Warren J, Sacksteder M R, Thuning C A
J Immunol. 1978 Jul;121(1):315-20.
Using protocols that incorporated double blind examination of animals sensitized to CNS antigen, we confirmed and amplified earlier findings of the complete suppression of EAE in rodents by hyperbaric oxygen. The effects of O2 were related to the gas pressure and duration of treatment. The development of paralytic disease was prevented for 34 days after sensitization (the longest interval studied). Compressed air or normobaric O2 administered under similar conditions did not modify the course of illness. Within 7 to 10 days after the discontinuance of oxygen therapy the majority of treated guinea pigs developed typical signs of EAE with characteristic lesions in the CNS. The relapses occurred sooner in the Lewis rat. The development of the delayed hypersensitivity reaction to myelin basic protein and to tuberculin is also suppressed by O2 therapy indicating that its effects upon autoimmune encephalomyelitis involves fundamental alterations of the cellular components of the immune response, some or all of which are reversible.
我们采用对中枢神经系统抗原致敏的动物进行双盲检查的方案，证实并拓展了早期的研究发现，即高压氧可完全抑制啮齿动物的实验性自身免疫性脑脊髓炎（EAE）。氧气的作用与气压和治疗时长有关。致敏后34天（研究的最长间隔时间）内，麻痹性疾病的发展得到了预防。在类似条件下给予压缩空气或常压氧气，并未改变疾病进程。在停止氧疗后的7至10天内，大多数接受治疗的豚鼠出现了EAE的典型症状，中枢神经系统出现了特征性病变。Lewis大鼠的复发出现得更快。氧疗还抑制了对髓鞘碱性蛋白和结核菌素的迟发型超敏反应的发展，这表明其对自身免疫性脑脊髓炎的作用涉及免疫反应细胞成分的根本性改变，其中一些或全部改变是可逆的。
