Qayyum M S, Barlow C W, O'Connor D F, Paterson D J, Robbins P A
University Laboratory of Physiology, Oxford.
J Physiol. 1994 Apr 15;476(2):365-72. doi: 10.1113/jphysiol.1994.sp020138.
The purpose of this study was to determine whether changes in arterial plasma potassium concentration [K+]a affect expired ventilation (VE) in euoxia, hypoxia and hyperoxia during rest and light exercise in humans. Three periods of ventilatory measurements were undertaken in eight healthy subjects at rest and in seven other subjects during cycle ergometry (70 W). The first period of measurement was before the ingestion of 64 mmol of potassium chloride (KCl), the second 20 min after ingestion of KCl when [K+]a levels were elevated, and the third 3 h after the ingestion of KCl when [K+]a had returned substantially to normal. During each period, end-tidal PO2 was cycled between euoxia, hypoxia and hyperoxia, whilst the end-tidal PCO2 was maintained constant. The acute ventilatory response to hypoxia (AHVR) was calculated as the difference in VE during hypoxia and hyperoxia within each period of measurement. Oral KCl produced a 1.3 +/- 0.2 mM (mean +/- S.E.M.) increase in [K+]a at rest and a 0.8 +/- 0.2 mM increase during exercise. There was no significant difference in ventilation during euoxia between the three periods of measurement at rest or during exercise. There was a significant increase in AHVR with the rise in [K+]a of 21 min-1 mM-1 at rest (arterial PO2 during hypoxia ca 57 Torr) and 10 l min-1 mM-1 during exercise (arterial PO2 during hypoxia ca 52 Torr). There was a significant difference in the absolute increase in AHVR with [K+]a between rest and exercise, but this difference was not significant if the increase in AHVR with [K+]a was expressed as a percentage of the initial AHVR. We conclude that changes in [K+]a of the order of 1 mM have little effect on euoxic ventilation at rest or during light exercise in humans. We also conclude that [K+]a changes of this order increase AHVR at rest and during light exercise and that increases in [K+]a contribute to the increase in AHVR with exercise in humans.
本研究的目的是确定在人类休息和轻度运动期间，动脉血浆钾浓度[K+]a的变化是否会影响常氧、低氧和高氧状态下的呼出通气量（VE）。对8名健康受试者在休息时以及另外7名受试者在进行自行车测力计运动（70瓦）时进行了三个阶段的通气测量。第一个测量阶段是在摄入64毫摩尔氯化钾（KCl）之前，第二个阶段是在摄入KCl 20分钟后，此时[K+]a水平升高，第三个阶段是在摄入KCl 3小时后，此时[K+]a已基本恢复正常。在每个阶段，呼气末PO2在常氧、低氧和高氧之间循环，同时呼气末PCO2保持恒定。急性低氧通气反应（AHVR）计算为每个测量阶段低氧和高氧期间VE的差值。口服KCl在休息时使[K+]a升高1.3±0.2毫摩尔/升（平均值±标准误），运动期间升高0.8±0.2毫摩尔/升。在休息或运动时的三个测量阶段中，常氧状态下的通气量没有显著差异。随着[K+]a升高，休息时（低氧期间动脉PO2约为57托）AHVR显著增加，增加幅度为21升/分钟·毫摩尔/升，运动时（低氧期间动脉PO2约为52托）为10升/分钟·毫摩尔/升。休息和运动时，AHVR随[K+]a的绝对增加量存在显著差异，但如果将AHVR随[K+]a的增加量表示为初始AHVR的百分比，则这种差异不显著。我们得出结论，在人类休息或轻度运动期间，1毫摩尔左右的[K+]a变化对常氧通气影响很小。我们还得出结论，这种程度的[K+]a变化在休息和轻度运动时会增加AHVR，并且[K+]a的增加有助于人类运动时AHVR的增加。
