Effect of nimodipine or methylprednisolone on recovery from acute experimental spinal cord injury in rats

The purpose of the present study was to examine the behavioral, electrophysiologic, and anatomic responses to nimodipine or methylprednisolone treatment of acute experimental spinal cord injury. Four groups of rats were injured at T1 by compressing the cord with a 52-g clip for 1 minute. The treatments were begun 15 minutes after injury, and the animals were observed thereafter for 8 weeks. Nimodipine 0.02 mg/kg/h intravenously (iv) for 8 hours with adjuvant albumen volume expansion, followed by 20 mg/kg nimodipine enterally three times per day for 7 days, produced a moderately better composite score comprising four endpoint parameters than the other treatments which consisted of nimodipine iv for 8 hours only, methylprednisolone 30 mg/kg iv bolus followed by 5.4 mg/kg/h iv for 8 hours, or control.     

Effect of vasodilators and myelotomy on recovery after acute spinal cord injury in rats.

The effect of papaverine, nitroprusside, or myelotomy on the recovery of spinal cord function was studied in rats after acute cord-compression injury. Spinal cord recovery was measured by a quantitative method of clinical assessment previously developed in our laboratory. Neither papaverine nor nitroprusside improved recovery of cord function. Dorsal midline myelotomy extending anteriorly as far as the central canal did not produce significant improvement (p greater than 0.05). However, when the myelotomy extended completely through the cord in the anteroposterior plane significant improvement (p less than 0.01) was obtained.     

异丙酚对大鼠急性脊髓损伤的影响

目的 研究异丙酚对大鼠急性脊髓损伤的影响.方法 雌性SD大鼠60只,体重230～270 g,随机分为3组(n=20):假手术组、脊髓损伤组和异丙酚组.采用改良的Allen打击法致伤大鼠脊髓,打击后30 min,异丙酚组经尾静脉持续输注1%异丙酚60 mg·lg-1·h-1 1 h,其余2组持续输注0.9%生理盐水6 ml·kg-1·h-1 1 h.应用斜板实验评分法和BBB联合评分法评价后肢运动功能;采用原位末端标记法(TUNEL法)检测脊髓组织细胞凋亡;HE染色后光镜下观察脊髓组织病理学.结果 异丙酚组行为学评分高于脊髓损伤组(P＜0.05);与假手术组相比,脊髓损伤组各时点单位面积凋亡细胞数均升高(P＜0.01);与脊髓损伤组相比,异丙酚组各时点单位面积凋亡细胞数均降低(P＜0.05);脊髓损伤组脊髓病理损伤较异丙酚组重,可见大量神经元坏死.结论 持续静脉输注1%异丙酚60 mg·kg-1·h-1 h可减轻大鼠急性脊髓损伤,其机制与抑制细胞凋亡有关.     

丙戊酸对大鼠急性脊髓损伤后神经功能恢复的影响及作用机制

目的:探讨丙戊酸(VPA)对大鼠脊髓损伤(SCI)后运动功能恢复的影响及作用机制。方法:60只雄性SD大鼠随机均分为3组:假手术组(C组)、损伤组(SCI组)和丙戊酸保护组(VPA组)。SCI组和VPA组采用改良Allen法制作大鼠T10 SCI模型。VPA组术后即刻及其后每12h皮下注射VPA 300mg/kg,至取材;C组和SCI组在相应时间点注射等体积的生理盐水。伤后6h,每组取5只大鼠处死取材,其余大鼠在伤后24h、48h和72h每组取5只先行后肢运动功能BBB评分,随后处死取材。切片后分别行HE染色观察脊髓组织病理变化,免疫荧光双标法在激光共聚焦显微镜下观察核因子κB(NF-κB)途径的激活状态,免疫组化法检测白介素1β(IL-1β)的表达。结果:C组大鼠各时间点BBB评分均为21分,VPA组和SCI组各时间点的评分均低于C组(P<0.05),但VPA组各时间点的评分均高于同时间点SCI组,在伤后48h和72h两组差异有显著性(P<0.05)。病理检查显示C组脊髓组织形态正常,VPA组和SCI组伤后6h损伤中央区即可见明显出血灶,灰质中神经元肿胀坏死,白质中神经纤维肿胀;伤后24h、48h出血灶界限更明显,并可见空洞形成和炎症细胞浸润;伤后72h上述病理变化仍明显;VPA组各时间点的病理变化与SCI组相似,但炎症细胞浸润减少。C组偶见或未见NF-κB核阳性细胞和IL-1β表达,与C组相比,SCI组和VPA组NF-κB核阳性细胞百分比和IL-1β表达量从伤后6h即显著性增高,24h达高峰,以后逐渐减少,72h仍显著性高于C组(P<0.05);VPA组各时间点NF-κB核阳性细胞百分比和IL-1β表达量均低于同时间点SCI组(P<0.05)。结论:VPA可促进大鼠SCI后运动神经功能恢复,其机制可能与抑制炎症反应有关。     

