Inhaled cigarette smoke selectively reverses human hypoxic vasoconstriction

The acute effects of the inhaled gas phase of cigarette smoke on pulmonary (PAP) and systemic (SAP) arterial pressures and on plasma arterial cGMP content were compared with those of inhaling 10, 20 and 80 ppm nitric oxide (NO) in one healthy adult volunteer spontaneously breathing a hypoxic gas mix...

Full description

Saved in:
Bibliographic Details
Published in:Intensive care medicine 1995-11, Vol.21 (11), p.941-944
Main Authors: DUPUY, P. M, LANCON, J.-P, FRANCOISE, M, FROSTELL, C. G
Format: Article
Language:English
Subjects:
Administration, Inhalation
Adult
Biological and medical sciences
Cyclic GMP - blood
Dose-Response Relationship, Drug
Humans
Hypoxia - blood
Hypoxia - chemically induced
Hypoxia - physiopathology
Medical sciences
Medicin och hälsovetenskap
Nitric Oxide - pharmacology
Oxygen - blood
Pulmonary Circulation - drug effects
Smoking - blood
Smoking - physiopathology
Tobacco, tobacco smoking
Toxicology
Vasoconstriction - drug effects
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The acute effects of the inhaled gas phase of cigarette smoke on pulmonary (PAP) and systemic (SAP) arterial pressures and on plasma arterial cGMP content were compared with those of inhaling 10, 20 and 80 ppm nitric oxide (NO) in one healthy adult volunteer spontaneously breathing a hypoxic gas mixture. Hypoxia (FIO2 0.12) induced a sustained, stable pulmonary vasoconstriction. Inhaled NO induced a dose-dependent fall in PAP; plasma cGMP rose from 39.4 (hypoxia) to 164 pmol/ml (hypoxia plus 80 ppm NO). Exposure to cigarette smoke induced a rapid, consistent and reversible fall in PAP; plasma cGMP rose from 45.5 (hypoxia) to 138 pmol/ml (hypoxia plus cigarette smoke). Neither NO nor cigarette smoke inhalation induced any change in SAP. These data suggest that exposure to cigarette smoke is able selectively to reverse acute hypoxic vasoconstriction in humans without causing systemic vasodilation, an effect likely mediated through the NO-cGMP pathway.
ISSN:0342-4642
1432-1238
DOI:10.1007/BF01712337