Engelstein E D, Lerman B B, Somers V K, Rea R F
New York Hospital-Cornell Medical Center, NY 10021.
Circulation. 1994 Dec;90(6):2919-26. doi: 10.1161/01.cir.90.6.2919.
Exogenous adenosine has been shown to increase muscle sympathetic nerve activity (MSNA), blood pressure, heart rate, and ventilation in conscious humans, effects attributed to peripheral chemoreceptor activation.
To determine whether endogenous adenosine has similar effects and whether they are mediated through chemoreceptor activation, we examined the effects of dipyridamole, an inhibitor of adenosine reuptake, on sympathetic nerve activity and ventilation. Twenty studies were conducted on separate days in 15 healthy volunteers. We examined responses to dipyridamole 0.56 mg/kg during room air breathing (n = 7), during hyperoxia (100% O2, n = 6), and during room air breathing after pretreatment with aminophylline (n = 7). During room air breathing, dipyridamole increased MSNA from 231 +/- 42 to 504 +/- 136 U/min, heart rate from 65 +/- 3.8 to 96 +/- 4.7 beats per minute, and systolic blood pressure from 129 +/- 3.5 to 140 +/- 4.8 mm Hg; central venous pressure decreased from 5.5 +/- 0.4 to 4.5 +/- 0.3 mm Hg (P < .01), and minute ventilation increased from 7.8 +/- 0.6 to 9.1 +/- 0.5 L/min (P < .01). During peripheral chemoreceptor suppression (with hyperoxia), there was a dissociation of the effects of dipyridamole on ventilation and sympathoexcitation. Effects on ventilation were attenuated, but sympathoexcitatory effects were not. Pretreatment with aminophylline, an adenosine receptor antagonist, either abolished (blood pressure, minute ventilation, and end-tidal CO2) or markedly attenuated (MSNA and heart rate) the effects of dipyridamole during room air breathing.
Augmentation of endogenous adenosine with dipyridamole increases sympathetic nerve activity and ventilation in conscious humans. The ventilatory effects of endogenous adenosine are mediated predominantly by chemoreceptor activation, but the sympathetic and hemodynamic responses to endogenous adenosine are probably mediated by an additional afferent mechanism that is independent of peripheral chemoreceptor activation.
外源性腺苷已被证明可增加清醒人类的肌肉交感神经活动（MSNA）、血压、心率和通气，这些效应归因于外周化学感受器激活。
为了确定内源性腺苷是否有类似作用以及这些作用是否通过化学感受器激活介导，我们研究了腺苷再摄取抑制剂双嘧达莫对交感神经活动和通气的影响。在15名健康志愿者身上于不同日期进行了20项研究。我们在室内空气呼吸期间（n = 7）、高氧期间（100% O₂，n = 6）以及用氨茶碱预处理后在室内空气呼吸期间（n = 7）检测了对0.56 mg/kg双嘧达莫的反应。在室内空气呼吸期间，双嘧达莫使MSNA从231±42增加至504±136 U/分钟，心率从65±3.8增加至96±4.7次/分钟，收缩压从129±3.5增加至140±4.8 mmHg；中心静脉压从5.5±0.4降至4.5±0.3 mmHg（P < 0.01），分钟通气量从7.8±0.6增加至9.1±0.5 L/分钟（P < 0.01）。在周围化学感受器受抑制（高氧）期间，双嘧达莫对通气和交感神经兴奋的作用出现分离。对通气的作用减弱，但交感神经兴奋作用未减弱。用腺苷受体拮抗剂氨茶碱预处理，要么消除（血压、分钟通气量和呼气末二氧化碳）要么显著减弱（MSNA和心率）双嘧达莫在室内空气呼吸期间的作用。
用双嘧达莫增强内源性腺苷可增加清醒人类的交感神经活动和通气。内源性腺苷的通气作用主要通过化学感受器激活介导，但内源性腺苷对交感神经和血流动力学的反应可能由一种独立于外周化学感受器激活的额外传入机制介导。
