Role of airway nitric oxide on the regulation of pulmonary circulation by carbon
dioxide.
Yamamoto, Yasushi, Hitoshi Nakano, Hiroshi Ide, Toshiyuki Ogasa, Toru Takahashi,
Shinobu Osanai, Kenjiro Kikuchi, and Jun Iwamato.
1Department of Internal Medicine and 2Division of Applied Physiology, School of
Nursing, Asahikawa Medical College, Asahikawa 078«hyphen»8510, Japan
APStracts 8:0295A, 2001.
The effects of hypercapnia (CO2) confined to either the alveolar space or the
intravascular perfusate on exhaled nitric oxide (NO), perfusate NO metabolites (NOx),
and pulmonary arterial pressure (Ppa) were examined during normoxia and progressive
20-min hypoxia in isolated blood- and buffer-perfused rabbit lungs. In blood-perfused
lungs, when alveolar CO2 concentration was increased from 0 to 12%, exhaled NO
decreased, whereas Ppa increased. Increments of intravascular CO2 levels increased Ppa
without changes in exhaled NO. In buffer-perfused lungs, alveolar CO2 increased Ppa
with reductions in both exhaled NO from 93.8 to 61.7 (SE) nl/min (P < 0.01) and
perfusate NOx from 4.8 to 1.8 nmol/min (P < 0.01). In contrast, intravascular CO2 did
not affect either exhaled NO or Ppa despite a tendency for perfusate NOx to decline.
Progressive hypoxia elevated Ppa by 28% from baseline with a reduction in exhaled NO
during normocapnia. Alveolar hypercapnia enhanced hypoxic Ppa response up to 50%
with a further decline in exhaled NO. Hypercapnia did not alter the apparent Km for O2,
whereas it significantly decreased the Vmax from 66.7 to 55.6 nl/min. These results
suggest that alveolar CO2 inhibits epithelial NO synthase activity noncompetitively and
the suppressed NO production by hypercapnia augments hypoxic pulmonary
vasoconstriction, resulting in improved ventilation-perfusion matching.
Received 12 January 2001; accepted in final form 30 April 2001
APS Manuscript Number A33-1.
Article publication pending J Appl Physiol
ISSN 1080-4757 Copyright 2001 The American Physiological Society.
Published in APStracts on 18 June 2001