罗西格列酮对脊髓损伤大鼠神经功能恢复的作用及机制

目的:观察罗西格列酮对脊髓损伤(SCI)大鼠后肢运动功能恢复的作用,探讨其作用机制。方法:75只成年SD大鼠,应用Allen改良法制作大鼠T10SCI模型,随机分为A、B、C三组,每组25只,B、C组于损伤后5min、6h、24h腹腔注射罗西格列酮,C组在腹腔注射罗西格列酮前1h给予G3335,A组于相应时间点腹腔注射等体积生理盐水作为对照组。每组取6只大鼠于伤后1d、7d、2w、4w、6w时对后肢运动功能进行BBB评分;伤后3d每组取4只动物脊髓组织行免疫组织化学染色法检测核转录因子κB(nuclear factor kappa-light-chain-enhancer of activated B cells,NF-κB)的表达;伤后1、3、5、7d和2w每组取3只应用Westernblot法检测脊髓组织中凋亡相关蛋白caspase-3和Bcl-2的表达。结果:伤后1d、7d时3组大鼠BBB评分均为0分,伤后2w开始B组BBB评分高于A组和C组,4w和6w时与A、C组比较有显著性差异(P0.05);伤后3d时三组NF-κB表达均为阳性,但B组平均光密度值明显低于A、C组(P0.05),B组与C组比较无显著性差异(P0.05);伤后各时间点B组caspase-3表达量均低于A组和C组(P0.05),而Bcl-2表达均高于A组和C组(P0.05),其差异均在伤后5d达到高峰,A组与C组同时间点比较无显著性差异(P0.05)。结论:罗西格列酮可促进SCI大鼠神经功能恢复,其机制可能与抑制炎症反应及细胞凋亡有关。     

Uncontrollable stimulation undermines recovery after spinal cord injury

Prior studies have shown that neurons within the spinal cord are sensitive to response-outcome relations, a form of instrumental learning. Spinally transected rats that receive shock to one hind leg learn to maintain the leg in a flexed position that minimizes net shock exposure (controllable shock). Prior exposure to uncontrollable stimulation (intermittent shock) inhibits this spinally mediated learning. Here it is shown that uncontrollable stimulation undermines the recovery of function after a spinal contusion injury. Rats received a moderate injury (12.5 mm drop) and recovery was monitored for 6 weeks. In Experiment 1, rats received varying amounts of intermittent tailshock 1-2 days after injury. Just 6 min of intermittent shock impaired locomotor recovery. In Experiment 2, rats were shocked 1, 4, or 14 days after injury. Delaying the application of shock exposure reduced its negative effect on recovery. In Experiment 3, rats received controllable or uncontrollable shock 24 and 48 h after injury. Only uncontrollable shock disrupted recovery of locomotor function. Uncontrollably shocked rats also exhibited higher vocalization thresholds to aversive stimuli (heat and shock) applied below the injury. Across the three experiments, exposure to uncontrollable shock, (1) delayed the recovery of bladder function; (2) led to greater mortality and spasticity; and (3) increased tissue loss (white and gray matter) in the region of the injury. The results indicate that uncontrollable stimulation impairs recovery after spinal cord injury and suggest that reducing sources of uncontrolled afferent input (e.g., from peripheral tissue injury) could benefit patient recovery.     

