Spatial and temporal profile of apoptosis following lateral fluid percussion brain injuury

OBJECTIVE: To investigate the spatial and temporal profile of neural cell apoptosis following traumatic brain injury (TBI). METHODS: In addition to morphological evidence of apoptosis, TUNEL histochemistry assay was used to identify DNA fragmentation in situ at both light and electron microscopic levels, whereas characteristic internucleosomal DNA fragmentation of apoptosis was demonstrated by DNA gel electrophoresis. RESULTS: Using TUNEL method, we detected massive cells with extensive DNA fragmentation in different regions of the brains of rats subjected to experimental traumatic brain injury. Compared with the sham controls, in the injured cortex, the apoptotic cells were detectable for up to 24 h and reached a peak at 1 week after injury. The number of apoptotic cells in the white matter h ad a significant increase as early as 12 h after injury and peaked at 1 wee k. The number of apoptotic cells increased in the hippocampus at 72 h, whereas i n the thalamus, the peak of apoptotic cells was at 2 weeks after injury. The number of apoptotic cells in most regions returned to sham values 2 months after in jury. Gel electrophoresis of DNA extracted from affected areas of the injured br ain revealed only internucleosomal fragmentation at 185-bp intervals, a feature originally described in apoptotic cell death. And no DNA ladder was detectable in the cortex and hippocampus contralateral to the injured hemisphere. CONCLUSIONS: These data suggest that in addition to the well described necrotic cell death, a temporal course of apoptotic cell death is initiated after brain trauma in selected brain regions.     

Treatment window for hypothermia in brain injury.

OBJECT: The goal of this study was to evaluate the therapeutic window for hypothermia treatment following experimental brain injury by measuring edema formation and functional outcome. METHODS: Traumatic brain injury (TBI) was produced in anesthetized rats by using cortical impact injury. Edema was measured in the ipsilateral and contralateral hemispheres by subtracting dry weight from wet weight, and neurological function was assessed using a battery of behavioral tests 24 hours after TBI. In injured rats, it was found that brain water levels were elevated at I hour postinjury, compared with those in sham-injured control animals, and that edema peaked at 24 hours and remained elevated for 4 days. Hypothermia (3 hours at 30 degrees C) induced either immediately after TBI or 60 minutes after TBI significantly reduced early neurological deficits. Delay of treatment by 90 or 120 minutes postinjury did not result in this neurological protection. Immediate administration of hypothermia also significantly decreased the peak magnitude of edema at 24 hours and 48 hours postinjury, compared with that in normothermic injured control animals. When delayed by 90 minutes, hypothermia did not affect the pattern of edema formation. CONCLUSIONS: When hypothermia was administered immediately or 60 minutes after TBI, injured rats showed an improvement in functional outcome and a decrease in edema. Delayed hypothermia treatment had no effect on functional outcome or on edema.     

Changes of evoked potentials and evaluation of mild hypothermia for treatment of severe brain injury

ＣＤｅｐａｒｔｍｅｎｔｏｆＮｅｕｒｏｓｕｒｇｅｒｙ,ＴｈｅＦｉｒｓｔＡｆｆｉｌｉａｔｅｄＨｏｓｐｉｔａｌｏｆＣｈｏｎｇｑｉｎｇＵｎｉｖｅｒｓｉｔｙｏｆＭｅｄｉｃａｌＳｃｉｅｎｃｅｓ,Ｃｈｏｎｇｑｉｎｇ400016,Ｃｈｉｎａ(ＹａｎＹａｎｄＴａｎｇＷＹ)ｅｒｅｂｒａｌｉｓｃｈｅｍｉａｉｎｐａｔｉｅｎｔｓｗｉｔｈａｃｕｔｅｓｅｖｅｒｅｂｒａｉｎｉｎｊｕｒｙｉｓｔｈｅｍａｊｏｒｃａｕｓｅｏｆｓｅｃｏｎｄａｒｙｂｒａｉｎｄａｍａｇｅ.1Ｍｉｌｄｈｙｐｏｔｈｅｒｍｉａｍａｙｌｉｍｉｔｉｓｃｈｅｍｉｃｄａｍａｇｅｂｙ…     

