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睡眠中犬类对颈动脉窦压力升高和降低的呼吸及心血管反应。

Respiratory and cardiovascular responses to increased and decreased carotid sinus pressure in sleeping dogs.

作者信息

Saupe K W, Smith C A, Henderson K S, Dempsey J A

机构信息

John Rankin Laboratory of Pulmonary Medicine, Department of Preventive Medicine, University of Wisconsin, Madison 53705, USA.

出版信息

J Appl Physiol (1985). 1995 May;78(5):1688-98. doi: 10.1152/jappl.1995.78.5.1688.

Abstract

The purpose of this study was to determine the effects of changing blood pressure in the carotid sinus (Pcs) on ventilatory output during wakefulness and non-rapid-eye-movement sleep in unanesthetized dogs. Eight dogs were chronically instrumented so that ventilation, heart rate, and blood pressure could be measured while pressure in the isolated carotid sinus was rapidly changed by means of an extracorporeal perfusion circuit. Raising Pcs 35-75 mmHg consistently reduced ventilation 15-40% in a dose-response fashion, with little or no further diminution in minute ventilation as Pcs was further increased > 75 mmHg above control level. This decrease in minute ventilation was immediate, due primarily to a decrease in tidal volume, and was sustained over the 20-s period of elevated Pcs. Increases in Pcs also caused immediate sustained reductions in systemic blood pressure and heart rate, both of which also fell in a dose-dependent fashion. The ventilatory and systemic cardiovascular responses to increased Pcs were the same during wakefulness and non-rapid-eye-movement sleep. Decreasing Pcs 40-80 mmHg caused a sudden carotid chemoreceptor-mediated hyperpnea that was eliminated by hyperoxia. We conclude that increasing Pcs causes a reflex inhibition of ventilation and that this reflex may play a role in sleep-disordered breathing.

摘要

本研究的目的是确定在未麻醉犬的清醒和非快速眼动睡眠期间,改变颈动脉窦压力(Pcs)对通气输出的影响。八只犬被长期植入仪器,以便在通过体外灌注回路快速改变孤立颈动脉窦压力的同时,测量通气、心率和血压。将Pcs升高35 - 75 mmHg会持续以剂量反应方式使通气减少15 - 40%,当Pcs在高于对照水平75 mmHg以上进一步升高时,分钟通气量几乎没有或没有进一步减少。分钟通气量的这种减少是即刻的,主要由于潮气量减少,并且在Pcs升高的20秒期间持续存在。Pcs升高还会导致全身血压和心率即刻持续降低,两者也呈剂量依赖性下降。在清醒和非快速眼动睡眠期间,对Pcs升高的通气和全身心血管反应是相同的。将Pcs降低40 - 80 mmHg会导致突然的颈动脉化学感受器介导的呼吸急促,而高氧可消除这种呼吸急促。我们得出结论,升高Pcs会引起通气的反射性抑制,并且这种反射可能在睡眠呼吸障碍中起作用。

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