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1 Department of Medicine, 2 Division of Applied Physiology, School of Nursing, Asahikawa Medical College, Asahikawa 078-8510, Japan
The effects of airway (AH) and vascular hypoxia
(VH) on the production of nitric oxide (NO;
NO) were
tested in isolated buffer-perfused (BFL) and blood-perfused rabbit
lungs (BLL). To produce AH and/or VH, the lung was
ventilated with 1% O2 gas, and/or
the perfusate was deoxygenated by a membrane oxygenator located on the
inlet limb to the pulmonary artery. We measured exhaled NO
(NO),
accumulation of perfusate NOx, and pulmonary arterial pressure (Ppa)
during AH (inspired O2 fraction = 0.01) and/or VH (venous PO2 = 26 Torr). In BFL, a pure AH without VH caused decreases in
NO and NOx
accumulation with a rise in Ppa. However, neither
NO, NOx
accumulation, nor Ppa changed during VH. Similarly, in BLL, only AH
reduced NO,
although NOx accumulation was not measurable because of Hb. When
alveolar PO2 was gradually reduced
from 152 to 0 Torr for 20 min, AH reduced NO
curvilinearly from 73.9 ± 8 to 25.6 ± 8 nl/min in BFL and from
26.0 ± 2 to 5.2 ± 1 nl/min in BLL. This plot was analogous to
that of a substrate-velocity curve for an enzyme obeying
Michaelis-Menten kinetics. The apparent Michaelis-Menten constant for
O2 was calculated to be 23.2 µM
for BLL and 24.1 µM for BFL. These results indicate that the
NO in the
airway epithelia is dependent on the level of inspired
O2 fraction, leading to the
tentative conclusion that epithelial NO synthase is
O2 sensitive over the
physiological range of alveolar PO2
and controls pulmonary circulation.
hypoxia; epithelium; oxygen
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