Role of Caspase 3 in neuronal apoptosis after acute brain injury

OBJECTIVE: To analyze the role of Caspase 3 in neuronal apoptosis after acute brain injury. METHODS: Experiments were carried out with rat diffuse brain trauma model. The neuronal DNA injury in cortex and hippocampus was observed by TUNEL stain. The mRNA and protein expressions and enzyme activation of Caspase 3 were observed by Northern blot, in situ hybridization, immunohistochemistry stain and Western blot, respectively. Special Caspase 3 enzyme inhibitor was used to observe the therapeutic effect. RESULTS: TUNEL positive neurons appeared 2 hours after severe trauma, peaked at 1 day and lasted for 7 days. Northern blot showed that the Caspase 3 mRNA expression was increased and peaked at 1 day, about twice higher than the control. In the area of cortex and hippocampus, positive mRNA staining neurons appeared most distinct on one day. With the antibody for Caspase 3 P20 subunit, the active Caspase 3 expression peaked at 1-3 days. The electrophoresis band of PARP degradation would be seen by Western blot. Caspase 3 enzyme inhibitor could reduce apoptotic neuronal death without any effect on Caspase 3 P20 subunit expression. CONCLUSIONS: After brain trauma, Caspase 3 mRNA and protein expressions and enzyme activation are enhanced in combination with neuronal apoptosis. Special Caspase 3 enzyme inhibitor can apparently decrease the neuronal apoptosis.     

复合膳食纤维对重型颅脑损伤大鼠肠屏障的保护作用

目的:研究膳食纤维对重型颅脑损伤大鼠肠屏障的保护作用。方法:Wistar 大鼠,致重型颅脑损伤,随机分为盐水组、能全力组、膳食纤维组,分别在伤后6、12、24、48、72h 活杀动物,另设正常对照组,取小肠回盲部在光镜下观察其病理形态变化,取门静脉血测血浆微量内毒素的变化,取腹主动脉血测血浆二胺氧化酶、D-乳酸的变化。结果:①致伤后各组肠粘膜组织结构受损,内毒素、二胺氧化酶、D-乳酸值明显高于对照组,伤后12～24h 最显著,至72h 不能恢复;②早期添加膳食纤维,伤后48h 对上述各观察指标有明显改善,加能全力48h 后有改善作用。结论:早期添加单纯膳食纤维作为肠内营养制剂对重型颅脑损伤大鼠肠屏障有保护作用。     

P53 gene transfer to the injured rat carotid artery promotes apoptosis

BACKGROUND: In a previous study we have demonstrated significant reduction of intimal hyperplasia after adenovirus-mediated gene transfer of p53 protein to the injured rat carotid artery. The purpose of this study was to elucidate whether apoptosis is one of the mechanisms responsible for this reduction. Apoptosis, a physiologic cell death process that stabilizes cell numbers in tissues, can be independently induced by p53. METHODS: In vivo gene transfer was used in isolated segments of balloon-injured rat carotid arteries. Genetically modified adenovirus encoding for wild-type p53 protein (AdWTp53) was applied at 8 x 10(10) plaque-forming units/mL. Control rats received either adenovirus null at the same concentration or balloon injury alone. Arteries were harvested at 24 and 48 hours after the procedure. Apoptosis was detected in tissue sections by in situ terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay. Specimens were graded either negative or positive less than 10%, 10% to 20%, 20% to 30%, or greater than 30% according to the number of apoptotic cells in the medial or intimal layer per high power field. Specimens were also subjected to DNA agarose gel electrophoresis and transmission electron microscopy. RESULTS: With the TUNEL assay no apoptosis was visualized at 24 and 48 hours in the controls (n = 5 in each group), whereas in the AdWTp53 groups (n = 5 in each) all specimens presented apoptosis (P < .05, AdWTp53 vs controls). The average grade of apoptotic cells detected in the medial layer in the AdWTp53 groups was less than 10% to 20% at 24 hours and 20% to 30% at 48 hours. The DNA agarose gel electrophoresis failed to detect a DNA laddering pattern, characteristic of apoptosis. Electron microscopy revealed morphologic changes typical of apoptosis in the treated group, whereas specimens from control group did not reveal any apoptotic features. CONCLUSIONS: At 48 hours after balloon injury alone, no apoptosis was observed in the vessel wall. However, when p53 gene was transferred, apoptosis was visualized in all specimens with greater intensity at 48 hours after injury. Promotion of apoptosis may play a key role in the mechanism by which p53 gene decreases intimal hyperplasia.     

