Andronikou S, Shirahata M, Mokashi A, Lahiri S
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia 19104.
Respir Physiol. 1988 Jun;72(3):361-74. doi: 10.1016/0034-5687(88)90094-1.
To understand the role of carotid chemoreceptor activity in the ventilatory responses to sustained hypoxia (30 min) the following measurements were made in cats anesthetized with alpha-chloralose: (1) carotid chemoreceptor and ventilatory responses to isocapnic hypoxia and to hypercapnia during hyperoxia; (2) carotid chemoreceptor responses to isocapnic hypoxia after dopamine receptor blockade; and (3) ventilatory responses to hypoxia after bilateral section of carotid sinus nerves (CSN). Transition to hypoxia (PaO2 approximately equal to 52 Torr) from hyperoxia gradually increased carotid chemoreceptor activity by ten fold and ventilation by two fold without any detectable overshoot. Termination of isocapnic hypoxia with hyperoxia (PaO2 greater than 300 Torr) at 30 min promptly restored the carotid chemoreceptor activity to prehypoxic level. Ventilation also decreased promptly, but remained above the control value. Induction of hypercapnia (from 31.8 Torr to 43.9 Torr) during hyperoxia was followed by a prompt increase in the chemoreceptor activity by four fold which subsequently diminished, and by a gradual four fold increase in ventilation. Termination of hypercapnia after 30 min was followed by a prompt return of chemoreceptor activity and by a slow return of ventilation to near control levels. Dopamine receptor blockade increased carotid chemoreceptor responsiveness to acute hypoxia but did not alter the response pattern during sustained hypoxia. After bilateral CSN section, ventilation decreased during maintained hypoxia. Thus, a stimulatory peripheral and inhibitory central effects of hypoxia could produce a biphasic ventilatory response to short-term hypoxia in the anesthetized cat with intact CSN but did not manifest it. The results suggest that the chemosensory input not only promptly stimulates ventilation but also prevents the subsequent depressant effect of hypoxia on the brain-stem respiratory mechanisms and hence presumably a biphasic ventilatory response in the anesthetized cat.
为了解颈动脉化学感受器活动在对持续性低氧(30分钟)的通气反应中的作用,在以α-氯醛糖麻醉的猫身上进行了以下测量:(1)在高氧期间对等碳酸性低氧和高碳酸血症的颈动脉化学感受器及通气反应;(2)多巴胺受体阻断后对等碳酸性低氧的颈动脉化学感受器反应;(3)双侧切断颈动脉窦神经(CSN)后对低氧的通气反应。从高氧过渡到低氧(动脉血氧分压约等于52托)使颈动脉化学感受器活动逐渐增加10倍,通气增加2倍,且无任何可检测到的过冲。在30分钟时用高氧(动脉血氧分压大于300托)终止等碳酸性低氧可使颈动脉化学感受器活动迅速恢复到低氧前水平。通气也迅速下降,但仍高于对照值。在高氧期间诱发高碳酸血症(从31.8托升至43.9托)后,化学感受器活动迅速增加4倍,随后减弱,通气逐渐增加4倍。30分钟后终止高碳酸血症,化学感受器活动迅速恢复,通气缓慢恢复到接近对照水平。多巴胺受体阻断增加了颈动脉化学感受器对急性低氧的反应性,但未改变持续性低氧期间的反应模式。双侧切断CSN后,在持续性低氧期间通气下降。因此,低氧的刺激性外周作用和抑制性中枢作用可在CSN完整的麻醉猫中对短期低氧产生双相通气反应,但未表现出来。结果表明,化学感受性输入不仅能迅速刺激通气,还能防止低氧随后对脑干呼吸机制的抑制作用,从而推测在麻醉猫中产生双相通气反应。