Graham M S, Turner J D, Wood C M
Vancouver Public Aquarium, B.C., Canada.
Respir Physiol. 1990 May-Jun;80(2-3):259-77. doi: 10.1016/0034-5687(90)90088-g.
In order to study the role of CO2 and acid-base status in contributing to ventilatory drive, skate were exposed to normoxic hypercapnia (PICO2 = 7.5 Torr) under conditions where the primary O2 drive would remain unaltered. Blood O2 transport was markedly insensitive to CO2, with no Root effect and only a small Bohr effect. Red blood cell pHi was not preferentially regulated, and there was no evidence of RBC swelling or nucleoside triphosphate adjustment. Although there were no changes in arterial O2 levels during hypercapnia, ventilation immediately increased 2.7-fold through large changes in stroke volume and small changes in frequency, and declined only slightly through 24-48 h. PaCO2 equilibrated rapidly with PICO2, driving down arterial pHa, which was 65% corrected through HCO3- accumulation by 24 h. In contrast, the extradural fluid outside the brain equilibrated only very slowly, and was clearly not involved in the ventilatory stimulation. Increased ventilation during hypercapnia may be related to depression in pHa.
为了研究二氧化碳和酸碱状态在通气驱动中的作用，在主要氧气驱动保持不变的条件下，使鳐鱼暴露于常氧高碳酸血症（末梢二氧化碳分压 = 7.5 托）环境中。血液氧气运输对二氧化碳明显不敏感，不存在鲁特效应，只有轻微的波尔效应。红细胞内pH值没有受到优先调节，也没有红细胞肿胀或核苷三磷酸调节的迹象。虽然在高碳酸血症期间动脉血氧水平没有变化，但通气量立即通过每搏输出量的大幅变化和频率的小幅变化增加了2.7倍，并且在24 - 48小时内仅略有下降。动脉血二氧化碳分压迅速与末梢二氧化碳分压达到平衡，导致动脉血pH值下降，到24小时时通过碳酸氢根离子积累使下降的pH值得到了65%的纠正。相比之下，脑外硬膜外液平衡非常缓慢，显然与通气刺激无关。高碳酸血症期间通气量增加可能与动脉血pH值降低有关。
