Khodadadeh Bradley, Badr M Safwan, Mateika Jason H
John D. Dingell Veterans Administration Medical Center, 4646 John R (11R), Room 4308, Detroit, MI 48201, USA.
Respir Physiol Neurobiol. 2006 Feb 28;150(2-3):122-34. doi: 10.1016/j.resp.2005.04.019. Epub 2005 Jun 2.
Our primary hypothesis was that the acute ventilatory response to carbon dioxide in the presence of sustained hypoxia {VRCO2 (hypoxia)} or hyperoxia {VRCO2 (hyperoxia)} would increase in subjects with obstructive sleep apnea (OSA) after exposure to episodic hypoxia. Secondarily, we hypothesized that chronic (i.e. years) exposure to episodic hypoxia, a hallmark of OSA, would facilitate persistent augmentation of respiratory activity (i.e. long-term facilitation) after acute (i.e. minutes) exposure to episodic hypoxia. Nine healthy males with OSA that were healthy otherwise completed a series of rebreathing trials before and after exposure to eight 4 min episodes of hypoxia. On a separate occasion, the rebreathing trials were repeated before and after exposure to atmospheric air for a duration equivalent to the episodic hypoxia protocol (i.e. sham episodic hypoxia). During the rebreathing trials, subjects initially hyperventilated to reduce the partial pressure of carbon dioxide (P(ET)CO2) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr) or high oxygen gas mixture (140 Torr). During the trials, P(ET)CO2 increased while the selected level of oxygen was maintained. The point at which ventilation began to rise in a linear fashion as P(ET)CO2 increased was the ventilatory threshold. The ventilatory response below and above the threshold was determined. The results showed that the VRCO2 (hypoxia) and the VRCO2 (hyperoxia) was increased after exposure to episodic hypoxia {VRCO2 (hypoxia): 7.9 +/- 1.3 versus 10.5 +/- 1.3, VRCO2 (hyperoxia): 5.9 +/- 1.1 versus 6.7 +/- 1.1 L/min/Torr}. However, only the increase in the VRCO2 (hypoxia) after episodic hypoxia was greater than the increase measured after exposure to sham episodic hypoxia. Long-term facilitation of ventilation, tidal volume and breathing frequency was not evident after episodic hypoxia. We conclude that the VRCO2 (hypoxia) is enhanced after exposure to acute episodic hypoxia and that enhancement of the VRCO2 (hypoxia) occurs even though long-term facilitation is not evident.
我们的主要假设是，在阻塞性睡眠呼吸暂停（OSA）患者中，暴露于间歇性低氧后，在持续性低氧{VRCO2（低氧）}或高氧{VRCO2（高氧）}情况下对二氧化碳的急性通气反应会增加。其次，我们假设，慢性（即数年）暴露于间歇性低氧（OSA的一个标志）会在急性（即数分钟）暴露于间歇性低氧后促进呼吸活动的持续增强（即长期易化）。九名其他方面健康的OSA男性在暴露于八次4分钟的低氧发作前后完成了一系列重复呼吸试验。在另一个场合，在暴露于与间歇性低氧方案持续时间相同的常压空气（即假间歇性低氧）前后重复进行重复呼吸试验。在重复呼吸试验期间，受试者最初过度通气以将二氧化碳分压（P(ET)CO2）降低至25 Torr以下。然后受试者从装有正常二氧化碳分压（42 Torr）、低氧（50 Torr）或高氧气体混合物（140 Torr）的袋子中重复呼吸。在试验期间，P(ET)CO2升高，同时维持选定的氧气水平。随着P(ET)CO2升高通气开始呈线性上升的点即为通气阈值。确定阈值以下和以上的通气反应。结果显示，暴露于间歇性低氧后VRCO2（低氧）和VRCO2（高氧）增加{VRCO2（低氧）：7.9±1.3对10.5±1.3，VRCO2（高氧）：5.9±1.1对6.7±1.1 L/min/Torr}。然而，仅间歇性低氧后VRCO2（低氧）的增加大于假间歇性低氧暴露后测得的增加。间歇性低氧后通气、潮气量和呼吸频率的长期易化并不明显。我们得出结论，暴露于急性间歇性低氧后VRCO2（低氧）增强，并且即使长期易化不明显，VRCO2（低氧）也会增强。
