Experimental study of the delayed axonal damages and demyelination in the rat spinal cord after continuous epidural compression

连续硬膜外压迫大鼠脊髓迟发性轴索损伤和脱髓鞘的实验研究

• 批准号: 11671399
• 负责人: IIZUKA Hideaki
• 金额: $ 1.09万
• 依托单位: KANAZAWA MEDICAL UNIVERSITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671399/
• 关键词: compressive myelopathy; demyelination; axonal degeneration; apoptosis; 圧泊性脊髄症

We studied experimentally using a spinal cord continuous compression model in rats to analyze the mechanism of chronic compression myelopathy. The rat thoracic spinal cord was epidurally pressured continuously with uterine-cervical dilator Dilapan, which has the character of slow expanding. The lesions were investigated morphologically, by histochemistry, electron microscopy, immunohistochemistry, as well as conventional histology for 1 days to 3 months..Histologically, in acute stage (within 7 days), mildly necrotic changes of the spinal cord occurred, mostly localized in the pressured sites, however, no apparent hemorrhagic necrosis was observed. In the white matter, edema but not destructive changes were seen at 24 hours. The spongy change with axonal degeneration was prominent for 1-2 weeks, which were not localized at the compression site but distributed diffusely in the white matter, continuing for 3 months later. Histochemistry disclosed that the spongy change of white matter wa … More s associated with decrease of axons and myelin 2 weeks later. EM examinations demonstrated that main change in the lateral column was degeneration of axon of myelinated fibers, such as edematous swelling, myelintangles, detachment from myelin sheath, and demyelinated axons. These axonopathy and demyelinating changes had been continuously seen as long as 3 months. Immunnohistochemistry using monoclonal antibody, APC (Ab-7), specific antibody against oligodendrocytes, showed the decrease of the cell number after 1-week compression, and most prominent at 2-4 weeks. Furthermore, by TUNEL examination, TUNEL positive cells were observed in the white matter at 24-48 hours with peak at 72 hours.Tease results indicate that our experimental model is suitable for the analysis of chronic compression myelopathy. The continuous axonopathy with demyelinating changes occurred in the white matter may be the main changes in compression myelopathy. Oligodendrocyte damage, probably due to apoptotic cell death, may cause demyelination of the remaining after continuous compression. Less

本实验采用大鼠脊髓持续压迫模型，探讨慢性压迫性脊髓病的发病机制。用具有缓慢扩张特性的子宫颈扩张器Dilapan对大鼠胸段脊髓持续加压。通过组织化学、电子显微镜、免疫组织化学以及常规组织学对病变进行形态学研究1天至3个月。组织学上，急性期（7天内）脊髓出现轻度坏死变化，主要位于受压部位，但未观察到明显的出血性坏死。在24小时的白色物质中，观察到水肿，但未观察到破坏性变化。海绵样改变伴轴索变性1-2周明显，不局限于受压部位，弥漫性分布于白色物质内，持续3个月。组织化学显示，白色物质呈海绵状改变， ...更多信息 与2周后轴突和髓鞘减少有关。电镜检查显示侧柱主要改变为有髓纤维轴突变性，如水肿肿胀、髓鞘缠结、髓鞘脱离、脱髓鞘等。这些轴突病变和脱髓鞘改变已经持续了长达3个月。用抗少突胶质细胞的单克隆抗体APC（Ab-7）进行免疫组化染色，结果显示，压迫1周后，少突胶质细胞数量减少，以2-4周最为明显。TUNEL法检测发现，在24-48 h的白色物质中有TUNEL阳性细胞，72 h达高峰，提示本实验模型可用于慢性压迫性脊髓病的分析。白色物质内发生的持续性轴突病变伴脱髓鞘改变可能是压迫性脊髓病的主要改变。少突胶质细胞损伤，可能是由于凋亡细胞死亡，可能会导致脱髓鞘的其余后，持续压缩。少

项目成果

Akai T, Iizuka H, Okamoto K: "Migrated disc in the lumbar spinal canal."Neurol Med Chir. 39. 693-695 (1999)

Akai T、Iizuka H、Okamoto K：“腰椎管内的椎间盘迁移。”Neurol Med Chir。

Sato S, Iizuka H, et al: "Surgical therapy for degenerative lumbar spinal canal stenosis in the elderly."Spinal Surg. 13. 149-156 (1999)

Sato S、Iizuka H 等人：“老年人退行性腰椎管狭窄的手术治疗。”脊柱外科。

Akai T.: "Migrated disc in the lumbar spinal canal"Neurolgia medico-chirurgica. 39. 693-695 (1999)

Akai T.：“腰椎管内的椎间盘移位”Neurolgia medico-chirurgica。

飯塚秀明: "上位頸椎損傷の臨床的検討"JINE. 12. 46-49 (1999)

Hideaki Iizuka：“上颈椎损伤的临床研究”JINE 12. 46-49 (1999)。

飯塚秀明: "上位頚椎の臨床.外傷性疾患"南江堂. 6 (2000)

Hideaki Iizuka：“上颈椎的临床研究。创伤性疾病”Nankodo 6 (2000)。