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1: Eur J Pharmacol 2001 Aug 10;425(2):141-8

Alleviation of wood smoke-induced lung injury by tachykinin receptor antagonist
and hydroxyl radical scavenger in guinea pigs.

Lin YS, Ho CY, Tang GJ, Kou YR.

Institute of Physiology, School of Medicine and Life Science, National Yang-Ming
University, Taipei, Taiwan.

We recently reported that wood smoke inhalation initially (within 5 min) causes
airway injury and subsequently produces both airway and parenchymal injury after

a delay (within 2 h). In this study, we investigated the mediator mechanisms of
this delayed smoke-induced lung injury in 126 anesthetized and artificially
ventilated guinea pigs who received challenges of either air or 40 tidal breaths
of wood smoke. Two hours after inhalation, wood smoke produced various injurious
responses, including increases in alveolar-capillary permeability, microvascular
permeabilities, and histological injury scores, in airway and parenchymal
tissues. Pre-treatment given before smoke challenge with CP-96,345 [a tachykinin
NK1 receptor antagonist;
bicyclo(2.2.2.)-octan-3-amine], dimethylthiourea (a hydroxyl radical scavenger),
or a combination of these two drugs largely alleviated both the airway and
parenchymal responses, whereas pre-treatment with SR-48,968 [a tachykinin NK2
receptor antagonist;
)benzamide] or a combination of CP-96,344 and SR-48,965 (inactive enantiomers)
failed to do so. Post-treatment given at 5 min after smoke challenge with
CP-96,345 or dimethylthiourea significantly alleviated the parenchymal
responses, while having no effect on the airway responses. Pre-treatment with
dimethylthiourea prevented the smoke-induced reduction in airway neutral
endopeptidase activity (an enzyme for tachykinin degradation). We concluded that
(1) tachykinins and hydroxyl radical play important roles in producing
smoke-induced delayed lung injury in guinea pigs, and both may be involved in
the spread of injury from the airways to the pulmonary parenchyma, and (2) the
contribution of tachykinins is mediated via the activation of tachykinin NK1
receptors, and is associated with the hydroxyl radical-induced inactivation of
airway neutral endopeptidase.

PMID: 11502280 [PubMed - indexed for MEDLINE]

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