胶质细胞源性神经营养因子对大鼠脊髓损伤后运动功能的影响

目的:研究胶质细胞源性神经营养因子（GDNF）对大鼠脊髓损伤后后肢运动功能恢复的影响。方法:采用改良Nystr(?)m法后路压迫大鼠胸段脊髓造成损伤模型,经蛛网膜下腔置管局部连续给予NGF （10μg/d）或GDNF（10μg/d）1周,对照组给予生理盐水。伤后4周3组分别观测:①伤段脊髓残存组织面积;②采用斜板试验和运动功能评分观察大鼠后肢运动功能恢复情况。结果:大鼠脊髓损伤后4～14d,GDNF治疗组后肢运动功能评分明显高于NGF组和生理盐水对照组（P<0.05）。伤后28d GDNF组伤段残存脊髓组织面积大于对照组和NGF组（P<0.01）。结论:外源性GDNF能减少脊髓损伤后伤区的坏死、萎缩并促进大鼠后肢运动功能的早期恢复。     

硫酸软骨素酶ABC置管灌注治疗对大鼠脊髓损伤后神经功能恢复的影响

目的探讨硫酸软骨素酶ABC（ehondroitinase ABC,ChABC）置管灌注治疗对大鼠脊髓完全性横断伤后脊髓功能恢复的影响。方法采用大鼠胸段（T7-8）脊髓完全横断损伤模型,将SD大鼠随机分为4组：正常组（n=6）、假手术组（n=6）、单纯脊髓横断组（n=10）、ChABC置管灌注组（n=10）。正常组不进行任何干预处理;假手术组只切除T7-8椎板,不损伤硬脊膜;在横断节段下方蛛网膜下腔放置PE-10导管灌注,单纯脊髓横断组给予生理盐水10μl/d灌注,连续10 d;ChABC置管灌注组给予ChABC 6μl/次灌注,隔日1次,共5次。大鼠脊髓损伤术后1～8周,1周1次,12～24周,2周1次,进行行为学评估;24周时行大脑皮层诱发电位检测。结果（1）行为学评估：损伤后3周内,评分均在8分左右[单纯脊髓损伤组为（6.5±1.14）分,ChABC置管灌注组为（9.0±2.20分）],3周后ChABC置管灌注组的评分有明显提高,并于14～16周达到峰值,然后呈下降趋势,22～24周时稳定在10周时的水平。单纯脊髓横断组的最高评分为（11.0±1.47）分,ChABC置管灌注组的最高评分为（30.0±4.55）分,正常组的评分为53.5分。假手术组术后2周时的评分与正常组无明显差异,4周后ChABC置管灌注组的评分高于单纯脊髓横断组（P〈0.05）。（2）大脑皮层诱发电位检测：术后24周时,所有脊髓横断组中均未记录到体感诱发电位（somatosensory evoked potentia,SEP）波形。结论ChABC置管灌注治疗后,改善脊髓损伤区及两端的神经细胞功能,促进轴突再生,促进双下肢运动功能的恢复,动物行为学评分有明显提高。     

