage.     

Effect of the free radical scavenger MCI-186 on spinal cord reperfusion after transient ischemia in the rabbit

Objective: Paraplegia remains a serious complication of aortic operations. The production of free radicals during reperfusion after transient ischemia is believed to induce secondary spinal neuronal injury, resulting in paraplegia. The aim of the present study was to clarify the protective effect and method of administration of antioxidants on the neurological and histological outcome in the animal model for reperfusion injury after transient spinal cord ischemia. Methods: New Zealand white rabbits underwent surgical exposure of the abdominal aorta that was clamped for 15 minutes to achieve spinal cord ischemia. Group A animals received two 10 mg/kg doses of 3-methyl-l-phenyl-2-pyrazolin-5-one (MCI-186) at the time of release of the aortic clamp and 30 minutes later. In group B, MCI-186, 5 mg/kg, was given three times, at the time of aorta clamp release, 30 minutes and 12 hours later. In group C (control group), one dose of vehicle was administered. Neurological status was assessed using modified Tarlov’s score until 168 hours after operation. Spinal cord sections were examined microscopically to determine the extent of ischemic neuronal damage. Results: Groups A and B animals had better neurological function than group C (p(0.001). In contrast, group C animals exhibited paraplegia or paraparesis with marked neuronal necrosis. The number of surviving neurons within examined sections of the spinal cord was significantly greater in group B than in group C (p(0.001). Conclusion: In a 15-minute ischemia-reperfusion model using rabbits, systemic repetitious administration of MCI-186, a free radical scavenger, was found to have a protective effect on the spinal cord neurons both neurologically and histologically. We postulate that the drug minimizes the delayed neuronal cell death for reperfusion injury after transient ischemia by reducing the free radical molecules. Moreover, it was thought that we could protect delayed neuronal cell death more effectively by administering MCI-18612 hours later.     

Critical ischemia time in a model of spinal cord section. A study performed on dogs

Vascular changes after acute spinal cord trauma are important factors that predispose quadriplegia, in most cases irreversible. Repair of the spinal blood flow helps the spinal cord recovery. The average time to arrive and perform surgery is 3 h in most cases. It is important to determine the critical ischemia time in order to offer better functional prognosis. A spinal cord section and vascular clamping of the spinal anterior artery at C5–C6 model was used to determine critical ischemia time. The objective was to establish a critical ischemia time in a model of acute spinal cord section. Four groups of dogs were used, anterior approach and vascular clamp of spinal anterior artery with 1, 2, 3, and 4 h of ischemia and posterior hemisection of spinal cord at C5–C6 was performed. Clinical evaluation was made during 12 weeks and morphological evaluation at the end of this period. We obtained a maximal neurological coordination at 23 days average. Two cases showed sequels of right upper limb paresis at 1 and 3 ischemia hours. There was nerve conduction delay of 56% at 3 h of ischemia. Morphological examination showed 25% of damaged area. The VIII and IX Rexed’s laminae were the most affected. The critical ischemia time was 3 h. Dogs with 4 h did not exhibit any recovery.     

脑缺血浅低温治疗时间窗的研究进展

背景 动物实验和临床研究证实浅低温(32℃～34℃)对脑缺血神经元有显著的保护作用.但是,何时开始浅低温,以及浅低温需要维持多长时间(即浅低温治疗时间窗)才能起到最大限度的神经保护作用,尚无明确定论.目的 综述脑缺血浅低温治疗时间窗的研究进展情况.内容 阐述治疗时间窗概念及脑缺血浅低温治疗时间窗的研究进展;讨论早期浅低温和晚期浅低温脑保护的可能作用机制.趋向 阐明浅低温治疗时间窗及机制,更好地应用浅低温于临床脑保护.     

Spinal cord blood flow after intrathecal injection of ropivacaine and bupivacaine with or without epinephrine in rats