反义bax对创伤后神经元的保护作用

目的 观察bax反义寡核苷酸对创伤后迟发性神经元死亡的疗效。方法 在自由落体打击大鼠弥漫性脑创伤模型中转染反义寡核苷酸药物，以大鼠神经功能行为评分及脱氧核糖核酸末端转移酶介导的缺口末端标记法(TUNEL)检测大鼠脑皮层神经元DNA损伤情况作为治疗评价；用原位杂交、免疫组织化学法对bax在mRNA与蛋白质水平表达变化进行观察。结果 大鼠打击后。神经功能行为评分下降，皮层打击区出现神经元凋亡现象。脑组织中持续表达高水平的bax，mRNA及蛋白。脑创伤后bax mRNA及蛋白表达进一步增加。bax反义寡核苷酸转染后的大鼠，神经功能评分明显改善，神经元凋亡数量明显减少。明显抑制因创伤诱发的bax蛋白表达增加。结论 细胞凋亡在创伤性脑损伤中起重要作用，对创伤后神经功能的缺损有重要影响，因而抑制脑创伤后细胞凋亡的发生可能成为治疗创伤性脑损伤后迟发性神经元死亡的新途径。     

Multiple immunostaining methods to detect traumatic axonal injury in the rat fluid-percussion brain injury model

Immunohistochemistry using beta-amyloid precursor protein (APP) N-terminus antibodies is routinely used to detect traumatic axonal injury (TAI). The temporal and regional distributions of APP C- and N-terminus immunoreactivity were investigated in rats with experimental brain injury and compared to distribution of neurofilament (NF) immunoreactivity. Male Sprague-Dawley rats underwent right lateral fluid-percussion (FP) brain injury or sham injury. Six FP injury rats and two control rats were transcardially fixed with 10% formalin at 1, 6, 24, and 48 hours, and 1 and 2 weeks after injury and serial 6 microm-thick paraffin sections were prepared. At 6 hours after injury, APP C-terminus immunostaining labeled small neurons and axonal deposits in the injured parasagittal cortex, striatum, thalami, and dorsal medulla, whereas APP N-terminus and NF immunostaining showed few axonal deposits in the parasagittal cortex. At 24-48 hours post-injury, marked axonal damage, including axonal swelling and bulbs, was observed in the injured cerebral hemisphere, cerebellar white matter, and medulla. NF immunostaining was most sensitive for axonal damage in the injured deep cortical layers, cerebellum, and medulla. At 1-2 weeks after injury, APP N-terminus immunostaining mainly showed dot-like axonal profiles in the injured thalamus. APP C-terminus immunoreactivity may serve as an early marker of TAI, and the C-terminal fragments of APP may be involved in the evolution of TAI because C-terminal fragments of APP are neurotoxic and pro-apoptotic. Multiple immunostaining methods may be required to fully recognize the extent of TAI.     

Effects of delayed, prolonged hypothermia on the pial vascular response after traumatic brain injury in rats

