CAJ | 학술논문

目的：电镜观察Ⅱ型减压病家兔脊髓神经轴突的超微结构改变，探讨减压病所致脊髓损伤的机制。方法将15只新西兰大耳白家兔按数字表法随机分为3组：减压病组、安全减压组和正常对照组，每组5只。减压病组行快速减压制作减压病动物模型，安全减压组采用安全减压，正常对照组行常压空气暴露，各组动物出舱后30 min内处死，取脊髓组织进行超微结构观察。结果减压病组神经细胞水肿，细胞内线粒体轻度肿胀，游离核糖体聚集；轴突水肿，髓鞘松解、褶曲，部分剥离，轴突内线粒体肿胀，微管排列紊乱，并见许多大小不等的空泡形成。安全减压组神经细胞和轴突轻度水肿，胞质和轴索内可见小空泡形成，髓鞘板层结构松散。正常对照组脊髓组织超微结构未见明显改变。结论神经纤维水肿、轴突脱髓鞘为Ⅱ型减压病家兔脊髓损伤的基本病变，脊髓血管内气泡及“原位气泡”可能同为导致脊髓损伤的直接原因。
목적：전경관찰Ⅱ형감압병가토척수신경축돌적초미결구개변，탐토감압병소치척수손상적궤제。방법장15지신서란대이백가토안수자표법수궤분위3조：감압병조、안전감압조화정상대조조，매조5지。감압병조행쾌속감압제작감압병동물모형，안전감압조채용안전감압，정상대조조행상압공기폭로，각조동물출창후30 min내처사，취척수조직진행초미결구관찰。결과감압병조신경세포수종，세포내선립체경도종창，유리핵당체취집；축돌수종，수초송해、습곡，부분박리，축돌내선립체종창，미관배렬문란，병견허다대소불등적공포형성。안전감압조신경세포화축돌경도수종，포질화축색내가견소공포형성，수초판층결구송산。정상대조조척수조직초미결구미견명현개변。결론신경섬유수종、축돌탈수초위Ⅱ형감압병가토척수손상적기본병변，척수혈관내기포급“원위기포”가능동위도치척수손상적직접원인。
Objective To observe changes in the ultra-structure of spinal neuraxon in rabbits with type Ⅱ decompression sickness ( DCS) and also to investigate the mechanism involved in the damage of spinal cord.Methods Fifteen New Zealand white rabbits were randomly divided into 3 groups:the DCS group, the safe decompression group and the control group.The rabbits in the DCS group were decompressed in rapid pace to develop the DCS animal model, the animals in the safe decompression group were safely decompressed to normal pressure and the animals in the control group were just exposed to normal air pressure.The animals in all groups were sacrificed within 30 minutes after they were brought out of the chamber.Then, spinal cord samples were collected for the observation of ultra-structure.Results Edema of neurocytes, slight swelling of mitochondria and aggregation of free ribosomes could be observed in the rabbits of the DCS group.Electron microscopic detection indicated that there were axon edema, myelin sheath relaxia-tion, partial demyelination, mitochondria swelling in neuraxon, disturbance in microtubule and bubble formation of various sizes.For the animals in the safe decompression group, slight edema of neurocytes and neuraxon, formation of small bubbles in cytoplasm and ax-on and loose structure of myelin sheath could be observed in them.However, for the animals in the normal control group, there were no significant changes in the ultra-structure of spinal cord tissue.Conclusion Nerve fiber edema and axon demyelination were primary pathological changes in the animals with spinal cord damage induced by typeⅡdecompression sickness.Air bubbles in spinal cord ves-sels and"pre-invasive air bubbles"might be the direct cause for spinal cord damage.