Background: Ropivacaine is a new local anaesthetic available for spinal and epidural anaesthesia. When new drugs are being introduced for spinal application, their effect on spinal cord blood flow (SCBF) should be studied for safety and toxicological aspects. In the present study, SCBF was studied after intrathecal (i. t.) application of ropivacaine and bupivacaine with and without epinephrine.
Method: SCBF was measured continuously in spontaneously breathing, enflurane/N₂O anaesthetized rats, using laser-Doppler flowmetry technique. The spinal cord was exposed by laminectomy at the L₁-L₂ level, and a laser-Doppler probe was placed over the dorsal horn, allowing on-line registration of SCBF in a tissue hemisphere of 1–2 mm. Relative changes in SCBF were then measured on-line after i. t. administration of increasing doses of ropivacaine, bupivacaine or bupivacaine with epinephrine.
Results: Ropivacaine and bupivacaine decreased SCBF in a dose-dependent manner. In contrast, the reduction in SCBF produced by bupivacaine + epinephrine (Bupi+Epi) was equal for all doses of bupivacaine. The order of magnitude of SCBF decreases was Bupi + Epi >ropivacaine>bupivacaine. The maximal decrease in SCBF at the highest concentration given (10 mg/ml) was 37±6% for ropivacaine, 27±7% for bupivacaine and 40 ±6% for bupivacaine + epinephrine.
Conclusion: Ropivacaine and bupivacaine produce a dose-related, transient decrease in SCBF following i. t. administration in anaesthetized rats. However, the decrease in SCBF produced by both ropivacaine and bupivacaine was less than that produced by bupivacaine, when epinephrine was added in a concentration of 5 μg/ml. These results suggest that ropivacaine, like bupivacaine, may be used for spinal anaesthesia without important effects on SCBF.     

Beneficial effects of local profound hypothermia and the possible mechanism after experimental spinal cord injury in rats

Objective: The primary focus of this study was to investigate the effects of local profound hypothermia and to explore the possible mechanism in adult rats with spinal cord injury.

Study Design and Methods: Spinal cord injury models were established by placing aneurysm clips on T10. An epidural perfusion device was applied to maintain a steady temperature (18?°C) for 120?min with gradual rewarming to 37?°C Total hypothermic duration lasted up to about 170?min. The expression of axon regeneration inhibitors was tested by Western blot and real-time PCR. Luxol Fast Blue (LFB) stain and Bielschowsky silver stain were used to observe spinal cord morphology. Motor function of the hind limbs (BBB score) was monitored for 21 days.

Results: The expressions of RhoA, ROCK-II, NG2, Neurocan, Brevican, and Nogo-A were downregulated by regional hypothermia (RH) after spinal cord injury. Subsequent observation showed that rats that had received RH had an alleviated demyelinating condition and a greater number of nerve fibers. Furthermore, the RH group achieved higher BBB scores than the spinal cord injury (SCI) group.

Conclusions: Recovery of hind limb function in rats can be promoted by local profound hypothermia; this may be caused by the suppression of axon regeneration inhibitors.     

Unilateral spinal anaesthesia with hyperbaric bupivacaine

Background: The dosage of local anaesthetic and the time the patient must be kept in the lateral decubitus position for a unilateral spinal anaesthesia is not known. The aim of this study was to determine the ideal dosage of hyperbaric bupivacaine and the time required for the lateral decubitus position for a unilateral spinal block. Methods: Ninety patients who were scheduled to receive spinal block for surgery in the lower extremity were randomised into 9 groups (n=10). The spinal block was performed through the L₄–L₅ intervertebral space with the patient in the lateral decubitus position. Patients in groups Ia, Ib, Ic; IIa, IIb, IIc; IIIa, IIIb, IIIc received 1.5 ml of 0.5%, 2 ml of 0.5%, and 2.5 ml of 0.5% hyperbaric bupivacaine solutions, respectively. The patients were turned to the supine position for 5 min after the injection in groups Ia, IIa, IIIa, 10 min after the injection in groups Ib, IIb, IIIb, and 15 min after the injection in groups Ic, IIc, IIIc. The onset and regression of sensory and motor block were checked and compared between the dependent and non-dependent sides in each group. Results: The rate of block progression of the non-dependent side was higher in the groups receiving 2.5 ml 0.5% hyperbaric bupivacaine solution than in the other groups; at the same time the level of block was higher and the duration of block was longer. The incidence of hypotension was 10–20% in these groups. In the 2 ml 0.5% hyperbaric bupivacaine solution groups, a satisfactory block level and duration of anaesthesia for surgery was obtained. The rate of block progression to non-dependent side in the groups receiving 1.5 ml of 0.5% hyperbaric bupivacaine solution was lower than the other groups, but the duration of block was shorter and the level of block was lower than the other groups. Conclusion: For unilateral spinal anaesthesia in lower extremity operations, 2ml 0.5% hyperbaric bupivacaine solution for operations above the knee and 1.5 ml 0.5% hyperbaric bupivacaine solution for operations below the knee and keeping the patients for 10 min in the lateral decubitus position were found to be appropriate.     

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.