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1 Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75390; 2 San Antonio Military Pediatric Center, Lackland Air Force Base 78235; and 3 The Southwest Foundation for Biomedical Research, San Antonio, Texas 78245
Nitric oxide (NO), produced by NO synthase
(NOS), serves multiple functions in the perinatal lung. In fetal
baboons, neuronal (nNOS), endothelial (eNOS), and inducible NOS (iNOS)
are all primarily expressed in proximal respiratory epithelium. In the
present study, NOS expression and activity in proximal lung and minute
ventilation of NO standard temperature and pressure
(
ENOSTP) were evaluated in a
model of chronic lung disease (CLD) in baboons delivered at 125 days
(d) of gestation (term = 185 d) and ventilated for 14 d,
obtaining control lung samples from fetuses at 125 or 140 d of
gestation. In contrast to the normal 73% increase in total NOS
activity from 125 to 140 d of gestation, there was an 83% decline with
CLD. This was related to marked diminutions in both nNOS and eNOS
expression and enzymatic activity. nNOS accounted for the vast majority
of enzymatic activity in all groups. The normal 3.3-fold maturational
rise in iNOS protein expression was blunted in CLD, yet iNOS activity
was elevated in CLD compared with at birth. The contribution of iNOS to
total NOS activity was minimal in all groups.
ENOSTP remained stable in the range of 0.5-1.0
nl · kg
1 · min1
from birth to day 7 of life, and it then rose by 2.5-fold.
Thus the baboon model of CLD is characterized by deficiency of the principal pulmonary isoforms, nNOS and eNOS, and enhanced iNOS activity
over the first 2 wk of postnatal life. It is postulated that these
alterations in NOS expression and activity may contribute to the
pathogenesis of CLD.
endothelial nitric oxide synthase; exhaled nitric oxide; inducible nitric oxide synthase; neuronal nitric oxide synthase; primate
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