Davies D G, McGrath J J
Department of Physiology, Texas Tech University Health Sciences Center, Lubbock 79430.
Respir Physiol. 1989 Feb;75(2):193-8. doi: 10.1016/0034-5687(89)90063-7.
Arterial blood gases were measured in 52 unanesthetized Sprague-Dawley rats following six weeks exposure to either room air at ambient altitude (950 m), room air containing 100 ppm CO at ambient altitude, room air at 4575 m simulated high altitude, or room air containing 100 ppm CO at 4575 m simulated high altitude. PaCO2 was significantly higher in animals exposed to CO both at ambient altitude (38.2 vs 34.5 Torr) and simulated high altitude (28.3 vs 23.6 Torr). The data show that chronic exposure to low concentrations of CO depresses ventilatory drive at both ambient and simulated high altitude. This depression could be related to changes in brain blood flow and the acidity of the central medullary chemosensitive area or to changes in peripheral chemoreceptor activity.
在52只未麻醉的斯普拉格-道利大鼠中测量动脉血气,这些大鼠在环境海拔(950米)下暴露于室内空气、环境海拔下含100 ppm一氧化碳的室内空气、4575米模拟高海拔下的室内空气或4575米模拟高海拔下含100 ppm一氧化碳的室内空气中六周。在环境海拔(38.2对34.5托)和模拟高海拔(28.3对23.6托)下暴露于一氧化碳的动物中,动脉血二氧化碳分压均显著更高。数据表明,长期暴露于低浓度一氧化碳会抑制环境海拔和模拟高海拔下的通气驱动。这种抑制可能与脑血流量和延髓中央化学敏感区酸度的变化有关,或者与外周化学感受器活性的变化有关。