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This Article Full Text Full Text (PDF) All Versions of this Article: 91/5/935    most recent expphysiol.2006.034421v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ito, S. Articles by Katsuya, H. Search for Related Content PubMed PubMed Citation Articles by Ito, S. Articles by Katsuya, H. Related Collections Respiratory

¹ Department of Anaesthesiology and Medical Crisis Management² Core Laboratory, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan ³ Department of Anaesthesia, University Health Network, University of Toronto, Toronto, Canada, M5G 2C4

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 O₂ (P_aO2) and arterial oxygen saturation (S_pO2) were measured, and alveolar-to-arterial P_O2 difference (D_A–aO2) 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_aO2 and S_pO2 (P < 0.05 and P < 0.01, respectively) and an increase in D_A–aO2 (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.

(Received 10 May 2006; accepted after revision 26 June 2006; first published online 29 June 2006)
Corresponding author H. Sasano: Department of Anaesthesiology and Medical Crisis Management, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi Mizuho-cho Mizuho-ku Nagoya, Aichi 467-8601, Japan.  Email: hirosasano{at}aol.com

This article has been cited by other articles:

				A. Beda, F. C. Jandre, and A. Giannella-Neto Changes in dead space can explain part of the reduction in gas exchange efficiency found, not necessarily linked to respiratory sinus arrhythmia Exp Physiol, April 1, 2008; 93(4): 513 - 514. [Full Text] [PDF]

				H. Sasano, S. Ito, and N. Sasano Reply from H. Sasano and colleagues Exp Physiol, April 1, 2008; 93(4): 515 - 515. [Full Text] [PDF]