Clinical features of diffuse axonal injury

ＤＤｅｐａｒｔｍｅｎｔｏｆＮｅｕｒｏｓｕｒｇｅｒｙ ,ＦｉｒｓｔＡｆｆｉｌｉａｔｅｄＨｏｓｐｉｔａｌ,ＷｅｓｔＣｈｉｎａＵｎｉｖｅｒｓｉｔｙｏｆＭｅｄｉｃａｌＳｃｉｅｎｃｅｓ ,Ｃｈｅｎｇｄｕ 6 10 0 41,Ｃｈｉｎａ (ＪｉａｎｇＳ ,ＪｕＹ ,ＨｅＭａｎｄＭａｏＢＹ)ＤｅｐａｒｔｍｅｎｔｏｆＦｏｒｅｉｇｎＬａｎｇｕａｇｅｓ ,ＷｅｓｔＣｈｉｎａＵｎｉｖｅｒｓｉｔｙｏｆＭｅｄｉｃａｌＳｃｉｅｎｃｅｓ ,Ｃｈｅｎｇｄｕ 6 10 0 41,Ｃｈｉｎａ (ＨｅＹ)ｉｆｆｕｓｅａｘｏｎａｌｉｎｊｕｒｙ (ＤＡＩ)ｗａｓｔｅｒｍｅｄｆｏｒ…     

Effect of dexamethasone by local treatment on cerebral edema and serum myelin basic protein after brain injury in rabbits

ＳＤｅｐａｒｔｍｅｎｔｏｆＮｅｕｒｏｓｕｒｇｅｒｙ ,ＴｈｅＦｉｒｓｔＡｆｆｉｌｉａｔｅｄＨｏｓｐｉｔａｌ,ＨｅｎａｎＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ ,Ｚｈｅｎｇｚｈｏｕ 45 0 0 5 2 ,Ｃｈｉｎａ (ＹａｎｇＢａｎｄＳｏｎｇＬＪ)ＡｌｂｅｒｔＥｉｎｓｔｅｉｎＣｏｌｌｅｇｅｏｆＭｅｄｉｃｉｎｅｏｆＹｅｓｈｉｖｅＵｎｉｖｅｒｓｉｔｙ ,ＮｅｗＹｏｒｋ ,10 46 1(ＧｕａｎＦＸ)ＴｈｅＰｈｙｓｉｃｓＤｅｐａｒｔｍｅｎｔｏｆＨｅｎａｎＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ ,Ｚｈｅｎｇｚｈｏｕ 45 0 0 5 2 ,Ｃｈｉｎａ (Ｌｉ…     

Anatomic basis of vascularized ulnar nerve graft by the pedicle of the superior collateral ulnar artery

ＩＤｅｐａｒｔｍｅｎｔｏｆＯｒｔｈｏｐｅｄｉｃｓａｎｄＨａｎｄＳｕｒｇｅｒｙ ,ＦｕｊｉａｎＰｒｏｖｉｎｃｉａｌＨｏｓｐｉｔａｌ,Ｆｕｚｈｏｕ 35 0 0 0 1,Ｃｈｉｎａ (ＸｕＪ)ＤｅｐａｒｔｍｅｎｔｏｆＨａｎｄＳｕｒｇｅｒｙ ,ＨｕａｓｈａｎＨｏｓｐｉｔａｌ ,ＳｈａｎｇｈａｉＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ ,Ｓｈａｎｇｈａｉ 2 0 0 0 40 ,Ｃｈｉｎａ (ＧｕＹＤ ,ＬａｏＪ ,ＣｈｅｎｇＸＭａｎｄＤｏｎｇＺ)ｎ 1986ＧｕｉｎｖｅｎｔｅｄｃｏｎｔｒａｌａｔｅｒａｌＣ7ｒｏｏｔｔｒａｎｓｆｅｒｆｏｒｔｒｅａｔｍｅｎｔｏ…     