OBJECT: In the experimental setting, hypothermia has been demonstrated to attenuate the damaging consequences of stroke and traumatic brain injury (TBI). Laboratory studies of TBI have focused primarily on the use of early hypothermic intervention, with little consideration of the potential efficacy of more delayed but prolonged hypothermia, which would constitute a more clinically relevant approach. In this investigation, the authors evaluated whether delayed, prolonged hypothermia after TBI protected the cerebral microcirculation. METHODS: Male Sprague-Dawley rats were equipped with cranial windows for direct visualization of the pial arterial circulation and then subjected to impact-acceleration brain injury. The rats were randomly divided into four experimental groups: Group 1 consisted of normothermic animals; in Group 2 the rats received a 1-hour period of hypothermia (32 degrees C) 30 minutes posttrauma, followed by slow rewarming (32-37 degrees C/90 minutes); and in Groups 3 and 4 the rats received a more delayed induction (at 1 hour postinjury) of either 1 hour (Group 3) or 2 hours (Group 4) of hypothermia, followed by the slow rewarming. The pial arteriolar responses to acetylcholine (ACh) or hypercapnia were measured until up to 6 hours postinjury. With this approach the authors found that the normothermic group demonstrated severely impaired vasoreactivity in terms of ACh-dependent dilation and CO2 reactivity in comparison to baseline values (p < 0.001). In contrast, hypothermia of short duration that was initiated early (30 minutes postinjury) conferred significant cerebrovascular protection (p < 0.001), yet this protection was reduced when the onset of this 1-hour hypothermic period was postponed to 1 hour postinjury. Nevertheless, reduced protection could be significantly improved (p < 0.001) with prolongation of the hypothermic period to 2 hours. CONCLUSIONS: The results of this study show that early as well as delayed but prolonged hypothermia attenuate the impaired vascular responsiveness seen after TBI, indicating the potential clinical usefulness of this treatment.     

脑损伤后不同时间给予高渗盐-羟乙基淀粉液的治疗效应

目的探讨在创伤性脑损伤后不同时间给予高渗盐-羟乙基淀粉液(HSH)对脑损伤的影响。方法选用SD大鼠64只,采用Feeney自由落体损伤模型,于伤后早期(伤后10min)和后期(伤后6h)分别经尾静脉注射HSH、生理盐水(4mg/kg),并据此分为四组,24h后处死动物,干湿重法测定脑组织含水量,伊文氏兰(EB)测定对血脑屏障的影响及应用流式细胞仪测定各组对损伤区周围皮质调亡的影响。结果伤后10minHSH10组的脑组织含水量和EB含量略高于NS10组,而皮层脑细胞调亡数明显低于NS10组(P<0.05);伤后6hHSH6组的脑组织含水量、EB含量和皮层脑细胞调亡数均明显低于NS6组(P<0.05);HSH6组的脑组织含水量、EB含量和皮层脑细胞调亡数均明显低于HSH10组(P<0.05)。结论脑损伤早期给予HSH会加重脑水肿,伤后6h给予HSH不会加重脑水肿;无论伤后早期还是晚期给予HSH均可减少皮层脑细胞调亡数,晚期给药效果更佳。     

大剂量甲基强的松龙对大鼠慢性压迫性脊髓损伤后神经细胞凋亡影响的实验研究

目的:观察大剂量甲基强的松龙对大鼠慢性压迫性脊髓损伤后神经细胞凋亡及神经功能恢复的影响。方法:将60只同龄Wistar大鼠,置入后路渐进式压迫装置,制作成中度慢性压迫性脊髓损伤模型。随机分为大剂量甲基强的松龙治疗组(A组,30只)和单纯慢性压迫性脊髓损伤组(B组,30只)。应用原位末端脱氧核糖核苷酸转移酶介导dUTP标记(TUNEL)技术,分别于慢性压迫性脊髓损伤后1、3、7、14、28d对脊髓损伤区进行细胞凋亡检测。结果:A、B两组均发现细胞凋亡,两组细胞凋亡率比较,差异有显著性(P<0.01和0.05)。治疗组细胞凋亡的减少与神经功能的恢复相一致。结论:慢性压迫性脊髓损伤可导致细胞凋亡,大剂量甲基强的松龙对神经细胞凋亡可起到抑制作用。     

反义p53对创伤后神经元的保护作用

目的 观察p53反义寡核苷酸对创伤后迟发性神经元死亡的防治效果。方法在自由落体打击大鼠弥漫性脑创伤模型中,转染反义寡核苷酸药物,以大鼠神经功能行为评分及Tunel法检测鼠脑皮层神经元DNA损伤情况作为疗效评价指标;用原位杂交、免疫组化法检测p53 mRNA与蛋白质的表达水平。结果大鼠打击后,神经功能行为评分下降,皮层打击区伤后1周内出现神经元凋亡现象。脑创伤后2～4h p53 mRNA及蛋白表达增加。p53反义寡核苷酸转染后的大鼠,神经功能评分明显改善;神经元凋亡数量明显减少;p53 mRNA及蛋白表达减少。结论细胞凋亡在创伤性脑损伤中起重要作用,对创伤后神经功能的缺损有重要影响;反义p53抑制脑创伤后细胞凋亡的发生可能成为治疗创伤性脑损伤后迟发性神经元死亡的新途径。     

