Kimura H, Mikami M, Kuriyama T, Fukuda Y
Department of Chest Medicine and Physiology II, School of Medicine, Chiba University, Japan.
J Appl Physiol (1985). 1989 Nov;67(5):1754-8. doi: 10.1152/jappl.1989.67.5.1754.
Effects on ventilatory responses to progressive isocapnic hypoxia of a synthetic potent progestin, chlormadinone acetate (CMA), were determined in the halothane-anesthetized male rat. Ventilation during the breathing of hyperoxic gas was largely unaffected by treatment with CMA when carotid chemoreceptor afferents were kept intact. The sensitivity to hypoxia evaluated by hyperbolic regression analysis of the response curve did not differ between the control and CMA groups. The reduction of ventilation after bilateral section of the carotid sinus nerve (CSN) in hyperoxia was less severe in CMA-treated than in untreated animals. Furthermore, the CMA-treated rats showed a larger increase in ventilation during the hypoxia test and a lower PO2 break point for ventilatory depression. Inhibition of hypoxic ventilatory depression by CMA persisted even after the denervation of CSN. We conclude that exogenous progestin likely protects regulatory mechanism(s) for respiration against hypoxic depression through a stimulating action independent of carotid chemoreceptor afferents and without a change in the sensitivity of the ventilatory response to hypoxia.
在氟烷麻醉的雄性大鼠中,测定了合成强效孕激素醋酸氯地孕酮(CMA)对渐进性等碳酸血症性低氧通气反应的影响。当颈动脉化学感受器传入神经保持完整时,高氧气体呼吸期间的通气在很大程度上不受CMA治疗的影响。通过反应曲线的双曲线回归分析评估的对低氧的敏感性在对照组和CMA组之间没有差异。在高氧状态下,双侧切断颈动脉窦神经(CSN)后,CMA治疗组的通气减少程度比未治疗动物轻。此外,CMA治疗的大鼠在低氧试验期间通气增加幅度更大,通气抑制的PO2断点更低。即使在CSN去神经支配后,CMA对低氧通气抑制的作用仍然持续。我们得出结论,外源性孕激素可能通过一种独立于颈动脉化学感受器传入神经的刺激作用,保护呼吸调节机制免受低氧抑制,并且不会改变通气对低氧反应的敏感性。