Miller M J, Tenney S M
Respir Physiol. 1975 Jan;23(1):31-9. doi: 10.1016/0034-5687(75)90069-9.
Ventilation while breathing air and in response to hypoxia was studied in unanesthetized cats after carotid body chemo-defferentation. Hypoxic exposure (FIO2 equal to 0.07-0.12) of chemo-deafferented animals rapidly produced a high frequency, low tidal volume tachypnea. Tachypneic breathing, although usually associated with an increased expired ventilation, was accompanied by an increase in PACO2. In contrast to intact cats, behavioral arousal during hypoxic exposure was not observed after chemo-deafferentation. The response to milder hypoxia (FIO2 equal to 0.14-0.16) occurred with an increased latency, and there resulted a less marked depression of tidal volume and stimulation of respiratory frequency. Elevation of PACO2 to 5 mm Hg above the resting value, by addition of CO2 to the inspired gas, prevented the appearance of tachypnea upon subsequent reduction of FIO2 from 0.21 to 0.07. Depletion of central catecholamine stores, by administration of reserpine, did not prevent the tachypneic response to hypoxia. Following administration of anesthesia (pentobarbital, 30 mg/kg, IP), hypoxic exposure (FIO2 equal to 0.10) led to depression of both respiratory frequency and tidal volume, resulting in apnea within 1.5 minutes. It is concluded that hypoxia (FLO2 equal to 0.07-0.16) acts, in a concentration-related manner, as a powerful stimulant to central respiratory frequency generation and as a depressant of the tidal volume in the unanesthetized cat.
在对未麻醉的猫进行颈动脉体化学去传入神经支配后,研究了其在呼吸空气时以及对低氧的反应中的通气情况。对化学去传入神经支配的动物进行低氧暴露(吸入氧分数等于0.07 - 0.12),会迅速产生高频、低潮气量的呼吸急促。呼吸急促虽然通常与呼出通气量增加有关,但同时伴有动脉血二氧化碳分压(PACO2)升高。与完整的猫不同,化学去传入神经支配后,低氧暴露期间未观察到行为觉醒。对较轻低氧(吸入氧分数等于0.14 - 0.16)的反应潜伏期延长,潮气量的降低和呼吸频率的刺激也不太明显。通过向吸入气体中添加二氧化碳,使PACO2升高至高于静息值5 mmHg,可防止随后将吸入氧分数从0.21降至0.07时出现呼吸急促。给予利血平耗尽中枢儿茶酚胺储备,并未阻止对低氧的呼吸急促反应。给予麻醉(戊巴比妥,30 mg/kg,腹腔注射)后,低氧暴露(吸入氧分数等于0.10)导致呼吸频率和潮气量均降低,在1.5分钟内导致呼吸暂停。结论是,在未麻醉的猫中,低氧(吸入氧分数等于0.07 - 0.16)以浓度相关的方式,作为中枢呼吸频率产生的强大刺激物和潮气量的抑制剂起作用。