FTY720对大鼠急性脊髓损伤后神经功能恢复的影响及相关机制

目的:观察FTY720对大鼠急性脊髓损伤(ASCI)后神经功能的影响,并探讨其相关机制。方法:168只雌性SD大鼠,随机分成A、B、C三组,每组56只,A组(假手术组)大鼠麻醉后仅切除T9椎板,不打击脊髓,缝合后立即以0.3ml生理盐水灌胃。B、C组采用Allen′s法制作T9脊髓损伤模型,B组(对照组)以0.3ml生理盐水灌胃,C组(治疗组)以FTY720按3mg/kg生理盐水稀释至0.3ml灌胃。每组取8只大鼠分别于术后1d、3d、7d、14d、21d行斜板试验及BBB评分。分别于术后6h、12h、24h、48h、72h、7d、21d处死大鼠,每个时间点每组8只,取损伤段(A组取相应部位)脊髓行超薄切片,HE染色观察各组脊髓坏死情况、炎细胞浸润情况、胶质瘢痕形成情况及脊髓空洞大小,并计数各组术后12h淋巴细胞数、术后12h与72h炎性细胞、术后7d胶质瘢痕区细胞,计算伤后21d脊髓空洞面积与脊髓面积比值;取术后6h、12h、24h、72h的切片行SP免疫组化染色观察caspase-3表达及Tunel染色观察细胞凋亡情况,计算相应时间点免疫组化染色阳性细胞比值和凋亡指数。所有数据以SPSS 13.0进行统计学分析。结果:B、C两组各时间点斜板实验及BBB评分均较A组同时间点差(P<0.05),在术后1d时B、C组之间无显著性差异(P>0.05),术后3d、7d、14d、21d时C组优于B组(P<0.05)。HE染色结果显示A组各时间点脊髓形态正常;B、C组脊髓术后6h可见脊髓内出血、血肿形成,术后12h~48h脊髓进行性水肿、损伤中心区出现液化坏死,伴有炎细胞浸润,以中性粒细胞、淋巴细胞、单核细胞为主,至术后72h,损伤中心区形成无组织结构空洞,空洞周围有大量炎细胞浸润,以小胶质细胞/单核细胞为主;术后12h及72h,B组炎细胞浸润程度明显重于C组(P<0.05),术后12h C组淋巴细胞浸润程度相对B组明显减少(P<0.05),术后7d,脊髓水肿减轻,空洞周围形成胶质瘢痕,胶质瘢痕细胞计数B组明显大于C组(P<0.05),术后21d脊髓空洞形成,脊髓空洞比值B组明显大于C组(P<0.05)。SP免疫组化染色和Tunel染色结果显示A组各时间点几乎见不到caspase-3和细胞凋亡表达阳性细胞,B、C组脊髓损术后6h即可见凋亡细胞,到术后24h达高峰,而后随术后时间延长而逐渐减弱,但是仍然保持在较高水平;caspase-3表达与细胞凋亡同步,各时间点C组caspase-3表达阳性细胞比值和细胞凋亡指数均显著低于B组(P<0.05)。结论:FTY720可以显著改善大鼠ASCI后神经功能,其可能是通过抑制脊髓损伤后的炎症反应,减少caspase-3的表达及神经细胞凋亡,从而减轻脊髓继发性损伤。     

神经毒素在脊髓损伤中的作用

目的 探讨神经毒素兴奋性氨基酸（ＥＡＡ）和神经肽在脊髓损伤的作用。方法 应用高效液相色谱法检测脊髓损伤后伤段组织中谷氨酸（Ｇｌｕ）天门冬氨酸（Ａｓｐ）两种ＥＡＡ的含量变化；应用放射免疫分析技术测定脊髓损伤段组织中神经肽之一强腓肽ＤｙｎＡ１－１３含量的变化；观察了蛛网膜下腔注射Ｇｌｕ，ＤｙａｎＡ１－１３兴奋性氨基酸受体拮抗剂３－（２－羧基哌嗪）丙基－１－磷酸（ＣＰＰ），ＤｙｎＡ１－１３抗血清（Ａｎ－     

The comparison of recovery patterns between ischemic spinal cord injury and traumatic spinal cord injury from acute to chronic phase

