CAJ | 학술논문

背景：大量临床研究证实，脊髓损伤区域的微环境通过高压氧可获得显著改善，但高压氧对脑损伤微环境有何影响呢？目的：观察高压氧治疗对大鼠脑梗死区神经再生微环境及神经功能恢复的影响。方法：构建大脑中动脉阻断制作局灶性脑梗死模型大鼠，并进行高压氧治疗，设假手术组和模型组作对照，假手术组不结扎颈内动脉不干预，模型组造模后模拟除压力和氧浓度以外的其他高压氧治疗过程及环境条件。结果与结论：与模型组相比，治疗后第16天高压氧组的大鼠肢体功能评分、术后14 d脑梗死区组织生长相关蛋白43表达均升高(P<0.05)，术后24 h梗死灶体积均降低(P <0.05)。结果证实，高压氧治疗促进脑梗死模型大鼠神经再生微环境及神经功能的恢复。
배경：대량림상연구증실，척수손상구역적미배경통과고압양가획득현저개선，단고압양대뇌손상미배경유하영향니？목적：관찰고압양치료대대서뇌경사구신경재생미배경급신경공능회복적영향。방법：구건대뇌중동맥조단제작국조성뇌경사모형대서，병진행고압양치료，설가수술조화모형조작대조，가수술조불결찰경내동맥불간예，모형조조모후모의제압력화양농도이외적기타고압양치료과정급배경조건。결과여결론：여모형조상비，치료후제16천고압양조적대서지체공능평분、술후14 d뇌경사구조직생장상관단백43표체균승고(P<0.05)，술후24 h경사조체적균강저(P <0.05)。결과증실，고압양치료촉진뇌경사모형대서신경재생미배경급신경공능적회복。
BACKGROUND:Numerous clinical studies have confirmed that the microenvironment at a spinal cord injury site can be obviously improved through hyperbaric oxygen therapy; however, what effect does hyperbaric oxygen have on the microenvironment of the injured brain? OBJECTIVE:To investigate the effect of hyperbaric oxygen therapy on nerve regeneration microenvironment and the recovery of rat nerve function after focal cerebral infarction. METHODS:Rat models of focal cerebral infarction were established by occlusion of the middle cerebral artery and subjected to hyperbaric oxygen therapy. Sham group and model group were established as comparison. In the sham group, rat models of focal cerebral infarction were established but did not receive any treatment. Rats in the model group were placed in a hyperbaric oxygen therapy chamber but the pressure and oxygen concentration were not administered. RESULTS AND CONCLUSION:Compared with the model group, the score of rat limb function at 16 days after treatment and the expression of growth associated protein 43 in the rat cerebral infarcted area at postoperative 14 days were significantly increased , but infarct volume at postoperative 24 hours was al significantly decreased in the hyperbaric oxygen therapy group (alP < 0.05). These results confirmed that hyperbaric oxygen therapy can improve nerve regeneration microenvironment and promote the recovery of rat nerve function after focal cerebral infarction.