二甲双胍治疗坐骨神经结扎诱发大鼠神经病理性疼痛的效应

目的:探讨二甲双胍治疗坐骨神经慢性压迫损伤(chronic constriction injury,CCI)诱发大鼠神经病理性疼痛的效应。方法:SPF级健康雌性SD大鼠48只,7～9周龄,180～200 g,采用随机数字表法将其分为正常对照组(Naive组)、假手术组(Sham组)、CCI组和CCI+二甲双胍组(Met组),每组12只。二甲双胍采用灌胃方式给药,每次剂量45 mg/kg,从CCI建模前3 d开始给药,每天2次,持续至建模后第7天。分别于建模前(基线水平),术后3 d、7 d、10 d、14 d记录建模侧(左侧)后足机械缩足反射阈值(MWT)、热缩足潜伏期(TWL)和冷刺激诱发缩足次数(TNCW);第3、14天使用CatWalk步态分析系统测定各组大鼠的步态。结果:与Naive组比较,CCI组和Met组大鼠左足MWT降低、TWL缩短、TNCW减少(P0.05);CCI组大鼠左侧足印面积缩小、完整足印的平均强度减弱、站立时间缩短、步周长减小、摆动时间延长,并持续至建模后第14天(P0.05);Met组大鼠左侧足印面积缩小、完整足印的平均强度减弱;Sham组上述指标无明显改变。与CCI组相比,Met组大鼠左足MWT升高、TWL延长、TNCW增加(P0.05); Met组大鼠左侧足印面积增大、完整足印的平均强度增强、站立时间延长以及步周长增加(P0.05),摆动时间无明显改变。结论:二甲双胍可缓解CCI诱发神经病理性疼痛大鼠机械痛觉过敏和冷热痛觉过敏,且能改善神经病理性疼痛大鼠的步态。     

Effects of intrathecal lidocaine on hyperalgesia and allodynia following chronic constriction injury in rats

The present study investigated the effects of different doses of intrathecal lidocaine on established thermal hyperalgesia and tactile allodynia in the chronic constriction injury model of neuropathic pain, defined the effective drug dose range, the duration of pain‐relief effects, and the influence of this treatment on the body and tissues. Male Sprague–Dawley rats were divided into five groups and received intrathecal saline or lidocaine (2, 6.5, 15, and 35mg/kg) 7 days after loose sciatic ligation. Respiratory depression and hemodynamic instability were found to become more severe as doses of lidocaine increased during intrathecal therapy. Two animals in the group receiving 35mg/kg lidocaine developed pulmonary oedema and died. Behavioral tests indicated that 6.5, 15, and 35mg/kg intrathecal lidocaine showed different degrees of reversal of thermal hyperalgesia, and lasted for 2–8 days, while 2mg/kg lidocaine did not. The inhibition of tactile allodynia was only observed in rats receiving 15 and 35mg/kg lidocaine, and the anti‐allodynic effects were identical in these two groups. Histopathologic examinations on the spinal cords revealed mild changes in rats receiving 2–15mg/kg lidocaine. However, lesions were severe after administration of 35mg/kg lidocaine. These findings indicate that intrathecal lidocaine has prolonged therapeutic effects on established neuropathic pain. The balance between sympathetic and parasympathetic nervous activities could be well preserved in most cases, except for 35mg/kg. Considering the ratio between useful effects and side effects, doses of 15mg/kg are suitable for intrathecal injection for relief of neuropathic pain.     

Changes in cardiovascular parameters and plasma norepinephrine level in rats after chronic constriction injury on the sciatic nerve

To evaluate whether neuropathic pain affects autonomic nervous activities, we investigated daily change in cardiovascular parameters and plasma norepinephrine (NE) in free-moving rats after chronic constriction injury (CCI) on the sciatic nerve. Arterial blood pressure (BP), heart rate (HR), and the power spectrum of pulse interval variability were analyzed. Daily change in motor activity and nociceptive behavior was also measured from some CCI rats. In others, NE from daily blood samples was quantified and spontaneous pain was evaluated by daily monitoring of foot guarding behavior. We identified three stages in the daily change of cardiovascular parameters and plasma NE level over 3 weeks following CCI. The first stage (up to 3 days after the surgery) was characterized by increased MAP and HR, especially in the daytime, even though plasma NE was unchanged and motor activity decreased. The second stage (mid first to mid second postoperative weeks) was characterized by increased daytime MAP and HR, and the animals developed punctate hyperalgesia in the affected hindpaw. An NE surge that may have been related to spontaneous pain was present 3-5 days after CCI. The third stage, which appeared after the second postoperative week, was characterized by normalized MAP and decreased HR, and increased high-frequency (0.8-3.0Hz) power in pulse interval variability, which is an index of cardiac parasympathetic tone. These results demonstrated that cardiovascular function was kept high through sympathetic and non-sympathetic activity for 2 weeks after CCI, followed by a predominance of parasympathetic tone.     

