Wood C D
Undersea Biomed Res. 1982 Mar;9(1):15-20.
The role of CO2 in hyperbaric oxygen toxicity was investigated by administering acetazolamide (Diamox), Tris buffer [tris(hydroxymethyl)aminomethane], and sodium bicarbonate by i.p. injection, and by exposure of other groups of animals to an atmosphere of 5% CO2 and 95% O2. All animals were placed in a pressure chamber and maintained at 50 psig in 100% O2 until death. The Tris buffer and the sodium bicarbonate buffer significantly extended time to onset of convulsions and to time of death. Acetazolamide and also 5% CO2 shortened time to onset of convulsions and significantly shortened survival time. These results suggest that increased tissue levels of CO2 play an important role in hyperbaric oxygen toxicity. The cause of death in our animals exposed to hyperbaric oxygen was pulmonary edema secondary to a systemic hypertension.
通过腹腔注射乙酰唑胺（醋氮酰胺）、Tris缓冲液[三（羟甲基）氨基甲烷]和碳酸氢钠，并将其他几组动物置于含5%二氧化碳和95%氧气的环境中，研究了二氧化碳在高压氧中毒中的作用。所有动物均置于压力舱中，在100%氧气环境下维持在50磅力/平方英寸直至死亡。Tris缓冲液和碳酸氢钠缓冲液显著延长了惊厥发作时间和死亡时间。乙酰唑胺以及5%二氧化碳缩短了惊厥发作时间，并显著缩短了存活时间。这些结果表明，组织中二氧化碳水平升高在高压氧中毒中起重要作用。我们暴露于高压氧环境中的动物的死亡原因是继发于全身性高血压的肺水肿。
