Radziszewski E, Guillerm R, Badre R, Abran C
Bull Eur Physiopathol Respir. 1976 Jan-Feb;12(1):87-101.
Four groups of male volunteers have been exposed in a tight climatical chamber to PICO2 of 14, 21, 28 and 32 torr; exposure periods varied from two to 30 days, between two reference periods in normal air. The results deal with the evolution of arterial blood acid-base equilibrium and that of renal response in relation to PICO2. In all exposures, the carbon dioxide alveolar overload increases by several torr during the first 24 hours on account of attenuation of the initial hyperventilation. Kinetics of the respiratory acidosis compensation differs according to hypercapnia which is moderate (PICO2 of 14 and 21 torr) or relatively severe (PICO2 of 28 and 32 torr). The decrease in arterial pH lessens as early as the 24th hour at PICO2 28 and 32 torr, and only after two days at PICO2 14 and 21 torr. The renal response is characterized by a significant increase in aciduria during the first 24 hours at PICO2 28 and 32 torr; the changes are smaller and start latter at PICO2 14 torr.
四组男性志愿者被置于一个密闭的气候舱中,暴露于14、21、28和32托的二氧化碳分压环境下;暴露时间从两天到30天不等,处于正常空气中的两个参考期之间。研究结果涉及动脉血酸碱平衡的变化以及与二氧化碳分压相关的肾脏反应。在所有暴露过程中,由于初始过度通气的减弱,在最初的24小时内,肺泡二氧化碳负荷会增加几个托。呼吸性酸中毒代偿的动力学因高碳酸血症程度不同而有所差异,即中度(二氧化碳分压为14和21托)或相对重度(二氧化碳分压为28和32托)。在二氧化碳分压为28和32托时,动脉血pH值的下降早在第24小时就开始减轻,而在二氧化碳分压为14和21托时,两天后才开始减轻。肾脏反应的特点是,在二氧化碳分压为28和32托时,最初24小时内酸尿显著增加;在二氧化碳分压为14托时,变化较小且开始时间较晚。