Objective: To investigate the neurological and functional recovery patterns of ischemic spinal cord injury (ISCI) compared with traumatic spinal cord injury (TSCI) in the acute to chronic phase.Design: Retrospective cohort study.Settings: Department of Neurology, Neurosurgery, Rehabilitation Medicine at a tertiary hospital.Participants: Fifty-four patients with ISCI and 86 patients with TSCI.Interventions: Not applicable.Outcome measures: MRI findings, American Spinal Injury Association Impairment Scale (AIS), modified Rankin Scale (mRS), Korean Spinal Cord Independence Measure (KSCIM), ambulatory status, and bladder status were reviewed. The functional outcomes were measured at admission, discharge, and >6 months after discharge.Results: AIS classification did not significantly change after 6 months in both ISCI and TSCI groups. Between admission and discharge, the proportion of patients needing a wheelchair or assistive device to ambulate decreased more in the ISCI group compared with the TSCI group [odds ratio (OR) 0.40, P = 0.04]. In addition, the proportion of catheterized voiding in the ISCI group was significantly higher than in the TSCI group at all time points (OR 5.12, P < 0.001). Lastly, both groups showed that functional improvement was the greatest between admission and discharge. In addition, the proportion of catheterized voiding decreased (Diff = −0.12, P = 0.019) and mRS score decreased (Diff=−0.48, P < 0.001) significantly in the ISCI group at >6 months post discharge.Conclusion: The ISCI group showed better recovery of mobility during inpatient rehabilitation period and worse recovery of bladder function as demonstrated by higher number of patients requiring bladder catheterization at all time points when compared with the TSCI group.     

Quercetin promotes functional recovery following acute spinal cord injury

We tested the hypothesis that quercetin, a potent Fe(2+)-chelating flavonoid, would decrease secondary damage following spinal cord trauma. MRI studies using the relaxation of the T1 proton signal caused by Fe(2+) ions and the dose-dependent reversal of this effect by addition of quercetin in aqueous solution were used to guide us to the dosage of quercetin to be used in animal experimentations. Forty-four male Wistar rats were used in two experimental series to test the hypothesis that administration of quercetin improves recovery of motor function after acute traumatic spinal cord injury. Animals were subjected to laminectomy and subjected to an extradural 40-g force clip compression for 5 sec at T7. Quercetin or saline was administered intraperitoneally 1 h after injury and then every 12 hr thereafter. Recovery of motor function was assessed using BBB scores at weekly intervals for 4 weeks. A dose of 2.5 micromoles quercetin/kg body weight did not result in significantly better functional outcome, whereas doses ranging from 5 to 100 micromoles quercetin/kg body weight resulted in a significantly better functional outcome with half or more of the animals walking, although with deficit; in contrast, no animals walked in the group of saline-treated animals. No significant differences in behavioral outcome were seen amongst the doses ranging from 5 to 100 micromol/kg, nor was there a difference if animals were treated for 4 or 10 days. Therapeutic outcome was coincident with more efficient iron clearance, suggesting that one possible mechanism whereby quercetin decreases secondary damage is through iron chelation.     

Association of riluzole and dantrolene improves significant recovery after acute spinal cord injury in rats

Background Context

Damage to the spinal cord can result in irreversible impairment or complete loss of motor, sensory, and autonomic functions. Riluzole and dantrolene have been shown to provide neuroprotection by reducing neuronal apoptosis after brain and spinal cord injury (SCI) in several animal models of neurologic disorders. As these drugs protect the injured spinal cord through different mechanisms, we investigated the cumulative effects of riluzole and dantrolene.

