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Nitric oxide inhalation transiently elevates pulmonary levels of cGMP, iNOS mRNS, and TNF-alpha.

Authors
Brady-TC; Crapo-J; Mercer-RR
Source
Am J Physiol, Lung Cell Mol Physiol 1998 Sep; 275(3):L509-L515
NIOSHTIC No.
20000649
Abstract
The initial pulmonary vasodilation that occurs during nitric oxide. (NO) inhalation does not appear to be maintained chronically in many cases. NO may acutely relax vascular smooth muscle by increasing levels of guanosine 3',5'-cyclic monophosphate (cGMP), tumor necrosis factor (TNF) -alpha, and inducible nitric oxide synthase (iNOS) while decreasing levels of lipid peroxidation. It was hypothesized that the acute NO-induced changes in cGMP, TNF-alpha, iNOS, and lipid peroxidation, all of which may mediate vasodilation, are transient rather than sustained. Lungs from rats kept in chambers containing 6 parts/million. NO for 1 h, 1 day, or 1 wk were analyzed for levels of NO-induced vasodilatory mediators. Pulmonary cGMP, iNOS mRNA, and TNF-alpha were increased 1 h after NO exposure but decreased to control values at later times. Levels of malonyl dialdehyde, an indicator of lipid peroxidation, were decreased at all times during NO inhalation. As a whole, the data suggest that in lungs the vasodilatory mediators cGMP, iNOS, and TNF-alpha are only acutely and transiently elevated during inhalation of NO, consistent with the initially positive clinical response to inhaled NO that deteriorates over time.
Keywords
Gas-inhalation; Chronic-exposure; Muscle-relaxation; Rats; Biological-models
CODEN
APLPE7
CAS No.
10102-43-9; 542-78-9; 7665-99-8; 82115-62-6
Publication Date
19980901
Document Type
Journal Article
Fiscal Year
1998
NTIS Accession No.
NTIS Price
Issue of Publication
3
ISSN
1040-0605
NIOSH Division
DRDS
Priority Area
Pulmonary-system-disorders
Source Name
American Journal of Physiology: Lung Cellular and Molecular Physiology
State
WV
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