Nedoboy Polina E, Houlahan Callum B, Farnham Melissa M J
Cardiovascular Neuroscience Unit, Heart Research Institute, Newtown, NSW, Australia.
Department of Physiology, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW, Australia.
Front Physiol. 2021 Mar 5;12:645392. doi: 10.3389/fphys.2021.645392. eCollection 2021.
A key feature of sleep disordered breathing syndromes, such as obstructive sleep apnea is intermittent hypoxia. Intermittent hypoxia is well accepted to drive the sympathoexcitation that is frequently associated with hypertension and diabetes, with measurable effects after just 1 h. The aim of this study was to directly measure the glucose response to 1 h of acute intermittent hypoxia in pentobarbital anesthetized rats, compared to conscious rats. However, we found that while a glucose response is measurable in conscious rats exposed to intermittent hypoxia, it is suppressed in anesthetized rats. Intermittent hypoxia for 1, 2, or 8 h increased blood glucose by 0.7 ± 0.1 mmol/L in conscious rats but had no effect in anesthetized rats (-0.1 ± 0.2 mmol/L). These results were independent of the frequency of the hypoxia challenges, fasting state, vagotomy, or paralytic agents. A supraphysiological challenge of 3 min of hypoxia was able to induce a glycemic response indicating that the reflex response is not abolished under pentobarbital anesthesia. We conclude that pentobarbital anesthesia is unsuitable for investigations into glycemic response pathways in response to intermittent hypoxia in rats.
睡眠呼吸障碍综合征（如阻塞性睡眠呼吸暂停）的一个关键特征是间歇性缺氧。间歇性缺氧被广泛认为会引发交感神经兴奋，而交感神经兴奋常与高血压和糖尿病相关，且仅在1小时后就会产生可测量的影响。本研究的目的是直接测量戊巴比妥麻醉大鼠与清醒大鼠在急性间歇性缺氧1小时后的血糖反应。然而，我们发现，虽然在暴露于间歇性缺氧的清醒大鼠中可测量到血糖反应，但在麻醉大鼠中该反应受到抑制。在清醒大鼠中，间歇性缺氧1、2或8小时会使血糖升高0.7±0.1 mmol/L，但在麻醉大鼠中则无影响（-0.1±0.2 mmol/L）。这些结果与缺氧刺激的频率、禁食状态、迷走神经切断或麻痹剂无关。3分钟的超生理缺氧刺激能够诱导血糖反应，表明在戊巴比妥麻醉下反射反应并未消失。我们得出结论，戊巴比妥麻醉不适用于研究大鼠对间歇性缺氧的血糖反应途径。
