Biaggioni I, Olafsson B, Robertson R M, Hollister A S, Robertson D
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn 37232.
Circ Res. 1987 Dec;61(6):779-86. doi: 10.1161/01.res.61.6.779.
The cardiovascular and respiratory effects of intravenous adenosine were studied in conscious normal volunteers. Bolus injections of adenosine increased systolic and diastolic pressures initially (+15 and +13 mm Hg after 100 micrograms/kg) followed by a subsequent reduction in systolic and diastolic pressures (-12 and -16 mm Hg). Heart rate increased during trough blood pressure (R-R interval shortening of 298 msec after 100 micrograms/kg). Adenosine steady-state infusions increased heart rate (+30 beats/min during 140 micrograms/kg/min), systolic pressure (+16 mm Hg), and pulse pressure (+21 mm Hg) but decreased diastolic pressure slightly (-5 mm Hg), resulting in no significant change in mean arterial pressure. Adenosine stimulated respiration, resulting in decreased PaCO2 (41 to 31 mm Hg), increased PaCO2 (101 to 113 mm Hg), and increased pH (7.42 to 7.50). The increased ventilation was not explained by bronchoconstriction, hypotension, or hypoxia. The observed pressor and tachycardic effects are mediated through reflex autonomic mechanisms since they are completely abolished in patients with severe autonomic failure. These autonomic mechanisms probably involve chemoreceptor activation since adenosine is pressor when infused in the aortic arch proximal to the origin of the carotid arteries but depressor when infused in the descending aorta. It is concluded that the hemodynamic and respiratory effects of adenosine observed in normal volunteers are in part due to chemoreceptor stimulation. These findings raise the possibility that adenosine is an endogenous modulator of respiration in man.
在清醒的正常志愿者中研究了静脉注射腺苷对心血管和呼吸系统的影响。静脉推注腺苷最初会使收缩压和舒张压升高(100微克/千克后分别升高15和13毫米汞柱),随后收缩压和舒张压降低(分别降低12和16毫米汞柱)。在血压低谷时心率增加(100微克/千克后R-R间期缩短298毫秒)。腺苷稳态输注会使心率增加(140微克/千克/分钟时增加30次/分钟)、收缩压升高(16毫米汞柱)、脉压增大(21毫米汞柱),但舒张压略有降低(5毫米汞柱),导致平均动脉压无显著变化。腺苷刺激呼吸,导致动脉血二氧化碳分压降低(从41降至31毫米汞柱)、动脉血氧分压升高(从101升至113毫米汞柱)以及pH值升高(从7.42升至7.50)。通气增加并非由支气管收缩、低血压或低氧血症所致。观察到的升压和心动过速效应是通过反射性自主神经机制介导的,因为在严重自主神经功能衰竭的患者中这些效应完全消失。这些自主神经机制可能涉及化学感受器激活,因为腺苷注入颈动脉起源近端的主动脉弓时具有升压作用,而注入降主动脉时具有降压作用。结论是,在正常志愿者中观察到的腺苷对血流动力学和呼吸的影响部分归因于化学感受器刺激。这些发现增加了腺苷是人体呼吸内源性调节剂的可能性。