Gaba S J, Préfaut C
Service d'Exploration de la Fonction Respiratoire, Hôpital Aiguelongue, Montpellier, France.
Eur Respir J. 1990 Apr;3(4):450-5.
During stepwise incremental intravenous adenosine triphosphate (ATP) infusion, systemic and pulmonary vascular effects were compared in 10 patients with stable chronic obstructive pulmonary disease (COPD). Pulmonary vasodilation was: 1) predominant and maximal as early as the lowest dose infusion (0.1 mumol.kg-1.min-1) with pulmonary arterial mean pressure (Ppa) (-16%; p less than 0.01) and pulmonary vascular resistance (PVR) decreases (-28%; p less than 0.005) and simultaneous increasing delta PVR/delta SVR ratio; 2) associated with worsening hypoxaemia (-14%; p less than 0.001), but also with increasing alveolar-arterial oxygen pressure difference (P(A-a)O2) and venous admixture (Qs/Qt) suggesting some inhibition of hypoxic pulmonary vasoconstriction. Systemic vasodilation was: 1) clearly dose-dependent, but only reached significant level at 0.2 mumol.kg-1.min-1 with systemic arterial mean pressure (Psa) (-12.5%; p less than 0.05) and systemic vascular resistance (SVR) decreases (-30%; p less than 0.01); 2) associated with arterial carbon dioxide tension (PaCO2) decrease (-12.5%; p less than 0.005) and recurring uncontrollable hyperpnoea, suggesting a ventilatory stimulatory effect of ATP in man. In patients with stable COPD, ATP infusion has dual acute haemodynamic effects depending on the dose-level. The predominant pulmonary vasodilating effect occurs as early as the lowest dose-levels without any further increase of pulmonary vasodilation. This contrasts with the dose-related systemic vasodilation effect. Such a dual haemodynamic effect is an indirect indication of in vivo lung metabolism of ATP.
在逐步递增静脉注射三磷酸腺苷（ATP）的过程中，对10例稳定期慢性阻塞性肺疾病（COPD）患者的全身和肺血管效应进行了比较。肺血管舒张表现为：1）早在最低剂量输注（0.1μmol·kg⁻¹·min⁻¹）时即占主导且达到最大程度，肺动脉平均压（Ppa）下降（-16%；p<0.01），肺血管阻力（PVR）下降（-28%；p<0.005），同时ΔPVR/ΔSVR比值增加；2）与低氧血症加重（-14%；p<0.001）相关，但也与肺泡-动脉氧分压差（P(A-a)O2）和静脉血掺杂（Qs/Qt）增加有关，提示对低氧性肺血管收缩有一定抑制作用。全身血管舒张表现为：1）明显呈剂量依赖性，但仅在0.2μmol·kg⁻¹·min⁻¹时达到显著水平，此时体动脉平均压（Psa）下降（-12.5%；p<0.05），全身血管阻力（SVR）下降（-30%；p<0.01）；2）与动脉血二氧化碳分压（PaCO2）下降（-12.5%；p<0.005）和反复出现的无法控制的呼吸急促有关，提示ATP对人体有通气刺激作用。在稳定期COPD患者中，ATP输注根据剂量水平具有双重急性血流动力学效应。最早在最低剂量水平时即出现占主导的肺血管舒张作用，且肺血管舒张不再进一步增强。这与剂量相关的全身血管舒张效应形成对比。这种双重血流动力学效应间接提示了ATP在体内的肺代谢情况。
