CAJ | 학술논문

目的探讨高压氧对动物减压损伤的治疗效用。方法大鼠18只，随机分为3组，清醒状态置于加压舱内，进行加、减压实验，造成急性减压损伤。高压氧治疗组动物形成减压损伤后随即再置于小型高压氧舱内，在250kPa高压氧暴露60min。出舱后进行脑和肝胞液糖皮质激素受体结合量的检测。结果动物出现减压损伤后，脑和肝胞液糖皮质激素受体结合量分别比对照组减少25％和16.4％，尤其以脑胞液糖皮质激素受体结合量减少为明显，与对照组相比差异显著(P<0.05)。高压氧暴露后脑和肝胞液糖皮质激素受体结合量可比高压氧暴露前分别回升9.5％和9.2％，动物一般状态亦随之好转。结论(1)快速减压时可引起动物脑和肝胞液糖皮质激素受体结合量明显减少，并造成动物病理性应激反应；(2)高压氧暴露对减压损伤所致的糖皮质激素受体代谢具有调整作用。
목적탐토고압양대동물감압손상적치료효용。방법대서18지，수궤분위3조，청성상태치우가압창내，진행가、감압실험，조성급성감압손상。고압양치료조동물형성감압손상후수즉재치우소형고압양창내，재250kPa고압양폭로60min。출창후진행뇌화간포액당피질격소수체결합량적검측。결과동물출현감압손상후，뇌화간포액당피질격소수체결합량분별비대조조감소25％화16.4％，우기이뇌포액당피질격소수체결합량감소위명현，여대조조상비차이현저(P<0.05)。고압양폭로후뇌화간포액당피질격소수체결합량가비고압양폭로전분별회승9.5％화9.2％，동물일반상태역수지호전。결론(1)쾌속감압시가인기동물뇌화간포액당피질격소수체결합량명현감소，병조성동물병이성응격반응；(2)고압양폭로대감압손상소치적당피질격소수체대사구유조정작용。
Objective. To probe therapeutic mechanism of hyperbaric oxygen (HBO) in animals with decompression injury.Methods 18 rats were divided into 3 groups randomly. They were placed into compression chamber to study by compression and decompression in lucid state so that the decompression injury was formed. Then the HBO exposure group was placed into a small HBO chamber. The animals were exposed to at 250 kPa HBO for 60min. The binding capacity of glucocorticoid receptor (GR) in cerebral and hepatic cytosol was measured after decompression to normal pressure. Results The binding capacity of GR of cerebral and hepatic cytosol respectively reduced 25％ and 16.4％ after decompression injyry in rats. Especially the binding capacity of GR of cerebral cytosol,which is significantly different comparing with the normal control group(P<0.05).After HBO exposure, the binding capacity of GR in cerebral and hepatic cytosol was higher 9.5％ and 9.2％ than that of before HBO exposure respectively. Meanwhile, general state of the rats was improved relevantly. Conclusions (1) During fast decompression, the binding capacity of GR in cerebral and hepatic cytosol obviously reduced, resulting in pathological decompression stress reaction.(2) HBO has regulating role in metabolism of GR resulted from decompression injury in rats.