Rapid functional recovery after spinal cord injury in young rats

Responses to traumatic injury in the immature spinal cord may be different from those in adults. We modified an adult model of weight-drop injury to characterize the histopathology and functional recovery after spinal cord injury (SCI) in rat pups at postnatal day 14-15. A 10-g weight was dropped from 2.5 or 5.0 cm at T8-T9. Hindlimb function was evaluated at 24 h and 1, 2, 3, and 4 weeks after injury using the Combined Behavioral Score that estimates overall hind limb sensorimotor function, and the BBB scale for open field locomotion. Histopathology was examined at 15 min, 24 h, and 4 weeks after SCI. The initial hemorrhagic lesion was similar to that seen in adults, but the time course of secondary loss of ventral horn motor neurons was extended. By 4 weeks, only a partial rim of white matter surrounding a central cavity was seen. The 5.0 cm injury group exhibited significantly less recovery of function at 4 weeks than the 2.5 cm group. In the latter, the degree of hindlimb deficit at 4 weeks was similar to that previously described for adults with 10 g x 2.5 cm SCI. However, pups in both injury groups exhibited a significantly faster rate of recovery than adults. Recovery was maximal by 1 week after SCI in pups as compared to 3-4 weeks in adults. The more rapid functional recovery observed in the pups suggests that this new model may be useful for studying mechanisms of functional plasticity after SCI.     

丙戊酸对大鼠急性脊髓损伤后氧化应激的影响

[目的]探讨丙戊酸(VPA)对大鼠脊髓损伤(SCI)后氧化应激的影响。[方法]72只雄性SD大鼠随机分为3组:假手术组(C组)、损伤组(SCI组)和丙戊酸保护组(VPA组)。采用改良的Allen法制作脊髓损伤动物模型。VPA组术后即刻及其后每12 h皮下注射VPA 300 mg/kg至取材;C组和SCI组在相应时间点注射等体积的生理盐水。大鼠在伤后24、48、72 h和1周先行后肢运动功能BBB评分,随后处死取材。通过石蜡切片HE染色观察脊髓组织病理变化,并用免疫组化法检测诱导型一氧化氮合酶(iNOS)的表达;通过化学比色法测定脊髓组织中丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH-Px)的含量。[结果]BBB评分显示C组运动功能未受影响,VPA组的BBB评分均高于SCI组,两者相比在伤后48、72 h和1周差异有显著性(P<0.01)。HE染色示C组脊髓组织形态正常,VPA组各时间点的病理变化与SCI组相比没有明显改善。C组偶见或未见iNOS阳性表达细胞。与C组相比,SCI组和VPA组的iNOS表达均明显增加(P<0.05),在伤后72 h达高峰,但VPA组的iNOS表达在各时间点均明显低于SCI组(P<0.05)。SCI组和VPA组脊髓组织的MDA含量明显高于C组,而GSH-Px活性明显低于C组(P<0.05),VPA组和SCI组相比较,MDA含量在各时间点均明显下降,GSH-Px活性均明显升高(P<0.05)。[结论]VPA通过减轻SCI所诱导的氧化应激,从而对SCI发挥保护作用。     

FTY720对大鼠急性脊髓损伤后RhoA表达的影响

目的观察大鼠急性脊髓损伤(spinal cord injury,SCI)后芬戈莫德(fingolimod,FTY720)对RhoA表达的影响,进一步探讨FTY720治疗SCI的可能机制。方法采用改良Allen’s法建立大鼠急性SCI模型。雌性SD大鼠75只,随机分为假手术组(n=15)、损伤组(n=30)和FTY720组(n=30)。FTY720组伤后30min一次性腹腔注射FTY7200.5mg/kg,假手术组和损伤组以相同方法给予浓度为0.9%的生理盐水。分别于伤后1天、3天、7天、14天及21天,应用RT-PCR和Western印迹法分别检测RhoA mRNA和RhoA蛋白的表达。结果损伤组RhoA mRNA和蛋白的表达于伤后3天开始明显增加,7天达到高峰,21天仍维持高水平表达;在同一时间点,与FTY720组和假手术组比较,差异有统计学意义(P0.05)。FTY720组伤后1天、3天和7天的RhoA表达高于假手术组(P0.05)。假手术组各时间点RhoA表达维持在较恒定水平。结论大鼠急性SCI后RhoA表达增加,FTY720可能通过抑制SCI后RhoA的表达,以达到减轻继发性SCI、促进脊髓神经功能恢复的目的。     