Calcitonin ameliorates enhanced arterial contractility after chronic constriction injury of the sciatic nerve in rats

In addition to its regulatory effect on bone mass, calcitonin has been shown to relieve pain and alleviate peripheral circulatory disturbance in patients with Raynaud's syndrome and complex regional pain syndrome. In the present study, we investigated whether calcitonin ameliorates diminished blood flow and enhanced arterial contraction in response to noradrenaline in chronic constriction injury (CCI) of the sciatic nerve in rats. Following surgically induced CCI, laser Doppler flowmetry studies showed a significant decrease in plantar skin blood flow of the ipsilateral hind paw compared to the contralateral side. A subcutaneous bolus injection of elcatonin (20 U/kg), a synthetic derivative of eel calcitonin, significantly improved decreased skin blood flow in the ipsilateral side. In vitro analysis of plantar arteries isolated from the ipsilateral hind paw 7-13 days after the CCI procedure showed higher sensitivity to noradrenaline than the plantar arteries from the contralateral side. Elcatonin (0.1-10 nm) significantly reduced noradrenaline-induced contraction in the arteries of the ipsilateral side, whereas it had little effect on those of the contralateral side. These results suggest that calcitonin selectively ameliorates enhanced arterial contractility in CCI neuropathic rats, thus leading to its alleviating effect on peripheral circulatory disturbance.     

Effect of ursolic acid in attenuating chronic constriction injury‐induced neuropathic pain in rats

Ursolic acid (UA; 3b‐hydroxy‐12‐urs‐12‐en‐28‐oic acid), a natural pentacyclic triterpenoid carboxylic acid, has been known to possess potent anti‐inflammatory, antioxidant, and antinociceptive effects in various animal models. Therefore, this study was designed to investigate the antihyperalgesic, anti‐inflammatory, and antioxidant effects of UA at 5, 10, and 20 mg/kg of doses via per os (p.o.) route for 14 days in chronic constriction injury (CCI)‐induced neuropathic pain in rats. Pain behavior in rats was evaluated before and after UA administration via mechanical and heat hyperalgesia. CCI caused significant increase in levels of pro‐inflammatory cytokines and oxido‐nitrosative stress. In addition, significant increase in myeloperoxidase, malondialdehyde, protein carbonyl, nitric oxide (NO), and total oxidant status (TOS) levels in sciatic nerve and spinal cord concomitant with mechanical and heat hyperalgesia is also noted for CCI‐induced neuropathic pain. Administration of UA significantly reduced the increased levels of pro‐inflammatory cytokines and TOS. Further, reduced glutathione is also restored by UA. UA also showed in vitro NO and superoxide radical scavenging activity. UA has a potential in attenuating neuropathic pain behavior in CCI model which may possibly be attributed to its anti‐inflammatory and antioxidant properties.     

Effect of intrathecal octreotide on thermal hyperalgesia and evoked spinal c-Fos expression in rats with sciatic constriction injury

This study was designed to determine whether intrathecal octreotide (sandostatin), a synthetic octapeptide derivative of somatostatin, relieved thermal hyperalgesia and reduced the evoked spinal c-Fos expression in rats with chronic constriction injury (CCI) of the sciatic nerve. Intrathecal catheters were implanted in rats 7 days before CCI of the sciatic nerve over the left hind limb. After confirmation of the development of thermal hyperalgesia by decreased paw withdrawal latencies (PWL) to heat stimulation 7 days after CCI, intrathecal sandostatin at 20, 40, and 80 microg was administered, respectively. Rats in the control group received saline injections intrathecally. PWLs were evaluated at 30, 60, 120, 180, and 240 min after drug administration. Detection of Fos-like immunoreactivity (Fos-LI) neurons in the dorsal horn of the spinal cord following drug administration was performed after mechanical stimulation (stroking of the hind paws) on the 14th day after CCI. The reduction of PWL was attenuated significantly in the groups that received intrathecal sandostatin at 20, 40, and 80 g when compared with the saline group. However, PWL did not return to pre-CCI values in all groups. In the 40 microg group, PWL returned up to 76% of pre-CCI values 120 min after drug administration. Stroking of the hind paw in CCI-treated (ipsilateral) limbs induced a significantly greater expression of spinal Fos-LI neurons than that of non-CCI treated (contralateral) limbs in each group. The number of Fos-LI neurons in animals receiving intrathecal sandostatin was dose-dependently reduced. Expression of Fos-LI neurons in the 80 microg group was nearly completely inhibited. These data suggest that intrathecal sandostatin significantly relieved thermal hyperalgesia behaviorally but with limited effects and dose-dependently reduced spinal Fos-LI neurons expression evoked by stroking stimulation, which may reflect mechanical allodynia in rats with sciatic constriction injury. This implies that intrathecal sandostatin was effective in the treatment of neuropathic pain.     

