Journal of Applied Physiology AJP: Regulatory, Integrative and Comparative Physiology
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J Appl Physiol 87: 1629-1636, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 5, 1629-1636, November 1999

Regulation of pulmonary circulation by alveolar oxygen tension via airway nitric oxide

Hiroshi Ide1, Hitoshi Nakano1, Toshiyuki Ogasa1, Shinobu Osanai1, Kenjirou Kikuchi1, and Jun Iwamoto2

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; VNO) 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 (VNO), 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 VNO and NOx accumulation with a rise in Ppa. However, neither VNO, NOx accumulation, nor Ppa changed during VH. Similarly, in BLL, only AH reduced VNO, 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 VNO 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 VNO 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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