不同时间应用甲基强的松龙对大鼠急性脊髓损伤的作用

目的:观察不同时间应用甲基强的松龙(methylprednisolone,MP)对大鼠急性脊髓损伤的作用,为临床应用MP保护脊髓功能选择用药时间提供理论指导.方法:216只成年SD大鼠,体重190～240g,随机分为假手术组(A组)、脊髓损伤组(B组)、MP治疗组(C组)和MP防治组(D组),每组54只.A组不损伤脊髓.B、C、D组采用改良AUen's法建立脊髓损伤(T8～T9水平)模型,D组术前0.5h静脉注射MP(30mg/kg),C组术后1h静脉注射MP(30mg/kg),C、D组术后6、12、18、24h静脉注射MP(每次31.05mg/kg),A、B组相同时间点予生理盐水0.5ml静脉注射.各组术后24、48、72h采用后肢功能评分障碍率(n=6)及斜板障碍率(n=6)进行脊髓功能评价.B、C、D组术后8、24、48、72h取出损伤段脊髓,A组相同时间点取出相应部位脊髓,切片行光镜(n=6)和电镜(n=6)检查,结果:A、B组组内各时间点后肢功能评分障碍率均无显著性差别(P>0.05),C、D组随时间延长逐渐减小(P<0.05);A组各时间点斜板障碍率及B、D组组内48h和72h比较无显著性差异(P>0.05),而B组、D组组内24h分别与48h、72h比较以及C组组内各时间点比较均有显著性差异(P<0.05);B、C、D组各时间点后肢功能评分障碍率及斜板障碍率均高于A组(P<0.05);24h、48h时C组与B组差异无显著性(P>0.05),而72h时及D组各时间点两者均低于B组(P<0.05);D组72h时斜板障碍率与C组差异无显著性(P>0.05),而72h时后肢功能评分障碍率及24h、48h时两者均低于C组(P<0.05):A组脊髓灰白质交界清楚,神经元丰富,形念清晰;B组损伤脊髓多处出血、坏死,神经元减少,残留细胞内结构模糊,髓鞘板层结构紊乱,并逐渐加重:C组较B组损伤轻,残留细胞内结构稍模糊,24h后逐渐好转;D组较B、C组损伤轻,出血少,细胞器轻度肿胀,24h后肿胀长基本消退.结论:MP能减轻大鼠急性脊髓损伤后的继发性损伤程度,术前半小时开始预防应用MP较单纯术后应用效果更好.     

汉防己甲素对大鼠急性脊髓损伤的作用及意义

目的：探讨汉防己甲素（Tet）对急性脊髓损伤（ASCI）的保护作用及作用机制。方法：81只大鼠随机分为三组：生盐水对照组（NS组）、汉防己甲素治疗组（Tet组）和甲基强松龙治疗组（MP组），每组27只，用加速型Allen′s打击法制成脊髓急性损伤模型，监测大鼠ASCI后及用药后的血压变化，测定损伤区脊髓Ca^2 、MDA含量；采用氢清除法测定脊髓伤区血流量（SCBF）的变化；连续观测6周ASCI后运动功能评分情况，ASCI后4h,8h、6周取伤区标本进行组织病理检查，结果：ASCI后10s各组动物的MABP显著升高，1min内迅速降至正常水平，之后Tet组舒张压，平均动脉明显降低（P＜0．05），而收缩压降低不明显（P＞0．05）；ASCI后SCBF下降，但Tet组和MP组的SCBF较NS组高（P＜0．05）；损伤区Ca^2 及MDA含量Tet组和MP组均较NS组低，神经功能评分均较NS组高。结论：Tet能改善微循环，防止SCBF的减少；抗脂质过氧化损伤，减少脂质过氧化物MDA的生成；减轻Ca^2 的局部积聚，防止钙超载，阻断继发性损伤的链式反应，减轻组织继发性损伤。对实验性急性脊髓损伤有保护作用。