坐骨神经慢性挤压伤模型大鼠行为学及形态学变化

目的:观察大鼠坐骨神经慢性挤压伤模型所引起的行为学及病理形态学变化。方法:实验于2006-02/05在解放军军事医学科学院生物工程研究所完成。①SD大鼠24只,随机分为3组,坐骨神经结扎组12只制备右侧坐骨神经慢性挤压伤模型,正常对照组6只不干预,假手术组6只手术但不结扎,观察处理后42d内自发痛、触诱发痛、热刺激及冷刺激痛觉过敏等行为学变化。②SD大鼠54只,随机分为正常对照组、假手术组及坐骨神经结扎后3,7,14,21,28,35,42d组9组,处理同前,相应时间点处死大鼠观察坐骨神经和脊髓组织大体形态、苏木精-伊红染色和轴突髓鞘染色观察脊髓组织病理变化,电镜观察超微结构变化。结果:78只大鼠进入结果分析。①行为学变化:坐骨神经结扎组大鼠术后3d即出现明显的自发性疼痛,机械刺激痛阈值从术前的(17.33±5.42)g降至(3.28±1.37)g;热刺激爪退缩阈值从(12.13±2.37)s缩短至(10.43±1.65)s;冷刺激抬足次数从(3.50±1.09)次增加至(14.75±2.34)次。术后7￣14d这些阈值的变化逐渐达高峰,并持续至观察期结束(42d)。②坐骨神经结扎大鼠坐骨神经结扎部位及其远端轴突水肿,部分脱髓鞘。结论:大鼠坐骨神经慢性挤压伤模型可以产生明显的、稳定的自发性疼痛和诱发性疼痛等类似临床神经痛的症状和体征;其局部病理变化与症状相符。     

坐骨神经损伤后相应脊髓前角运动神经元的形态学变化

目的探讨坐骨神经损伤与修复过程中相应脊髓前角外侧核运动神经元的形态学变化,并对神经元尼氏染色法的应用价值进行评估。方法采用硅胶管套接切断的大鼠坐骨神经模型,应用焦油紫染色、甲苯胺蓝染色和硫堇染色等3种尼氏法对伤后7、14、30d脊髓前角运动神经元进行形态学观察。结果应用3种染色方法均观察到坐骨神经伤侧脊髓前角外侧核大、中型运动神经元的形态结构和存活率与对照侧有明显差别。与对照侧比较,伤后7d伤侧脊髓神经元数目减少,存活率降低;伤后14d和伤后30d,尤其是伤后30d,伤侧脊髓神经元数目减少更显著,存活率下降更明显,有些神经元轮廓不清且尼氏体模糊。结论随着大鼠坐骨神经损伤时间的延长,其相应脊髓前角运动神经元的损伤程度逐渐增加,尤其是伤后30d退变非常明显。焦油紫染色方法是显示神经元尼氏体及反映神经元生活状态的简捷有效的方法。     

