In:
Journal of Applied Physiology, American Physiological Society, Vol. 87, No. 5 ( 1999-11-01), p. 1629-1636
Abstract:
The effects of airway (AH) and vascular hypoxia (VH) on the production of nitric oxide (NO;V˙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% O 2 gas, and/or the perfusate was deoxygenated by a membrane oxygenator located on the inlet limb to the pulmonary artery. We measured exhaled NO (V˙no), accumulation of perfusate NOx, and pulmonary arterial pressure (Ppa) during AH (inspired O 2 fraction = 0.01) and/or VH (venous [Formula: see text] = 26 Torr). In BFL, a pure AH without VH caused decreases inV˙no and NOx accumulation with a rise in Ppa. However, neitherV˙no, NOx accumulation, nor Ppa changed during VH. Similarly, in BLL, only AH reduced V˙no, although NOx accumulation was not measurable because of Hb. When alveolar [Formula: see text] was gradually reduced from 152 to 0 Torr for 20 min, AH reducedV˙nocurvilinearly 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 O 2 was calculated to be 23.2 μM for BLL and 24.1 μM for BFL. These results indicate that theV˙no in the airway epithelia is dependent on the level of inspired O 2 fraction, leading to the tentative conclusion that epithelial NO synthase is O 2 sensitive over the physiological range of alveolar [Formula: see text]and controls pulmonary circulation.
Type of Medium:
Online Resource
ISSN:
8750-7587
,
1522-1601
DOI:
10.1152/jappl.1999.87.5.1629
Language:
English
Publisher:
American Physiological Society
Publication Date:
1999
detail.hit.zdb_id:
1404365-8
SSG:
12
SSG:
31
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