Treatment of recurrent traumatic carotid cavernous fistula via endovascular embo lism technique

ＥＤｅｐａｒｔｍｅｎｔｏｆＮｅｕｒｏｓｕｒｇｅｒｙ,1ｓｔＡｆｆｉｌｉａｔｅｄＨｏｓｐｉｔａｌ,ＨａｒｂｉｎＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ,Ｈａｒｂｉｎ150001,Ｃｈｉｎａ(ＳｈｉＺＳ,ＬｉｎＣＨ,ＣｈｕＭａｎｄＺｈａｎｇＸＤ)ＤｅｐａｒｔｍｅｎｔｏｆＮｅｕｒｏｓｕｒｇｅｒｙ,1ｓｔＡｆｆｉｌｉａｔｅｄＨｏｓｐｉｔａｌ,ＳｕｎＹａｔｓｅｎＵｎｉｖｅｒｓｉｔｙｏｆＭｅｄｉｃａｌＳｃｉｅｎｃｅ,Ｇｕａｎｇｚｈｏｕ,Ｃｈｉｎａ(ＨｕａｎｇＺＳ,ＱｉＴＷ)ｎｄｏｖａｓｃｕｌａｒｅｍｂｏｌｉｓｍｔｅｃｈｎｉｑｕｅｈａｓ…     

Alterations of bcl—2,bcl—x and bax protein expressions in area CA3 of rat hippocampus following fluid percussion brain injury

Ｉ　ＤｅｐａｒｔｍｅｎｔｏｆＮｅｕｒｏｓｕｒｇｅｒｙ,ＣｈａｎｇｚｈｅｎｇＨｏｓｐｉｔａｌ,ＳｅｃｏｎｄＭｉｌｉｔａｒｙＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ,Ｓｈａｎｇｈａｉ２００００３,Ｃｈｉｎａ（ＬｕｏＣ,ＺｈｕＣ,ＪｉａｎｇＪＹ,ＬｕＹＣ,ＺｈａｎｇＧＪ,ＹｕａｎＧＬ,ＣａｉＲＪ）ＤｅｐａｒｔｍｅｎｔｏｆＰａｔｈｏｌｏｇｙ,ＣｈａｎｇｚｈｅｎｇＨｏｓｐｉｔａｌ,ＳｅｃｏｎｄＭｉｌｉｔａｒｙＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ,Ｓｈａｎｇｈａｉ２００００３,Ｃｈｉｎａ（ＹｅＴＪ）ｎ１９９５,Ｒｉ…     

Schwann cells and fibronectin treating lesioned spinal cord of adult rats

Ｒ　ＤｅｐａｒｔｍｅｎｔｏｆＮｅｕｒｏｓｕｒｇｅｒｙ,ＧｕｌｏｕＨｏｓｐｉｔａｌ,Ｎａｎｊｉｎｇ２１０００８,Ｃｈｉｎａ（ＺｈａｏＹＴ）ＤｅｐａｒｔｍｅｎｔｏｆＮｅｕｒｏｓｕｒｇｅｒｙ,ＦｉｒｓｔＡｆｆｉｌｉａｔｅｄＨｏｓｐｉｔａｌ,ＮａｎｊｉｎｇＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ,Ｎａｎｊｉｎｇ２１００２９,Ｃｈｉｎａ（ＬｉＬＸａｎｄＤａｉＪＣ）ｅｇｅｎｅｒａｔｉｏｎｏｆｌｅｓｉｏｎｅｄａｘｏｎｓｉｎｔｈｅｃｅｎｔｒａｌｎｅｒｖｏｕｓｓｙｓｔｅｍ（ＣＮＳ）ｏｆａｄｕｌｔｍａｍｍａｌｓｉｓｖｅｒ…     

Relationship between changes of N-methyl-D-aspartate receptor activity and brain edema after brain injury in rats

