论文部分内容阅读
本工作设想,内啡肽参与了成人急性低氧通气压抑机制。受试者均为健康成年男子。6名受试者吸入中度低氧混合气(12.8％O_2)30min;7名吸入重度低氧混合气(10.8％O_2)20min,其中6名并在重度低氧下吸入三口纯氮气。吸入低氧气前先由静脉注入生理盐水(对照)或纳洛酮(中度低氧5mg,重度低氧10mg)。观察低氧时的通气反应、终末潮气二氧化碳分压(P_(ETCO2)、动脉血氧饱和度和外周低氧通气敏感性以及纳洛酮对上述测定的影响。结果表明,纳洛酮使重度低氧下的通气压抑明显减弱,低氧第3～15分钟的通气水平明显高于对照实验;而P_(ETCO2)明显低于对照值。但纳洛酮对中度低氧下的通气压抑无明显作用。此外,纳洛酮显著增强外周低氧敏感性。结果提示,在重度低氧下,内啡肽参与了成人低氧通气压抑机制,并对外周低氧敏感性有抑制作用。
This work envisions that endorphin is involved in the acute hypoxia-induced depression in adults. Subjects were healthy adult men. 6 subjects inhaled moderate hypoxia mixture (12.8% O 2) for 30 min; 7 inhaled severe hypoxia mixture (10.8% O 2) for 20 min, of which 6 inhaled three pure nitrogen under severe hypoxia. Inhaled low oxygen before the first intravenous injection of saline (control) or naloxone (moderate hypoxia 5mg, severe hypoxia 10mg). The effects of naloxone on naloxone and naloxone were investigated.Results showed that naloxone caused severe changes of the respiratory rate, the end-tidal carbon dioxide partial pressure (P_ (ETCO2), arterial oxygen saturation and peripheral hypoxemia sensitivity) Ventilatory pressure was significantly reduced in hypoxia, the level of hypoxia 3 to 15 minutes ventilation was significantly higher than the control experiment; and P_ (ETCO2) was significantly lower than the control value.But naloxone moderate hypoxia pressure was In addition, naloxone significantly enhanced peripheral hypoxia sensitivity.The results suggest that endorphins are involved in adult hypoxia-depression mechanism and inhibit peripheral hypoxia sensitivity under severe hypoxia.