Kaehny W D, Jackson J T
J Appl Physiol Respir Environ Exerc Physiol. 1979 Jun;46(6):1138-42. doi: 10.1152/jappl.1979.46.6.1138.
To test the participation of the carotid bodies in the respiratory response to metabolic acidosis, six dogs were infused with HCl for 2 h followed by HCl feeding to prolong the acidosis to 48 h. This protocol was repeated after carotid body denervation (CBD). Mean control PCO2 rose by 7.3 Torr after CBD. PCO2 fell comparably during acidosis before and after CBD at all time periods from 30 to 48 h and returned to control levels by 72 h. The pH ranged from 7.10 to 7.30 during acidosis pre- and post-CBD. The decreases in pH and bicarbonate concentration did not differ significantly at any time interval between the pre- and post-CBD studies. This study indicates that in dogs moderately severe HCl acidosis stimulates ventilation acutely and chronically through a central mechanism in the absence of the carotid bodies.
为了测试颈动脉体在对代谢性酸中毒的呼吸反应中的参与情况,对6只狗输注盐酸2小时,随后喂食盐酸以将酸中毒延长至48小时。在颈动脉体去神经支配(CBD)后重复该方案。CBD后平均对照二氧化碳分压升高了7.3托。在30至48小时的所有时间段内,CBD前后酸中毒期间二氧化碳分压下降程度相当,并在72小时时恢复到对照水平。CBD前后酸中毒期间pH值范围为7.10至7.30。在CBD前后研究的任何时间间隔内,pH值和碳酸氢盐浓度的降低均无显著差异。这项研究表明,在狗中,在没有颈动脉体的情况下,中度严重的盐酸酸中毒通过中枢机制急性和慢性地刺激通气。