Department of Physiology & Neurobiology, The Geisel School of Medicine at Dartmouth, USA.
Respir Physiol Neurobiol. 2013 Mar 1;186(1):109-13. doi: 10.1016/j.resp.2013.01.004. Epub 2013 Jan 22.
We have examined influence of hypocapnia, mild hypercapnia and hypoxia on the durations of fictive apnea and respiratory disruption elicited by injection of 0.1ml of water into the laryngeal lumen-the laryngeal chemoreflex (LCR)-in 20 unanesthetized, decerebrate, vagotomized piglets aged 4-10 days that were paralyzed and ventilated with a constant frequency and tidal volume. The LCR was enhanced by hypocapnia and attenuated by hypercapnia as reported by others. The responses to laryngeal stimulation during hypoxia were varied and complex: some animals showed abbreviated responses during the tachypnea of early hypoxia, followed after 10-15min by more prolonged apnea and respiratory disruption accompanying the reduction in ventilatory activity that commonly occurs during sustained hypoxia in neonates. We speculate that this later hypoxic enhancement of the LCR may be due to accumulation of adenosine in the brain stem.
我们研究了低碳酸血症、轻度高碳酸血症和缺氧对喉腔注射 0.1ml 水诱发的虚拟呼吸暂停和呼吸中断持续时间的影响,这是一种喉化学反射(LCR),在 20 只未麻醉、去大脑、迷走神经切断的 4-10 天大的猪只中进行,这些猪只在接受机械通气时被麻痹,并使用恒定的频率和潮气量进行通气。正如其他人所报道的那样,低碳酸血症增强了 LCR,高碳酸血症减弱了 LCR。在缺氧期间,对喉刺激的反应是多样且复杂的:一些动物在早期缺氧的呼吸急促期间表现出短暂的反应,随后在 10-15 分钟后,伴随着通气活动减少,出现更长时间的呼吸暂停和呼吸中断,这在新生儿持续缺氧期间很常见。我们推测,这种后期缺氧对 LCR 的增强可能是由于脑干中腺苷的积累。