Chastel C, Barthelemy L, Balouet G
Pathol Biol (Paris). 1977 May;25(5):307-13.
During a week, adult Swiss mice inoculated with LCM virus were exposed to hyperbaric environment (51 ATA) in He-O2 mixture. This exposure delayed the mortality by virus infection for 5-6 days and/or lowered or abolished the specific cerebral pathology. However, at the moment of death, the infectious titer of virus in the brain of exposed mice was not significantly decreased. Some physico-chemical factors involved in hyperbaric environment were investigated in order to determine their possible role in inducing the delayed mortality. Temperature has no effect on the course of experimental LCM in the mouse while He-O2 mixture at atmospheric pressure aggravate the viral disease. Pure O2 applied at 2 ATA intermittently has some beneficial effect but only on specific cerebral alterations. Thus, it seems likely that "per se" hydrostatic pressure and/or an hyperabaric helium specific effect is responsible for the delay of mortality after hyperbaric exposure. Possible mechanisms leading to this delay, i.e. a transient abolition of immunologic response of mice to LCM virus, are briefly discussed.
在一周时间内，接种淋巴细胞性脉络丛脑膜炎病毒（LCM病毒）的成年瑞士小鼠被置于氦氧混合气中的高压环境（51个绝对大气压）中。这种暴露使病毒感染导致的死亡率延迟了5至6天，和/或减轻或消除了特定的脑部病变。然而，在死亡时刻，暴露小鼠大脑中病毒的感染滴度并未显著降低。为了确定高压环境中一些物理化学因素在导致死亡率延迟方面可能发挥的作用，对其进行了研究。温度对小鼠实验性淋巴细胞性脉络丛脑膜炎的病程没有影响，而常压下的氦氧混合气会加重病毒性疾病。以2个绝对大气压间歇性施加纯氧有一定益处，但仅对特定的脑部病变有作用。因此，似乎“本身的”静水压力和/或高压氦的特定效应是高压暴露后死亡率延迟的原因。文中简要讨论了导致这种延迟的可能机制，即小鼠对LCM病毒免疫反应的短暂消除。