Cell-specific upregulation of survivin after experimental traumatic brain injury in rats

In this study, we examined the expression and cellular localization of survivin and proliferating cell nuclear antigen (PCNA) after controlled cortical impact traumatic brain injury (TBI) in rats. There was a remarkable and sustained induction of survivin mRNA and protein in the ipsilateral cortex and hippocampus of rats after TBI, peaking at five days post injury. In contrast, both survivin mRNA and protein were virtually undetectable in craniotomy control animals. Concomitantly, expression of PCNA was also significantly enhanced in the ipsilateral cortex and hippocampus of these rats with similar temporal and spatial patterns. Immunohistochemistry revealed that survivin and PCNA were co-expressed in the same cells and had a focal distribution within the injured brain. Further analysis revealed a frequent co-localization of survivin and GFAP, an astrocytic marker, in both the ipsilateral cortex and hippocampus, while a much smaller subset of cells showed co-localization of survivin and NeuN, a mature neuronal marker. Neuronal localization of survivin was observed predominantly in the ipsilateral cortex and contralateral hippocampus after TBI. PCNA protein expression was detected in both astrocytes and neurons of the ipsilateral cortex and hippocampus after TBI. Collectively these data demonstrate that the anti-apoptotic protein survivin, previously characterized in cancer cells, is abundantly expressed in brain tissues of adult rats subjected to TBI. We found survivin expression in both astrocytes and a sub-set of neurons. In addition, the expression of survivin was co-incident with PCNA, a cell cycle protein. This suggests that survivin may be involved in regulation of neural cell proliferative responses after traumatic brain injury.     

低温联合地塞米松对大鼠睾丸扭转复位后eNOS表达及生精细胞凋亡的影响

目的:探讨低温联合地塞米松对睾丸扭转复位后的保护作用,以及对eNOS表达及生精细胞凋亡的影响。方法:将80只青春期SD大鼠随机分为4组,每组20只。4组大鼠分别扭转左侧睾丸720°2 h,建立单侧睾丸扭转模型,随后各组做如下处理,A组:常温+生理盐水、B组:低温+生理盐水、C组:低温+地塞米松、D组:常温+地塞米松;术后48 h采集睾丸,通过HE染色光镜观察睾丸组织病理学改变、免疫组化法检测eNOS表达、TUNEL法检测睾丸生精细胞凋亡。结果:HE染色光镜下见4组大鼠扭转侧睾丸组织均有不同程度损伤,其中A组睾丸损伤最明显,其余3组扭转侧睾丸得到不同程度保护;睾丸组织eNOS免疫组化检测结果:A组扭转侧(左侧)睾丸组织阳性细胞数及阳性细胞着色强度明显强于B、C、D 3组,差异具有显著性(P<0.05、P<0.01、P<0.01);凋亡细胞染色:细胞核呈深棕黄色或棕褐色,A组扭转侧(左侧)睾丸可见大量生精细胞凋亡,凋亡指数AI(31.12±4.68)明显高于B组(16.58±6.22)(P<0.05)及C(8.60±1.15)、D组(13.52±3.06)(P<0.01)。结论:睾丸扭转复位后的缺血再灌注损伤可导致生精细胞凋亡增加、睾丸生殖能力下降;应用低温联合地塞米松能显著增强睾丸组织的抗损伤能力,较好地保护了扭转复位后睾丸的生精功能。     

Cognitive impairment and synaptosomal choline uptake in rats following impact acceleration injury

