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First published online on June 29, 2006.
Experimental Physiology (2006)
DOI: 10.1113/expphysiol.2006.034421
© The Physiological Society 2006

A more recent version of this article appeared on September 1, 2006
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Received May 10, 2006
Revised May 24, 2006
Accepted after revision June 26, 2006


Respiratory [290]

Vagal nerve activity contributes to improve the efficiency of pulmonary gas exchange in hypoxic humans

Shoji Ito 1, Hiroshi Sasano 2*, Nobuko Sasano 2, Junichiro Hayano 2, Joseph A Fisher 3, Hirotada Katsuya 2

1 Nagoya City University Graduate School of
2 Nagoya City University Graduate School of Medical Sciences
3 University Health Network, University of Toronto

* To whom correspondence should be addressed. E-mail: hirosasano{at}aol.com.


   Abstract
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 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, achieved with atropine, on pulmonary gas exchange. Ten healthy volunteers inhaled hypoxic gas with constant tidal volume and respiratory frequency through a respiratory circuit in which a respiratory analyzer was installed. Pao2, and oxygen saturation (Spo2) were measured and alveolar-to-arterial Po2 difference (A-a Do2) was calculated. Anatomical dead space (VDan), alveolar dead space (VDalv) and the ratio of physiological dead space and tidal volume (VD/VT phys) were measured. Electrocardiogram was recorded and the amplitude of R-R interval variability in the high frequency (0.15-0.2 Hz) component (RRIHF) was utilized as an index of respiratory sinus arrhythmia (RSA) magnitude. These parameters of pulmonary function were measured before (control) and after atropine administration (0.02 mg/kg-1). Decreased RRIHF (P<0.01) was accompanied by decreases in Pao2 and Spo2 (P <0.05, P<0.01 respectively) and an increase in A-a Do2 (P<0.05). VDan, VDalv, and VD/VT phys 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 VDan and VDalv 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.

Key Words: Pulmonary circulation, Respiratory control, Vagus




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