Curran A K, Rodman J R, Eastwood P R, Henderson K S, Dempsey J A, Smith C A
The John Rankin Laboratory of Pulmonary Medicine, Department of Preventive Medicine, University of Wisconsin, Madison, Wisconsin 53705, USA.
J Appl Physiol (1985). 2000 May;88(5):1840-52. doi: 10.1152/jappl.2000.88.5.1840.
Our study was concerned with the effect of brain hypoxia on cardiorespiratory control in the sleeping dog. Eleven unanesthetized dogs were studied; seven were prepared for vascular isolation and extracorporeal perfusion of the carotid body to assess the effects of systemic [and, therefore, central nervous system (CNS)] hypoxia (arterial PO(2) = 52, 45, and 38 Torr) in the presence of a normocapnic, normoxic, and normohydric carotid body during non-rapid eye movement sleep. A lack of ventilatory response to systemic boluses of sodium cyanide during carotid body perfusion demonstrated isolation of the perfused carotid body and lack of other significant peripheral chemosensitivity. Four additional dogs were carotid body denervated and exposed to whole body hypoxia for comparison. In the sleeping dog with an intact and perfused carotid body exposed to specific CNS hypoxia, we found the following. 1) CNS hypoxia for 5-25 min resulted in modest but significant hyperventilation and hypocapnia (minute ventilation increased 29 +/- 7% at arterial PO(2) = 38 Torr); carotid body-denervated dogs showed no ventilatory response to hypoxia. 2) The hyperventilation was caused by increased breathing frequency. 3) The hyperventilatory response developed rapidly (<30 s). 4) Most dogs maintained hyperventilation for up to 25 min of hypoxic exposure. 5) There were no significant changes in blood pressure or heart rate. We conclude that specific CNS hypoxia, in the presence of an intact carotid body maintained normoxic and normocapnic, does not depress and usually stimulates breathing during non-rapid eye movement sleep. The rapidity of the response suggests a chemoreflex meditated by hypoxia-sensitive respiratory-related neurons in the CNS.
我们的研究关注脑缺氧对睡眠中犬类心肺控制的影响。对11只未麻醉的犬进行了研究；其中7只准备进行血管分离及颈动脉体的体外灌注，以评估在非快速眼动睡眠期间，在正常碳酸血症、正常氧合及正常水合状态的颈动脉体存在时，全身性[以及因此的中枢神经系统（CNS）]缺氧（动脉血氧分压=52、45和38托）的影响。在颈动脉体灌注期间，对全身性注射氰化钠缺乏通气反应，表明灌注的颈动脉体已分离且不存在其他显著的外周化学敏感性。另外4只犬进行了颈动脉体去神经支配并暴露于全身缺氧状态以作比较。在具有完整且灌注的颈动脉体并暴露于特定中枢神经系统缺氧的睡眠犬中，我们发现以下情况。1）中枢神经系统缺氧5 - 25分钟导致适度但显著的通气过度和低碳酸血症（在动脉血氧分压=38托时，分钟通气量增加29±7%）；去神经支配的颈动脉体犬对缺氧无通气反应。2）通气过度是由呼吸频率增加引起的。3）通气过度反应迅速出现（<30秒）。4）大多数犬在缺氧暴露长达25分钟期间维持通气过度。5）血压和心率无显著变化。我们得出结论，在完整的颈动脉体维持正常氧合和正常碳酸血症的情况下，特定的中枢神经系统缺氧在非快速眼动睡眠期间不会抑制且通常会刺激呼吸。反应的迅速性表明这是一种由中枢神经系统中对缺氧敏感的呼吸相关神经元介导的化学反射。