2-氨基-5-磷酰基戊酸酯对大鼠坐骨神经慢性压迫性损伤的机械痛敏和热痛敏的影响

目的:建立大鼠坐骨神经慢性压迫性损伤(CCI)动物模型,腹腔注射N-甲基-D-天冬氨酸(NMDA)受体竞争性拮抗剂2-氨基-5-磷酰基戊酸酯(AP5)后观察腹腔用药对大鼠坐骨神经慢性压迫性损伤(CCI)动物模型机械痛敏和热痛敏的影响.方法:48只成年Wistar大鼠,雌雄不拘,随机分成3组,即Ⅰ组,假手术组(Sham),8只大鼠;Ⅱ组,CCI组,8只大鼠;Ⅲ组,治疗组,32只大鼠再分为4个亚组,Ⅲa组(CCI+NS),mb组[CCI+AP50.1mg/(kg·d)]、Ⅷc组(CCI+AP50.2 mg/kg)、Ⅲd组(CCI+AP50.5 mg/kg),每个亚组8只大鼠.48只大鼠分别于术前(0 d)及术后1、3、5、7、14、21 d测量每组大鼠的机械性缩足反射阈值(MWT)和热缩腿潜伏期(TWL).结果:CCI组从术后第3天开始直到本实验观察的术后第21天,MWT和TWL均明显降低,与假手术组Sham相比具有显著性(P＜0.01);CCI加生理盐水组大鼠与CCI组大鼠的MWT和TWL相比无明显改变(P＞0.05);腹腔注射AP5各个剂量的CCI组在术后5～21 d的MWT和TWL明显增加,与给药前和生理盐水组相比具有显著性(P＜0.01).结论:腹腔注射AP5有明显减轻大鼠CCI模型的机械性痛敏和热痛敏的作用.     

Advances in stem cell treatment for sciatic nerve injury

Introduction: The sciatic nerve is one of the peripheral nerves that is most prone to injuries. After injury, the connection between the nervous system and the distal organs is disrupted, and delayed treatment results in distal organ atrophy and total disability. Regardless of great advances in the fields of neurosurgery, biological sciences, and regenerative medicine, total functional recovery is yet to be achieved.

Areas covered: Cell-based therapy for the treatment of peripheral nerve injuries (PNIs) has brought a new perspective to the field of regenerative medicine. Having the ability to differentiate into neural and glial cells, stem cells enhance neural regeneration after PNIs. Augmenting axonal regeneration, remyelination, and muscle mass preservation are the main mechanisms underlying stem cells’ beneficial effects on neural regeneration.

Expert opinion: Despite the usefulness of employing stem cells for the treatment of PNIs in pre-clinical settings, further assessments are still needed in order to translate this approach into clinical settings. Mesenchymal stem cells, especially adipose-derived stem cells, with the ability of autologous transplantation, as well as easy harvesting procedures, are speculated to be the most promising source to be used in the treatment of PNIs.     

坐骨神经损伤与修复过程中相应脊髓神经元变化的形态学观察

目的探讨坐骨神经损伤与再生修复过程中相应脊髓前角运动神经元的形态学变化和嗅被膜细胞(OECs)对神经元的保护作用。方法采用硅胶管套接切断的大鼠坐骨神经实验模型,将30只大鼠随机分为两组,治疗组硅胶管内注射OECs悬液,对照组注射生理盐水(SAL),应用尼氏法对术后7d、14d、30dSAL组与OECs组脊髓前角运动神经元进行形态学观察,比较两组同类神经元的存活率。结果OECs组治疗侧脊髓前角外侧核大、中型运动神经元的形态结构和存活率与对照组有明显差别。术后7d,OECs组治疗侧神经元数目较SAL组伤侧丢失减少,存活率上升。术后14d和30d,OECs组治疗侧神经元数目较SAL组伤侧明显增加,存活率明显升高,大多数神经元轮廓清楚,尼氏体清晰。结论OECs能减少坐骨神经损伤后相应脊髓前角运动神经元的退行性变。     

苦参碱对小鼠坐骨神经损伤后脊髓运动神经元的影响

目的探讨BALB/c小鼠坐骨神经损伤后应用苦参碱后对坐骨神经相应脊髓节段中gap-43的表达变化。方法健康成年BALB/c小鼠320只,单侧坐骨神经切断吻合后,随机分组给药,不同时间获取L4-6脊髓节段,用Real time-PCR检测坐骨神经相应脊髓节段gap-43的表达变化,同时进行髓鞘LFB染色观察坐骨神经的恢复情况。结果 Real time-PCR结果显示高剂量和中剂量组12h,24h3d5d1w,2w,4w,gap-43表达量明显高于低剂量组和空白对照组,8w各组比较无明显差异。LFB染色表明高中剂量组坐骨神经恢复情况明显优于低剂量组和对照组。结论坐骨神经损伤后应用苦参碱对坐骨神经脊髓相应节段细胞中gap-43的活化起到促进作用,减少炎症细胞的浸润从而达到促进神经再生的目的。     

Long-term changes of c-Fos expression in the rat spinal cord following chronic constriction injury.

