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睡眠不足对β-内啡肽活性、肾上腺素水平和通气反应性的影响。

Effect of sleep loss on beta-endorphin activity, epinephrine levels, and ventilatory responsiveness.

作者信息

Phillips B, Cooper K R, Newsome H H, Dewey W L

出版信息

South Med J. 1987 Jan;80(1):16-20. doi: 10.1097/00007611-198701000-00004.

Abstract

Sleep loss impairs ventilatory responsiveness to hypercapnia and hypoxia, and also interferes with performance on spirometry. To test the hypothesis that the decline in hypercapnic drive due to sleep loss is mediated by endorphin production, we measured loaded and unloaded CO2 response after injection of placebo and naloxone in 11 normal subjects who were alternately rested and sleep-deprived. Blood for beta-endorphin and epinephrine assay was drawn before testing each day. Unloaded CO2 response was lower after sleep loss than after sleep restoration; naloxone had no effect on this difference. Likewise, there was no difference between CO2 response after naloxone administration and CO2 response in control subjects. beta-Endorphin activity did not rise after sleep loss. Loaded CO2 response was reduced compared to unloaded response and was not affected by sleep loss or by naloxone. The serum epinephrine level rose significantly with sleep loss. We conclude that naloxone is not a respiratory stimulant in normal people, and that it does not reverse the fall in CO2 response that follows sleep loss.

摘要

睡眠不足会损害对高碳酸血症和低氧血症的通气反应,还会干扰肺活量测定的结果。为了检验睡眠不足导致的高碳酸驱动下降是由内啡肽产生介导的这一假设,我们在11名正常受试者中,交替进行休息和睡眠剥夺后,注射安慰剂和纳洛酮,测量了加载和未加载二氧化碳的反应。每天测试前采集血液用于检测β-内啡肽和肾上腺素。睡眠剥夺后的未加载二氧化碳反应低于睡眠恢复后;纳洛酮对此差异无影响。同样,纳洛酮给药后的二氧化碳反应与对照受试者的二氧化碳反应之间也没有差异。睡眠不足后β-内啡肽活性没有升高。与未加载反应相比,加载二氧化碳反应降低,且不受睡眠剥夺或纳洛酮的影响。血清肾上腺素水平随着睡眠剥夺显著升高。我们得出结论,纳洛酮对正常人不是呼吸兴奋剂,并且它不会逆转睡眠剥夺后二氧化碳反应的下降。

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