ＩＤｅｐａｒｔｍｅｎｔｏｆＮｅｕｒｏｓｕｒｇｅｒｙ ,ＺｈｕｊｉａｎｇＨｏｓｐｉｔａｌ ,ＦｉｒｓｔＭｉｌｉｔａｒｙＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ ,Ｇｕａｎｇｚｈｏｕ 5 10 2 82 ,Ｃｈｉｎａ (ＸｕＲＸａｎｄＬｕｏＣＹ)ＳｕｐｐｏｒｔｅｄｂｙＮａｔｕｒａｌＳｃｉｅｎｃｅＦｏｕｎｄａｔｉｏｎｏｆＧｕａｎｇｄｏｎｇＰｒｏｖｉｎｃｅ (ＧＤ990 416 )ａｎｄＮａｔｕｒａｌＳｃｉｅｎｃｅＦｏｕｎｄａｔｉｏｎｏｆＣｈｉｎａ(39770 76 0 )ｔｉｓｅｘｐｅｒｉｍｅｎｔａｌｌｙｆｏｕｎｄｔｈａｔｇｌｕｔａｍａｔｅｍａｙｉｎ…     

L—arginine promotes the repair process of endothelium in ischemia—reperfused arteries of rats

ＴＤｅｐａｒｔｍｅｎｔｏｆＢｉｏｐｈｙｓｉｃｓ ,ＳｈａｎｇｈａｉＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ ,Ｓｈａｎｇｈａｉ2 0 0 0 32 ,Ｃｈｉｎａ (ＺｈｏｕＷＸ ,ＪｉａｎｇＪＷ ,ＱｉＬａｎｄＺｈｏｎｇＣＳ)ＤｅｐａｒｔｍｅｎｔｏｆＮｅｕｒｏｂｉｏｌｏｇｙ ,ＳｈａｎｇｈａｉＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ ,Ｓｈａｎｇｈａｉ 2 0 0 0 32 ,Ｃｈｉｎａ (ＳｕｎＡＹ)ＨｕａｓｈａｎＨｏｓｐｉｔａｌ,ＳｈａｎｇｈａｉＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ ,Ｓｈａｎｇｈａｉ2 0 0 0 40 ,Ｃｈｉｎａ (ＧｕＹＤ)Ｔｈｉｓｗｏｒｋ…     

Remote therapeutic effect of early nerve transposition in treatment of obstetric al brachial plexus palsy

ＭＤｅｐａｒｔｍｅｎｔｏｆＯｒｔｈｏｐａｅｄｉｃｓａｎｄＨａｎｄＳｕｒｇｅｒｙ,ＦｕｊｉａｎＰｒｏｖｉｎｃｉａｌＨｏｓｐｉｔａｌ,Ｆｕｚｈｏｕ350001,Ｃｈｉｎａ(ＸｕＪ)ＤｅｐａｒｔｍｅｎｔｏｆＨａｎｄＳｕｒｇｅｒｙ,ＨｕａｓｈａｎＨｏｓｐｉｔａｌ,ＳｈａｎｇｈａｉＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ,Ｓｈａｎｇｈａｉ200040,Ｃｈｉｎａ(ＣｈｅｎｇＸＭ,ＤｏｎｇＺａｎｄＧｕＹＤ)ｏｓｔｐａｔｉｅｎｔｓｗｉｔｈｏｂｓｔｅｔｒｉｃａｌｂｒａｃｈｉａｌｐｌｅｘｕｓｐａｌｓｙ(ＯＢＰＰ)ｃａｎｂｅｅｘｐｅｃｔｅｄｔｏｒ…     

Effect of bactericidal／permeability—increasing protein on sepsis induced by intra—abdominal infection in rats