The expression of c-Fos protein has been used as a relative marker of nociceptive neuronal activity in the spinal cord following various noxious stimuli. Experiments were conducted to examine c-Fos expression in lumbar spinal cord (L3-L6) following chronic constriction injury (CCI) in relation to nociceptive behavior over longer survival period up to 28 days. Development of mechanical allodynia was observed in the ipsilateral hind paw of CCI rats at day 3 and lasted up to 28 days. In contrast, the spinal c-Fos expression in CCI rats appeared in a biphasic manner. The highest number of c-Fos positive neurons occurred during the first week, followed by a decline at 7 and 14 days and reappearance at day 28 following injury. The early increase of c-Fos expression correlated with allodynia development, however, at longer survival period (28 days) c-Fos positivity become comparable in both CCI and sham groups despite their obvious behavior differences. Our results suggest that, at least in the CCI model, the c-Fos protein expression should not be considered as a reliable index of pain sensation disorders.     

电针对坐骨神经损伤大鼠背根神经节中神经营养因子-3及其受体TrkC的影响

目的:观察电针对坐骨神经损伤大鼠行为学、神经生长因子-3及其受体Trk C的影响,探讨电针治疗坐骨神经损伤的生物学机制。方法:建立大鼠坐骨神经夹持损伤模型,观察各组大鼠的行为学改变与背根神经节(DRG)中NT-3与Trk C表达情况。结果:模型组、模型对照组的大鼠行为学检测表明,造模后大鼠的感觉功能显著下降(P<0.05),电针治疗后有显著改善(P<0.05),与正常组无显著差异;电针组的NT-3与Trk C表达显著升高(P<0.05),第20天时模型组与正常组相比,NT-3分泌显著增多(P<0.05)。结论:电针治疗可以通过提高NT-3与Trk C的表达,维持神经元存活,促进受损神经修复,改善坐骨神经损伤大鼠的感觉功能。     

Bilateral chronic constriction of the sciatic nerve: a model of long-term cold hyperalgesia.

Effects of chronic constriction injury (CCI) and sham surgery of both sciatic nerves were evaluated for reflex lick/guard (L/G) and operant escape responses to thermal stimulation of rats. Experiment 1 compared L/G and escape responses to 0.3 degrees C, 43 degrees C, and 47 degrees C stimulation during a period of 60 days after CCI. Experiment 2 evaluated escape from 44 degrees C, 47 degrees C, and 10 degrees C for 100 days after CCI. The rats escaped from heat or cold stimulation of the paws in a dark compartment by climbing on a thermally neutral platform in a brightly lit compartment. For reflex testing, a single compartment provided no escape option. There was no significant effect of bilateral CCI on reflex or escape responses to nociceptive heat. However, there were long-term increases in the duration of L/G responding during trials of 0.3 degrees C stimulation and in the duration of escape responding to 10 degrees C. Hyperalgesia for cold was confirmed by a preference test, with a 2-compartment shuttle box with one floor heated (45 degrees C) and the other floor cooled (10 degrees C). Occupancy of the heated compartment was significantly increased by CCI (indicating a relative aversion for cold). PERSPECTIVE: For preclinical testing of treatments for allodynia/hyperalgesia after nerve injury, it is crucial to use methods of testing that are sensitive to effects on nociception throughout the neuraxis. Operant escape testing satisfies this criterion and is sensitive to bilateral CCI of rats, which avoids asymmetric postural/motor influences of unilateral CCI.     

电针改善坐骨神经损伤大鼠步行能力及跨半球可塑性机制研究

目的:采用静息态fMRI体素-镜像同伦连接(VMHC)和Granger因果分析(GCA)方法,探讨电针改善坐骨神经损伤大鼠步行能力的作用及跨半球可塑性机制。方法:16只右侧坐骨神经横断外膜缝合模型大鼠,随机等分为治疗组和对照组。治疗组予电针治疗,对照组无特殊干预。于术后1月、4月行步态分析和静息态fMRI扫描。结果:治疗组术后1月、4月步态分析最大接触平均强度均较对照组显著提高(P0.05)。术后1月两组VMHC差异无显著性,术后4月治疗组运动皮质、杏仁核、嗅皮质VMHC较对照组显著降低(FDR校正,P0.01)。GCA结果显示术后4月治疗组大鼠左侧运动皮质到右侧运动皮质的效应连接较对照组显著降低(P0.05)。结论:电针治疗可以改善坐骨神经损伤大鼠的步行能力,可能与电针调节了大鼠半球间功能连接和定向效应连接有关。     

