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Vagal nerve activity contributes to improve the efficiency of pulmonary gas exchange in hypoxic humans
Author(s) -
Ito Shoji,
Sasano Hiroshi,
Sasano Nobuko,
Hayano Junichiro,
Fisher Joseph A.,
Katsuya Hirotada
Publication year - 2006
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2006.034421
Subject(s) - atropine , vagal tone , respiratory system , tidal volume , anesthesia , dead space , chemistry , vagus nerve , heart rate , medicine , blood pressure , stimulation , autonomic nervous system
The aim of this study was to test our hypothesis that both phasic cardiac vagal activity and tonic pulmonary vagal activity, estimated as respiratory sinus arrhythmia (RSA) and anatomical dead space volume, respectively, contribute to improve the efficiency of pulmonary gas exchange in humans. We examined the effect of blocking vagal nerve activity with atropine on pulmonary gas exchange. Ten healthy volunteers inhaled hypoxic gas with constant tidal volume and respiratory frequency through a respiratory circuit with a respiratory analyser. Arterial partial pressure of O 2 ( P aO 2) and arterial oxygen saturation ( S pO 2) were measured, and alveolar‐to‐arterial P O 2difference ( D A − aO 2) was calculated. Anatomical dead space ( V D,an ), alveolar dead space ( V D,alv ) and the ratio of physiological dead space to tidal volume ( V D,phys / V T ) were measured. Electrocardiogram was recorded, and the amplitude of R–R interval variability in the high‐frequency component (RRIHF) was utilized as an index of RSA magnitude. These parameters of pulmonary function were measured before and after administration of atropine (0.02 mg kg −1 ). Decreased RRIHF ( P < 0.01) was accompanied by decreases in P aO 2and S pO 2( P < 0.05 and P < 0.01, respectively) and an increase in D A − aO 2( P < 0.05). Anatomical dead space, V D,alv and V D,phys / V T increased ( P < 0.01, P < 0.05 and P < 0.01, respectively) after atropine administration. The blockade of the vagal nerve with atropine resulted in an increase in V D,an and V D,alv and a deterioration of pulmonary oxygenation, accompanied by attenuation of RSA. Our findings suggest that both phasic cardiac and tonic pulmonary vagal nerve activity contribute to improve the efficiency of pulmonary gas exchange in hypoxic conscious humans.