ＡＲｅｓｅａｒｃｈＩｎｓｔｉｔｕｔｅｏｆＳｕｒｇｅｒｙ,ＤａｐｉｎｇＨｏｓｐｉｔａｌ,ＴｈｉｒｄＭｉｌｉｔａｒｙＭｅｄｉｃａｌＵｎｉｖｅｒｓｉｔｙ,Ｃｈｏｎｇｑｉｎｇ４０００４２,Ｃｈｉｎａ（ＪｉａｎｇＪＸ,ＸｉｅＧＱ,ＬｉｕＤＷ,ＺｈｕＰＦ,ＷａｎｇＺＧ,ＨｅＹＮ,ＺｈｏｕＪＨａｎｄＸｕＨ）ＴｈｉｓｓｔｕｄｙｗａｓｓｕｐｐｏｒｔｅｄｂｙｔｈｅＮａｔｉｏｎａｌＮａｔｕｒａｌＳｃｉｅｎｃｅＦｏｕｎｄａｔｉｏｎｏｆＣｈｉｎａ（Ｎｏ．３９４７０６７８）．ｌｔｈｏｕｇｈｇｒｅａｔａｔｔｅｎｔｉｏｎｈａｓ…     

Association of HIF- expression and cell apoptosis after traumatic brain injury in the rat

Objective: To explore the expression of hypoxia inducible factor-1α (HIF-1~) and the correlation between HIF-1α and apoptosis after traumatic brain injury.Methods: Using experimental traumatic brain injury in the rats, the expression of HIF-1α was studied by immunohisto-chemistry in cerebral tissue, apoptotic cell death was evaluated with TUNEL (transferase-mediated XdUTP nick end labeling ), and double-labeled immunohistochemistry and TUNEL methods were used to investigate the relationship between HIF-1α and apoptosis.Results: There was remarkable difference in the expression of HIF-1α between the experimental groups and the control groups (P ＜ 0.01), in the experimental groups,the expression of HIF-1α at 48 hours was highest; the evidence of apoptotic cell death after experimental traumatic brain injury was found by TUNEL; the apoptotic percentage increased or decreased according to the changes of the positive expression of HIF-1α (r = 0.99).Conclusions: The results suggest that secondary brain ischemia plays a crucial role in apoptotic cell death after traumatic brain injury; HIF-1α can prompt apoptotic cell death after experimental traumatic brain injury.*e expres     

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.     

Sequential changes of hypoxia—inducible factor 1 alpha in experimental spinal cord injury and its significance

Ｔｈｅｈｏｍｅｏｓｔａｓｉｓｏｆｏｘｙｇｅｎｉｓｉｍｐａｉｒｅｄｕｎｄｅｒｔｈｅｃｏｎｄｉｔｉｏｎｓｏｆｃａｒｃｉｎｏｇｅｎｅｓｉｓａｎｄｔｒａｕｍａ.Ｗｈｅｎｈｙｐｏｘｉａｏｃｃｕｒｓ ,ｔｈｅｉｎｔｒｉｎｓｉｃｍａｎｉｐｕｌａｔｉｎｇｍｅｃｈａｎｉｓｍｓａｒｅｉｎｉｔｉａｔｅｄ .Ｈｙｐｏｘｉａｉｎｄｕｃｉｂｌｅｆａｃｔｏｒ(ＨＩＦ)ｌｉｅｓｉｎｔｈｅｋｅｙｐｏｓｉｔｉｏｎｏｆａｄａｐｔａｔｉｏｎｔｏｈｙｐｏｘｉｃｓｔｒｅｓｓ.Ｉｔｓｅｆｆｅｃｔｓｏｎｃａｒｃｉｎｏｇｅｎｅｓｉｓａｎｄｃａｒｄｉｏ …     