Traumatic brain injury is well known to cause deficits in learning and memory, which typically improve with time. Animal studies with fluid percussion or controlled cortical impact injury have identified transient disturbances in forebrain cholinergic innervation which may contribute to such cognitive problems. This study examines the extent to which water maze performance and forebrain synaptosomal choline uptake are affected one week after injury using the newly developed impact acceleration injury model. Injury or sham injury was delivered to adult male Sprague-Dawley rats under halothane anesthesia using a 500-g 2.1-m weight drop. Based on righting reflex, injured rats were divided into moderate (< or = 12 min) or severe (>12 min) groups. Water maze testing was performed on days 5-7 postinjury. On day 7, choline uptake was determined in synaptosomes from hippocampus, a parietal cortex, and entorhinal cortex. Maze learning was severely impaired in the severe injury group but not in the moderate injury group. Learning retention was slightly impaired in the moderate injury group and severely affected in the severe injury group. There was a very strong correlation between the severity of injury as determined by prolongation of righting times and disruption of maze learning at 1 week postinjury. There was no change in synaptosomal choline uptake in any of the forebrain regions in the severe injury group, but a slight (14%) decrease in the hippocampus and parietal cortex of the moderate injury group. Correlation analysis showed no relationship between synaptosomal choline uptake in any brain region and performance in either water maze learning or retention. This study shows that the impact acceleration model produces cognitive impairments equivalent to those seen with fluid percussion injury and controlled cortical impact. Compared with those models, the impact acceleration model does not produce a similar disruption of forebrain cholinergic nerve terminals.     

Neuroprotective effects of citicoline on brain edema and blood-brain barrier breakdown after traumatic brain injury

OBJECT: Cytidine 5'-diphosphocholine (CDPC), or citicoline, is a naturally occurring endogenous compound that has been reported to provide neuroprotective effects after experimental cerebral ischemia. However, in no study has such protection been shown after traumatic brain injury (TBI). In this study the authors examined the effect of CDPC on secondary injury factors, brain edema and blood-brain barrier (BBB) breakdown, after TBI. METHODS: After anesthesia had been induced in Sprague-Dawley rats by using 1.5% halothane, an experimental TBI was created using a controlled cortical impact (CCI) device with a velocity of 3 m/second, resulting in a 2-mm deformation. Four sham-operated control animals used for brain edema and BBB breakdown studies underwent the same surgical procedure, but received no injury. Brain edema was evaluated using the wet-dry method 24 hours postinjury, and BBB breakdown was evaluated by measuring Evans blue dye (EBD) extravasation with fluorescein 6 hours after TBI. The animals received intraperitoneal injections of CDPC (50, 100, or 400 mg/kg two times after TBI [eight-10 animals in each group]) or saline (eight animals) after TBI. Traumatic brain injury induced an increase in the percentage of water content and in EBD extravasation in the injured cortex and the ipsilateral hippocampus. No significant benefit from CDPC treatment was observed at a dose of 50 mg/kg. Cytidine 5'-diphosphocholine at a dose of 100 mg/kg attenuated EBD extravasation in both regions, although it reduced brain edema only in the injured cortex. In both regions, 400 mg/ kg of CDPC significantly decreased brain edema and BBB breakdown. CONCLUSIONS: This is the first report in which dose-dependent neuroprotective effects of CDPC have been demonstrated in the injured cortex as well as in the hippocampus, a brain region known to be vulnerable to injury, after experimental TBI. The results of this study suggest that CDPC is an effective neuroprotective agent on secondary injuries that appear following TBI.     

Study on cognition disorder and morphologic change of neurons in hippocampus area following traumatic brain injury in rats

Ｃｏｇｎｉｔｉｖｅｄｅｆｉｃｉｔｓｏｆｌｅａｒｎｉｎｇａｎｄｍｅｍｏｒｙａｒｅｔｈｅｍｏｓｔｅｎｄｕｒｉｎｇａｎｄｄｉｓａｂｌｉｎｇｓｅｑｕｅｌａｏｆｈｕｍａｎｔｒａｕｍａｔｉｃｂｒａｉｎｉｎｊｕｒｙ (ＴＢＩ) .Ｔｈｅｃｏｇｎｉｔｉｖｅｆｕｎｃｔｉｏｎｏｆｌｅａｒｎｉｎｇａｎｄｍｅｍｏｒｙｉｓｏｎｅｏｆｔｈｅｅｓｓｅｎｔｉａｌｂｒａｉｎｆｕｎｃｔｉｏｎｓｆｏｒｐｅｏｐｌｅ ｓｌｉｆｅ ,ｗｈｉｃｈｄｅｖｅｌｏｐｓｉｎｔｈｅｈｉｐｐｏｃａｍｐｕｓ .Ｈｏｗｅｖｅｒ ,ｔｈｅｒｅｉｓｌｉｔｔｌｅｋｎｏｗｌｅ…     

