Modulation of human sinus node function by systemic hypoxia.
We studied sinus node responses to mild to moderate systemic hypoxia provoked by nitrogen inhalation in five healthy young men. Volunteers maintained their usual tidal volumes and respiratory frequencies at constant levels. We modified carotid arterial baroreceptor activity by applying neck suction or pressure during held expiration. Arterial oxygen saturation began to decline between 8.0 and 9.6 s after the onset of the first breath of nitrogen. Pulse interval declined in parallel with oxygen saturation. During mild hypoxia cardioacceleration was restricted primarily to the inspiratory phase of respiration. Moderate hypoxia diminished the magnitude of sinus arrhythmia. It did not alter baroreflex responsiveness. Our results suggest that in normal humans, augmentation of chemoreceptor input leads to reduction of cardiac vagal motoneuron output. This effect exhibits a distinct respiratory periodicity (more prominent in inspiration) and appears to be independent of any influence of hypoxia on ventilation or baroreflex responsiveness.
D000328:Adult; D002628:Chemoreceptor Cells / Q000502:physiology; D006339:Heart Rate; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D009584:Nitrogen; D010100:Oxygen / Q000097:blood; D011311:Pressoreceptors / Q000502:physiology; D012018:Reflex; D012119:Respiration; D012849:Sinoatrial Node / Q000502:physiology*; D013990:Tidal Volume; D014630:Vagus Nerve / Q000502:physiology
D009584:Nitrogen; D010100:Oxygen