Griffiths T L, Fernando S S, Saunders K B
Division of Physiological Medicine, St George's Hospital Medical School, London, UK.
Thorax. 1996 Nov;51(11):1083-6. doi: 10.1136/thx.51.11.1083.
In normal subjects intravenous adenosine infusion has been shown to stimulate ventilation with a consequent fall in arterial partial pressure of carbon dioxide (Paco2), probably by an action on the carotid bodies. The objective of this study was to determine whether the increase in Paco2 seen when patients with ventilatory failure secondary to chronic obstructive pulmonary disease (COPD) are given a high concentration of oxygen to breathe might be ameliorated by an intravenous infusion of adenosine.
Eight subjects with chronic stable ventilatory failure secondary to COPD were studied. Their mean (SE) forced expiratory volume in one second (FEV1) was 0.63 (0.12) 1 with forced vital capacity (FVC) of 1.63 (0.21) 1. They received continuous intravenous infusions of saline and adenosine in random order, double blind. The infusions were administered for two minutes at 20 micrograms/kg/min, increasing in increments of 20 micrograms/kg/min every two minutes to a maximum infusion rate of 80 micrograms/kg/min adenosine (or an equivalent saline infusion rate), or until side effects supervened. The infusions were continued at that rate for five minutes, after which the fractional inspired oxygen (FIO2) was raised to 0.50 during a further 20 minutes of the infusion at that rate. Haemoglobin oxygen saturation (SaO2) and transcutaneous PCO2 (PtcCO2) were monitored throughout the procedure. Spirometric tests were performed before and after each infusion.
Adenosine infusion was accompanied by a fall in PtcCO2 from a mean (SE) of 7.29 (0.42) kPa to 6.95 (0.48) kPa: mean difference -0.34 (95% confidence interval, -0.56 to -0.11) kPa. During saline infusion oxygen administration resulted in an increase in transcutaneous PtcCO2 from 7.35 (0.34) kPa to 7.88 (0.28) kPa: mean difference 0.53 (95% CI 0.20 to 0.85) kPa. PtcCO2 did not rise above baseline levels when oxygen was administered during the adenosine infusion. A small fall in FVC was seen following adenosine infusion.
The increase in PtcCO2 seen when patients with stable ventilatory failure secondary to severe COPD are given a high concentration of oxygen to breathe is counteracted by a continuous intravenous infusion of adenosine.
在正常受试者中,静脉输注腺苷已被证明可刺激通气,随后动脉血二氧化碳分压(Paco2)下降,这可能是通过作用于颈动脉体实现的。本研究的目的是确定,对于因慢性阻塞性肺疾病(COPD)导致通气衰竭的患者,给予高浓度氧气呼吸时出现的Paco2升高是否可通过静脉输注腺苷得到改善。
对8例因COPD导致慢性稳定通气衰竭的受试者进行研究。他们一秒用力呼气容积(FEV1)的平均值(标准误)为0.63(0.12)升,用力肺活量(FVC)为1.63(0.21)升。他们以随机顺序、双盲方式接受生理盐水和腺苷的持续静脉输注。输注以20微克/千克/分钟的速度持续两分钟,每两分钟以20微克/千克/分钟的增量增加,直至腺苷的最大输注速度达到80微克/千克/分钟(或等量的生理盐水输注速度),或直至出现副作用。以该速度继续输注五分钟,之后在以该速度进一步输注的20分钟内,将吸入氧分数(FIO2)提高至0.50。在整个过程中监测血红蛋白氧饱和度(SaO2)和经皮二氧化碳分压(PtcCO2)。在每次输注前后进行肺量计测试。
输注腺苷后,PtcCO2从平均值(标准误)7.29(0.42)千帕降至6.95(0.48)千帕:平均差值为-0.34(95%置信区间,-0.56至-0.11)千帕。在输注生理盐水期间给予氧气导致经皮PtcCO2从7.35(0.34)千帕增加至7.88(0.28)千帕:平均差值为0.53(95%置信区间0.20至0.85)千帕。在输注腺苷期间给予氧气时,PtcCO2未升高至基线水平以上。输注腺苷后可见FVC略有下降。
对于因严重COPD导致稳定通气衰竭的患者,给予高浓度氧气呼吸时出现的PtcCO2升高可通过持续静脉输注腺苷得到抵消。