Pokorski M, Lahiri S
Am J Physiol. 1983 Dec;245(6):R873-80. doi: 10.1152/ajpregu.1983.245.6.R873.
We investigated the relative contribution of peripheral and central chemosensory mechanisms to ventilatory responses to metabolic alkalosis in anesthetized cats by simultaneously measuring steady-state carotid body chemosensory activity and ventilation. The effects of graded steady-state levels of metabolic alkalosis at constant levels of arterial O2 and CO2 partial pressure (PaO2 and PaCO2, respectively) were studied first. Then the responses to isocapnic hypoxia and hyperoxic hypercapnia before and after the induction of a given level of metabolic alkalosis were studied. From the relationship between the carotid chemosensory activity and ventilation, the contribution of the two chemosensory mechanisms was estimated. The depression of ventilation that could not be accounted for by a decrease in the carotid chemosensory activity is attributed to the central effect. We found that metabolic alkalosis decreased both carotid chemosensory activity and ventilation at all levels of PaO2 or PaCO2. The ventilatory effect of alkalosis increased during hypoxia due to suppression of both peripheral chemosensory input and its interaction with the central CO2-H+ drive. During hyperoxia the central effect of alkalosis was predominant, although the peripheral effect increased with hypercapnia. We conclude that acute metabolic alkalosis suppresses both peripheral and central chemosensory drives, and its ventilatory effect grows larger with decreasing PaO2.
我们通过同时测量稳态颈动脉体化学感受活动和通气，研究了外周和中枢化学感受机制对麻醉猫代谢性碱中毒通气反应的相对贡献。首先研究了在恒定动脉血氧分压（PaO₂）和二氧化碳分压（PaCO₂）水平下，分级稳态代谢性碱中毒水平的影响。然后研究了在诱导给定水平的代谢性碱中毒之前和之后，对等碳酸血症性低氧和高氧性高碳酸血症的反应。根据颈动脉化学感受活动与通气之间的关系，估算了两种化学感受机制的贡献。不能用颈动脉化学感受活动降低来解释的通气抑制归因于中枢效应。我们发现，在所有PaO₂或PaCO₂水平下，代谢性碱中毒均降低了颈动脉化学感受活动和通气。由于外周化学感受输入及其与中枢CO₂ - H⁺驱动的相互作用均受到抑制，碱中毒的通气效应在低氧期间增强。在高氧期间，碱中毒的中枢效应占主导，尽管外周效应随高碳酸血症而增加。我们得出结论，急性代谢性碱中毒抑制外周和中枢化学感受驱动，并且随着PaO₂降低其通气效应增大。