Bcl-2 gene therapy for apoptosis following traumatic brain injury

Objective: Toinvestigatethetherapeuticeffect of Bcl-2 fusion protein on apoptosis in brain following traumatic brain injury. Methods: Bcl-2 gene was cloned by RT-PCR. Bcl-2 and EGFP genes were linked together and inserted into pAdeno-X vector. This recombinant vector was packaged into infectious adenovirus in HEK293 cells. Ninety Wistar rats were assigned randomly into experimental group (n=45) and control group (n=45). All rats were subjected to traumatic brain injury. Then recombinant adenovirus (for experimental group) or saline (for control group) was injected into the traumatic brain. The expression of Bcl-2 fusion protein was investigated by Western blotting, immunohistochemistry and fluorescence microscopy. Apoptosis in the injured brain was studied by TUNEL. Animals' behavior capacity was evaluated by tiltboard test. Results: In the experimental group, many fluorescent cells were found around the traumatic locus, which were also proven to be Bcl-2-positive by immunohistochemistry. On the contrary, few Bcl-2-positive cells and no fluorescent cell were detected in the control group. Bcl-2 expression of experimental group was much higher than that of control group, which was illustrated by Western blotting. The apoptosis index of experimental group was 0. 027±0. 005, and that of control group was 0.141±0.025 (P <0.01). Two weeks after injury, animals of the experimental group behaved better than those of the control group. Conclusions: A recombinant adenovirus vector expressing Bcl-2 fusion protein has been constructed. Bcl-2 fusion protein can suppress apoptosis and promote cell survival. Moreover, the behavior recovery of the injured animal is promoted. Bcl-2 fusion protein provides a way to track the target cells in vivo.     

Enhanced bone regeneration associated with decreased apoptosis in mice with partial HIF-1alpha deficiency.

HIF-1alpha activates genes under hypoxia and was hypothesized to regulate bone regeneration. Surprisingly, HIF-1alpha+/- fracture calluses are larger, stronger, and stiffer than HIF-1alpha+/+ calluses because of decreased apoptosis. These data identify apoptosis inhibition as a means to enhance bone regeneration. INTRODUCTION: Bone regeneration subsequent to fracture involves the synergistic activation of multiple signaling pathways. Localized hypoxia after fracture activates hypoxia-inducible factor 1alpha (HIF-1alpha), leading to increased expression of HIF-1 target genes. We therefore hypothesized that HIF-1alpha is a key regulator of bone regeneration. MATERIALS AND METHODS: Fixed femoral fractures were generated in mice with partial HIF-1alpha deficiency (HIF-1alpha+/-) and wildtype littermates (HIF-1alpha+/+). Fracture calluses and intact contralateral femurs from postfracture days (PFDs) 21 and 28 (N=5-10) were subjected to microCT evaluation and four-point bending to assess morphometric and mechanical properties. Molecular analyses were carried out on PFD 7, 10, and 14 samples (N=3) to determine differential gene expression at both mRNA and protein levels. Finally, TUNEL staining was performed on PFD 14 samples (N=2) to elucidate differential apoptosis. RESULTS: Surprisingly, fracture calluses from HIF-1alpha+/- mice exhibited greater mineralization and were larger, stronger, and stiffer. Microarray analyses focused on hypoxia-induced genes revealed differential expression (between genotypes) of several genes associated with the apoptotic pathway. Real-time PCR confirmed these results, showing higher expression of proapoptotic protein phosphatase 2a (PP2A) and lower expression of anti-apoptotic B-cell leukemia/lymphoma 2 (BCL2) in HIF-1alpha+/+ calluses. Subsequent TUNEL staining showed that HIF-1alpha+/+ calluses contained larger numbers of TUNEL+ chondrocytes and osteoblasts than HIF-1alpha+/- calluses. CONCLUSIONS: We conclude that partial HIF-1alpha deficiency results in decreased chondrocytic and osteoblastic apoptosis, thereby allowing the development of larger, stiffer calluses and enhancing bone regeneration. Furthermore, apoptosis inhibition may be a promising target for developing new treatments to accelerate bone regeneration.     

