Maxwell D L, Fuller R W, Nolop K B, Dixon C M, Hughes J M
J Appl Physiol (1985). 1986 Nov;61(5):1762-6. doi: 10.1152/jappl.1986.61.5.1762.
Adenosine infusion (100 micrograms X kg-1 X min-1) in humans stimulates ventilation but also causes abdominal and chest discomfort. To exclude the effects of symptoms and to differentiate between a central and peripheral site of action, we measured the effect of adenosine infused at a level (70-80 micrograms X kg-1 X min-1) below the threshold for symptoms. Resting ventilation (VE) and progressive ventilatory responses to isocapnic hypoxia and hyperoxic hypercapnia were measured in six normal men. Compared with a control saline infusion given single blind on the same day, adenosine stimulated VE [mean increase: 1.3 +/- 0.8 (SD) l/min; P less than 0.02], lowered resting end-tidal PCO2 (PETCO2) (mean fall: -3.9 +/- 0.9 Torr), and increased heart rate (mean increase: 16.1 +/- 8.1 beats/min) without changing systemic blood pressure. Adenosine increased the hypoxic ventilatory response (control: -0.68 +/- 0.4 l X min-1 X %SaO2-1, where %SaO2 is percent of arterial O2 saturation; adenosine: -2.40 +/- 1.2 l X min-1 X %SaO2-1; P less than 0.01) measured at a mean PETCO2 of 38.3 +/- 0.6 Torr but did not alter the hypercapnic response. This differential effect suggests that adenosine may stimulate ventilation by a peripheral rather than a central action and therefore may be involved in the mechanism of peripheral chemoreception.
人体静脉输注腺苷(100微克/千克/分钟)可刺激通气,但也会引起腹部和胸部不适。为排除症状的影响并区分中枢和外周作用部位,我们在低于症状阈值的水平(70 - 80微克/千克/分钟)输注腺苷并测量其作用。在6名正常男性中测量静息通气量(VE)以及对等容性低氧和高氧性高碳酸血症的渐进性通气反应。与同日单盲给予的生理盐水对照输注相比,腺苷刺激了VE[平均增加:1.3±0.8(标准差)升/分钟;P<0.02],降低了静息呼气末PCO₂(PETCO₂)(平均下降:-3.9±0.9托),并增加了心率(平均增加:16.1±8.1次/分钟),而未改变体循环血压。在平均PETCO₂为38.3±0.6托时,腺苷增加了低氧通气反应(对照:-0.68±0.4升/分钟/%SaO₂⁻¹,其中%SaO₂是动脉血氧饱和度百分比;腺苷:-2.40±1.2升/分钟/%SaO₂⁻¹;P<0.01),但未改变高碳酸血症反应。这种差异效应表明,腺苷可能通过外周而非中枢作用刺激通气,因此可能参与外周化学感受机制。