Acute brain edema in fatal head injury: analysis by dynamic CT scanning

Dynamic computerized tomography (CT) was performed on 42 patients with acute head injury to evaluate the hemodynamics and to elucidate the nature of fatal diffuse brain bulk enlargement. Patients were divided into two groups according to the outcome: Group A included 17 nonfatally injured patients, eight with acute epidural hematomas and nine with acute subdural hematomas; Group B included 25 fatally injured patients, 16 with acute subdural hematomas and nine with bilateral brain bulk enlargement. Remarkable brain bulk enlargement could be seen in all fatally injured patients with acute subdural hematoma. In 29 (69%) of 42 patients, dynamic CT was performed within 2 hours after the impact. In the nonfatally injured patients with brain bulk enlargement, dynamic CT scans suggested a hyperemic state. On the other hand, in 17 (68%) of the 25 fatally injured patients, dynamic CT scans revealed a severely ischemic state. In the fatally injured patients with acute subdural hematoma, CT Hounsfield numbers in the enlarged hemisphere (hematoma side) were significantly lower than those of the opposite side (p less than 0.001). Severe diffuse brain damage confirmed by follow-up CT scans and uncontrollable high intracranial pressure were noted in the fatally injured patients. Brain bulk enlargement following head injury originates from acute brain edema and an increase of cerebral blood volume. In cases of fatal head injury, acute brain edema is the more common cause of brain bulk enlargement and occurs more rapidly than is usually thought.     

Changes of metabotropic glutamate receptor subtype 1a in diffuse brain injury with secondary brain insults and the effects of 2-methyl-4-carboxyphenylglycine

Secondarybraininsults (SBI) ,firstlyputforwardbyMillerin 1978,indicatesthatsecondaryfactorssuchashypotensionandpyrexiafollowingprimarybraininjurycouldfurtheraggravatebraininjury .Researchesonithavebeengoingonandhavebecomehotpointinrecentyears .Headinjuryincombinationwithhypotensionresultingfromhemorrhagefromviscerainjuryinmultipletraumahasincreasedmortalityandmorbidity .1,2 However,developmentalmechanismofSBIafterdiffusebraininjury (DBI)isseldomstudied .OurpreviousresearchesshowedthatinDB…     

白细胞介素-10对大鼠脊髓损伤后神经细胞凋亡的影响

目的 观察白细胞介素-10(IL-10)对大鼠脊髓损伤(SCI)后脊髓细胞凋亡的影响,探讨IL-10对脊髓损伤的保护作用。方法 将SD大鼠随机分为3组:单纯SCI组(A组)、IL-10治疗组(B组)及假损伤组(Sham组)。除Sham组不致伤脊髓外,A、B两组应用改良的Allen打击法制作大鼠急性 SCI模型,B组大鼠于 SCI后 30 min腹腔注射 10 μg IL-10,再分别于伤后 12、24、48 h、4、8、16和 24 d应用苏木素-伊红(HE)染色、原位末端脱氧核糖核苷酸转移酶介导的脱氧尿苷三磷酸生物素缺口末端标记技术(TUNEL检测法)及开放野行为评分(BBB评分)观察IL-10治疗后脊髓细胞凋亡的变化及神经功能的恢复情况。结果 假损伤组未见凋亡细胞。A组大鼠伤后 12 h即可见零星的凋亡细胞,至 24 h渐增多,伤后 48 h脊髓组织凋亡细胞率达峰值。B组伤后 24、48 h及4d细胞凋亡率比单纯SCI组明显减少,差异具有显著性(P<0.01或P<0.05)。B组脊髓功能恢复亦比A组有明显提高(P<0.05)。结论 SCI后早期应用IL-10可抑制大鼠脊髓细胞凋亡,从而对脊髓损伤起到保护作用。