The effect of Spinal Cord Stimulation in mice with chronic neuropathic pain after partial ligation of the sciatic nerve

The effect of Spinal Cord Stimulation (SCS) in chronic neuropathic pain is inversely related to the severity of mechanical allodynia and the underlying mechanisms are poorly understood. To understand these mechanisms further we aimed to develop a model of SCS in a neuropathic mouse. Further, the CatWalk analysis, which is claimed to be an improved test for mechanical allodynia and therapeutic intervention, was used to analyze the effect of SCS on mechanical allodynia. Male C57BL/6 mice (N = 31) underwent partial ligation of the sciatic nerve. After 14 days an electrode was implanted and the effect of SCS (N = 22) on mechanical allodynia was tested. Unligated mice (N = 8) also received SCS. Behavioral analysis was performed using von Frey filaments and the CatWalk system. The withdrawal threshold showed a significant decrease which remained over time. Changes in CatWalk parameters were observed after 2 days, but tended to diminish during the next 14 days. Thirty minutes of SCS resulted in a 100% response and return to pre-neuropathy levels of the withdrawal threshold. The effect of SCS on the withdrawal threshold was comparable for the most severe and milder allodynic animals. SCS did not affect any of the CatWalk parameters in all mice. In conclusion, we developed a model of SCS in a chronic neuropathic pain C57BL/6 mouse. The CatWalk gait analysis does not result in the detection of behavioral changes to SCS in mice with chronic neuropathic pain and control animals. This model allows future molecular-genetic studies on the mechanisms of SCS in chronic neuropathic pain.     

Baroreceptor reflex is suppressed in rats that develop hyperalgesia behavior after nerve injury

The baroreceptor reflex buffers autonomic changes by decreasing sympathetic activity and increasing vagal activity in response to blood pressure elevations, and by the reverse actions when the blood pressure falls. Because of the many bidirectional interactions of pain and autonomic function, we investigated the effect of painful nerve injury by spinal nerve ligation (SNL) on heart rate (HR), blood pressure (BP) and their regulation by the baroreceptor reflex. Rats receiving SNL were separated into either a hyperalgesic group that developed sustained lifting, shaking and grooming of the foot after plantar punctate nociceptive stimulation by pin touch or a group of animals that failed to show this hyperalgesic behavior after SNL. SNL produced no effect on resting BP recorded telemetrically in unrestrained rats compared to control rats receiving either skin incision or sham SNL. However, two tests of baroreceptor gain showed depression only in animals that developed sustained hyperalgesia after SNL. The animals that failed to develop hyperalgesia after SNL were found to have elevations in HR both before and for the first 4 days after SNL, and HR variability analysis gave indications of decreased vagal control of resting HR and elevated sympatho-vagal balance at these same time intervals. In human patients, other research has shown that blunted baroreceptor reflex sensitivity predicts poor outcome during conditions such as hypertension, congestive heart failure, myocardial infarction, and stroke. If baroreceptor reflex suppression is also found in human subjects during chronic neuropathic pain, this may adversely affect survival.     

运动训练对慢性酒精中毒大鼠坐骨神经功能恢复的影响

目的：探讨长期饮酒对大鼠周围神经功能及形态的影响，并观察早期运动训练能否对其功能恢复产生促进作用，同时探讨其代偿机制。方法：将60只雄性Wistar大鼠随机分为3组：A组为对照组20只，B组为酒精中毒组20只，C组为康复组20只。采用灌胃法B、C组以50%（v/v）食用酒精，按10ml/kg·d 灌胃8周，康复组于灌胃第7周开始同时予游泳训练及跑笼训练2周，对照组则用等体积的生理盐水，每只大鼠每周称重，8周后做电生理测定，并做坐骨神经检查。结果：①酒精中毒组大鼠体重、食量、毛色均较对照组差，并出现酒精中毒性精神症状；②电生理检查酒精中毒组大鼠神经肌肉收缩阈值增高，峰值降低；③酒精中毒组微观结构显示轴索变性伴继发性节段性脱髓鞘改变，而其他两组则不显著。结论：①长期大量饮用高浓度白酒对大鼠周围神经肌肉形态及功能均有影响，其改变与人类慢性酒精中毒周围神经病相似；②早期运动训练对慢性酒精中毒大鼠坐骨神经肌肉损伤有一定治疗作用。