CAJ | 학술논문

目的探讨实验性减压病兔脑和脊髓组织损伤机制及高压氧(hyperbaric oxygen,HBO)的治疗作用.方法成年健康雄性新西兰大耳白兔28只,按数字表法随机分为正常对照组、减压病(DCS)组、安全减压组、HBO组,每组7只.DCS组,5 min空气加压至0.8 MPa(绝对压),停留60 min,5 min匀速减至常压;HBO组按DCS组操作,出舱后立刻用加压舱行HBO治疗;安全减压组参考我国海军空气潜水减压表减至常压.动物出舱后30 min内迅速处死,取各组胸腰段脊髓和脑,借助光镜观察脊髓和脑的病理形态学改变,用原位末端脱氧核糖核酸转移酶介导DUTP标记法(TUNNEL法)观察胸腰段脊髓和脑组织凋亡情况.结果 DCS组脊髓白质内空泡形成,损伤区周围胶质细胞增生;TUNNEL标记阳性凋亡细胞数为每高倍镜视野下(28.29 ±2.56)个,较正常对照组(0.57±0.54)个、安全减压组(2.29±1.11)个、HBO组(3.71±1.1 1)个均明显增多,差异均有统计学意义(P ＜0.05);HBO组阳性凋亡细胞数较正常对照组多,但较DCS组明显减少,差异均有统计学意义(P ＜0.05);HBO组与安全减压组阳性细胞数差异无统计学意义(P ＞0.05);DCS组脑组织凋亡细胞数[(1.43±0.54)个]较脊髓组织中凋亡细胞数[(28.29 ±2.56)个]明显减少,但多于正常对照组,差异具有统计学意义(P＜0.05).结论脊髓是减压病中枢神经系统损伤的主要部位;细胞凋亡是减压病脊髓损伤的原因之一;高压氧治疗能明显抑制大鼠脊髓损伤后的细胞凋亡,对减压病有良好的治疗作用.
목적 탐토실험성감압병토뇌화척수조직손상궤제급고압양(hyperbaric oxygen,HBO)적치료작용.방법 성년건강웅성신서란대이백토28지,안수자표법수궤분위정상대조조、감압병(DCS)조、안전감압조、HBO조,매조7지.DCS조,5 min공기가압지0.8 MPa(절대압),정류60 min,5 min균속감지상압;HBO조안DCS조조작,출창후립각용가압창행HBO치료;안전감압조삼고아국해군공기잠수감압표감지상압.동물출창후30 min내신속처사,취각조흉요단척수화뇌,차조광경관찰척수화뇌적병리형태학개변,용원위말단탈양핵당핵산전이매개도DUTP표기법(TUNNEL법)관찰흉요단척수화뇌조직조망정황.결과 DCS조척수백질내공포형성,손상구주위효질세포증생;TUNNEL표기양성조망세포수위매고배경시야하(28.29 ±2.56)개,교정상대조조(0.57±0.54)개、안전감압조(2.29±1.11)개、HBO조(3.71±1.1 1)개균명현증다,차이균유통계학의의(P ＜0.05);HBO조양성조망세포수교정상대조조다,단교DCS조명현감소,차이균유통계학의의(P ＜0.05);HBO조여안전감압조양성세포수차이무통계학의의(P ＞0.05);DCS조뇌조직조망세포수[(1.43±0.54)개]교척수조직중조망세포수[(28.29 ±2.56)개]명현감소,단다우정상대조조,차이구유통계학의의(P＜0.05).결론 척수시감압병중추신경계통손상적주요부위;세포조망시감압병척수손상적원인지일;고압양치료능명현억제대서척수손상후적세포조망,대감압병유량호적치료작용.
Objective To investigate the mechanism of brain and spinal cord injury in experimental rabbits with decompression sickness (DCS) and the effect of hyperbaric oxygen (HBO).Methods Twentyeight adult male healthy New Zealand rabbits were randomly divided into 4 groups:the normal control group,the DCS group,the safe decompression group and the HBO group,each consisting of 7 animals.The rabbits in the DCS group were compressed with air in 5 minutes to a pressure 0.8 MPa and maintained at the said pressure for 60 min,and then were decompressed to normal pressure within 5 min.The animals in the HBO group underwent the same compression and decompression procedures,as the animals in the DCS group,but were immediately put into the hyperbaric chamber to receive HBO therapy.The safe decompression group was compressed and decompressed with the profile of the Chinese Navy Diving Decompression Tables.Changes in pathological morphology and apoptosis of brain and spinal cord tissue cells in the thoracic and lumbar segments were observed with light microscopy and terminal deoxynucleotidyl transferase-mediated DUTP nick end labeling (TUNEL) method.Results For the animals in the DCS group,cavity in the white matter of the spinal cord and proliferation of gliocytes around the damaged tissue could obviously be observed.TUNEL results showed that more positive apoptotic cells were detected in the DCS group (28.29 ± 2.56)/HP,as compared with those of the normal control group (0.57 ± 0.54)/HP,the safe decompression group (2.29 ± 1.11)/HP and the HBO group (3.71 ± 1.11)/HP,with statistical significance (P ＜ 0.05).More positive apoptotic cells were also seen in the HBO group (3.71 ± 1.1 1)/HP,as compared with those of the normal control group (P ＜0.05),but were significantly less,as compared with those of the DCS group (P ＜ 0.05),also with statistical significance (P ＜ 0.05).Slightly more positive apoptotic cells were detected in the animals of the HBO group,when compared with those of the safe decompression group,but without statistical significance (P ＜ 0.05).No significant apoptosis of cells could be seen in the brain tissue.Conclusions Spinal core was the main site involved in the central nervous system injury induced by rapid decompression.The spinal cord injury induced by rapid decompression was the result of the apoptosis of gliocytes,and gliocytes might play a key role in the recovery of spinal cord injury.HBO therapy could obviously inhibit the apoptosis of gliocytes,following spinal cord injury.