Cerebral apoptosis in severe traumatic brain injury patients: an in vitro, in vivo, and postmortem study

One of the most important recent observations in traumatic brain injury (TBI) relates to the potential role of apoptosis in secondary brain injury. We aimed to analyze the presence of apoptosis and the expression of apoptosis-related proteins in brain samples from patients with TBI. We also tried to find any association between the in situ results and the in vitro observations in a neuronal model of induced-apoptosis. Brain tissue from the pericontusional zone (PCZ) of patients with traumatic contusions and from post-mortem samples was analyzed. Immunohistochemical analyses of apoptosis-related proteins and the terminal deoxynucleotide transferase-mediated nick end labeling (TUNEL) method to determine the presence of apoptotic cells were performed. Apoptotic rates on neuronal cells induced by jugular bulb vein sera was determined by flow cytometry. TUNEL-positive cells were detected in all PCZ of traumatic contusions and in most of PCZ in post-mortem specimens (none in control; p = 0.026). In vivo samples showed higher expression of antiapoptotic proteins Bcl-2 (p = 0.027) and Bcl-XL (p = 0.014) than post-mortem samples. In autopsies, the expression of Fas and Bim (p < 0.05) were higher in PCZ than in the zone distal from the contusion. In vitro studies showed that apoptotic rate was an independent factor associated with mortality at 6 months (p = 0.014). In the receiving operator curve (ROC) curve, a cut-off point of 66.5% showed a sensitivity of 89.5% and specificity of 66.7% in the prediction of patients' death. Cerebral apoptosis is a prominent form of cell death in the PCZ of human traumatic cerebral contusions, and high rates of in vitro apoptosis are associated with a poorer prognosis after TBI.     

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。     

纳洛酮对大鼠颅脑损伤后神经细胞凋亡的影响

目的　探讨纳络酮对大鼠颅脑损伤后神经细胞凋亡的影响。方法　采用Feeney氏自由落体法制备脑损伤动物的模型 ,将 90只大鼠随机分为实验组及对照组 ,于伤后 1 5、60min及2 4h分别给予纳洛酮或 0 .9%氯化钠溶液 ,伤后第 5天断头处死大鼠 ,采用原位末端脱氧核苷酸生物素末端标记 (TUNEL)法测定神经细胞原位凋亡情况 ,并用光镜观察细胞形态学改变。结果　与对照组比较 ,大鼠脑损伤后 1 5及 60min应用纳洛酮可明显减少神经细胞凋亡 ,而伤后 2 4h给药 ,则两组神经细胞的凋亡率差异无显著性 (P >0 .0 5)。结论　早期应用大剂量纳洛酮可明显减少脑损伤后神经细胞的凋亡 ,从而可有效地保护神经细胞功能     

大鼠脊髓损伤中的细胞凋亡及甲基强的松龙的干预作用

目的：探讨脊髓损伤（SCI）继发损伤机制,研究损伤脊髓细胞的凋亡及其意义,观察甲基强的松龙（MP）对细胞凋亡的影响。方法：使用改良Allen法制作大鼠急性SCI模型,实验分3组,假损伤（脊髓未受打击）,损伤组及MP治疗组,采用HE,荧光Hoechst 33342,TUNEL(末端脱氧核苷转移酶介导的脱氧尿苷三磷酸生物素缺口末端标记技术）等技术观察SCI后4h,8h,3d,7d,14d,21d及28d时损伤中心及邻近节段脊髓细胞的凋亡,治疗组损伤后30min给予大剂量MP,比较MP治疗组与损伤组脊髓细胞凋亡的变化,同时平行观察大鼠神经学和组织学恢复情况及两组神经丝蛋白（NF）含量的变化。结果：假损伤组各检测方法未见脊髓细胞凋亡,损伤组大鼠急性SCI后1d开始出现脊髓细胞凋亡,3d达高峰,自损伤中心向头尾端递减分布,持续21d,MP治疗组在伤后3d及7d凋亡脊髓细胞较损伤组显著减少,神经学恢复及组织学评分较损伤组有显著性提高,结论：凋亡是SCI后脊髓神经元死亡的一种重要方式,在继发性损伤中起极为重要的作用。MP的治疗作用可能与其干预SCI后细胞凋亡有关。