Chua T P, Ponikowski P P, Harrington D, Chambers J, Coats A J
Department of Cardiac Medicine, Royal Brompton Hospital, London.
Heart. 1996 Dec;76(6):483-9. doi: 10.1136/hrt.76.6.483.
To assess the contribution of peripheral chemoreceptors to ventilation and the effects of continuous inspired oxygen on exercise tolerance in chronic heart failure patients. The role of peripheral chemoreceptors in mediating hyperpnoea in chronic heart failure is unknown. Hyperoxia is known to suppress the peripheral chemoreceptor drive. The magnitude of decrease in ventilation with transient inhalations of oxygen thus provides a measure of the contribution of the peripheral chemoreceptors to ventilation.
Tertiary specialist hospital.
Three breaths of 100% oxygen were given at rest and also during cycle ergometry at 25 W to 8 healthy controls (age 52.0 (4.7) (SEM) years) and 13 patients with chronic heart failure (age 60.5 (2.1) years (P = NS); radionuclide left ventricular ejection fraction 25.5 (4.3)%). The peripheral chemoreceptor sensitivity was also measured by assessing the ventilatory response to hypoxia using transient inhalations of pure nitrogen. Another group of 12 patients with chronic heart failure (age 65.5 (1.5) years; left ventricular ejection fraction 21.3 (3.0)%) underwent treadmill exercise testing on 2 occasions, breathing air or 100% oxygen in a randomised single-blind manner, to examine the effects of continuous inspired oxygen on exercise tolerance.
The reduction in ventilation with transient hyperoxia was 18.1 (2.9)% v 17.9 (2.6)% (P = NS) at rest and 20.4 (2.8)% v 21.0 (1.6)% (P = NS) during cycle ergometry, for controls and patients respectively. The hypoxic chemosensitivity was higher in patients (0.232 (0.022) v 0.572 (0.082) 1/min/%SaO2; P = 0.002). Continuous inspired oxygen increased exercise time (517 (31) v 455 (27) seconds; P = 0.003), and a trend towards a reduction in the ventilatory response to exercise, characterised by the regression slope relating ventilation to carbon dioxide output, was evident (31.27 (2.60) v 34.19 (2.35); P = 0.08).
Despite an increased peripheral chemoreceptor sensitivity, the proportionate contribution of peripheral chemoreceptors to ventilation remained similar in heart failure patients (about 20%). This suggests that the peripheral chemoreceptors are not the main mediator of increased ventilation and there are other non-peripheral chemoreceptor-mediated mechanisms involved. Hyperoxia reduced ventilation at rest and during cycle ergometry. The increase in exercise duration with continuous inspired oxygen that was associated with a reduction in exercise ventilatory response suggests that suppression of the peripheral chemoreceptors may improve exercise tolerance; the effects of possible reduced skeletal muscle anaerobiosis cannot be excluded, however.
评估外周化学感受器对慢性心力衰竭患者通气的作用以及持续吸入氧气对运动耐力的影响。外周化学感受器在慢性心力衰竭介导呼吸急促中的作用尚不清楚。已知高氧会抑制外周化学感受器驱动。因此，短暂吸入氧气时通气量的下降幅度可衡量外周化学感受器对通气的作用。
三级专科医院。
对8名健康对照者（年龄52.0（4.7）（标准误）岁）和13名慢性心力衰竭患者（年龄60.5（2.1）岁（P =无显著性差异）；放射性核素左心室射血分数25.5（4.3）%）在静息时以及在功率为25 W的蹬车运动期间给予3次100%氧气呼吸。还通过短暂吸入纯氮评估对低氧的通气反应来测量外周化学感受器敏感性。另一组12名慢性心力衰竭患者（年龄65.5（1.5）岁；左心室射血分数21.3（3.0）%）以随机单盲方式在两种情况下进行跑步机运动测试，分别呼吸空气或100%氧气，以研究持续吸入氧气对运动耐力的影响。
对于对照组和患者，静息时短暂高氧通气量减少分别为18.1（2.9）%对17.9（2.6）%（P =无显著性差异），蹬车运动期间为20.4（2.8）%对21.0（1.6）%（P =无显著性差异）。患者的低氧化学敏感性更高（0.232（0.022）对0.572（0.082）1/分钟/%血氧饱和度；P = 0.002）。持续吸入氧气增加了运动时间（517（31）对455（27）秒；P = 0.003），并且以通气与二氧化碳排出量的回归斜率为特征的运动通气反应有降低趋势（31.27（2.60）对34.19（2.35）；P = 0.08）。
尽管外周化学感受器敏感性增加，但外周化学感受器对通气的相对作用在心力衰竭患者中仍相似（约20%）。这表明外周化学感受器不是通气增加的主要介导因素，还存在其他非外周化学感受器介导的机制。高氧在静息和蹬车运动期间降低了通气量。持续吸入氧气使运动持续时间增加且与运动通气反应降低相关，这表明抑制外周化学感受器可能改善运动耐力；然而，不能排除骨骼肌无氧代谢可能减少的影响。
