Thorning DR, Howard ML, Hudson LD, Schumacher RL.
Inhalation of smoke can adversely affect pulmonary function;
however, the lack
of detailed knowledge of exposure conditions and the overall complexity
of
ensuing clinical problems generally preclude an understanding
of the specific
role played by smoke in human victims. Using controlled exposures
of rabbits to
white pine wood smoke, an animal model of smoke inhalation
has been created.
Light and electron microscopic examinations of injured respiratory
tissues from
these animals have revealed a reproducible, necrotizing tracheobronchial
epithelial cell injury. By six hours after injury, the epithelium
remains
largely intact but is infiltrated by inflammatory cells; by 24
hours its
ciliated and secretory lining cells are largely destroyed, the
inflammatory
reaction is maximal, but basal epithelial cells retain their normal
structural
appearances; by 72 hours, its surfaces are largely covered by
a nonciliated,
stratified reparative epithelium, apparently derived from proliferating
and
migrating basal cells. The acute injury and early reactions to
injury resemble
lesions observed in the lungs of human smoke-injured victims,
and suggest
several physiologic consequences that would provide likely explanations
for some
of the disabilities observed in these victims.
PMID: 7076218 [PubMed - indexed for MEDLINE]
Hsu TH, Lai YL, Kou YR.
Wood smoke-induced airway hyperreactivity in guinea pigs: time
course, and role
of leukotrienes and hydroxyl radical.
Life Sci. 2000;66(11):971-80.
PMID: 10724444 [PubMed - indexed for MEDLINE]
1: Life Sci 2000;66(11):971-80
Hsu TH, Lai YL, Kou YR.
Department of Veterinary Medicine, College of Veterinary Medicine,
National
Chung Hsing University, Taichung, Taiwan, Republic of China.
A prior airway exposure to wood smoke induces a tachykinin-dependent
increase in
airway responsiveness to the subsequent smoke inhalation in guinea
pigs (Life
Sci. 63: 1513, 1998). To further investigate the time course of,
and the
contribution of other chemical mediators to, this smoke-induced
airway
hyperresponsiveness (SIAHR), two smoke challenges (each 10 ml)
separated by 30
min were delivered into the lungs of anesthetized guinea pigs
by a respirator.
In the control animals, the SIAHR was evidenced by the bronchoconstrictive
response to the second smoke challenge (SM2) which was approximately
5.2-fold
greater than that to the first challenge (SM1). This SIAHR was
alleviated by
shortening the elapsed time between SM1 and SM2 to 10 min or by
extending it to
60 min, and was abolished by extending it to 120 min. This SIAHR
was reduced by
pretreatment with either MK-571 (a leukotriene D4-receptor antagonist)
or
dimethylthiourea (a hydroxyl radical scavenger), but was not affected
by
pretreatment with either pyrilamine (a histamine H1-receptor antagonist)
or
indomethacin (a cyclooxygenase inhibitor). The smoke-induced reduction
in the
neutral endopeptidase activity (a major enzyme for tachykinin
degradation)
measured in airway tissues excised 30 min post SM1 was largely
prevented by
pretreatment with dimethylthiourea. However, this reduction was
not seen in
airway tissues excised 120 min post SM1. These results suggest
that 1) the SIAHR
to inhaled wood smoke has a rapid onset time following smoke inhalation
and
lasts for less than two hours, 2) leukotrienes and hydroxyl radical
may play
contributory roles in the development of this SIAHR, and 3) hydroxyl
radical is
the major factor responsible for the smoke-induced inactivation
of airway
neutral endopeptidase, which may possibly participate in the development
of this
SIAHR.
PMID: 10724444 [PubMed - indexed for MEDLINE]
J Appl Physiol 1998 Jan;84(1):30-6
Lai CJ, Kou YR.
Institute of Physiology, School of Medicine and Life Science,
National Yang-Ming
University, Taipei, Taiwan, Republic of China.
This study investigated the stimulation of vagal pulmonary
C fibers (PCs) by
wood smoke. We recorded impulses from PCs in 58 anesthetized,
open-chest, and
artificially ventilated rats and delivered 6 ml of wood smoke
into the lungs.
Within 1 or 2 s after the smoke delivery, an intense and nonphasic
burst of
discharge [delta = +7.4 +/- 0.7 (SE) impulses/s, n = 68] was evoked
in 60 of the
68 PCs studied and lasted for 4-8 s. This immediate stimulation
was usually
followed by a delayed and more sustained increase in C-fiber activity
(delta =
+2.0 +/- 0.4 impulses/s). The overall stimulation was not influenced
by removal
of smoke particulates (n = 15) or by pretreatment with vehicle
(n = 8) for
dimethylthiourea (DMTU; a hydroxyl radical scavenger) or indomethacin
(Indo; a
cyclooxygenase inhibitor). The immediate-phase stimulation was
not affected by
pretreatment with Indo (n = 8) but was largely attenuated by pretreatment
with
DMTU (n = 12) or by a combined treatment with DMTU and Indo (DMTU
+ Indo; n =
8). Conversely, the delayed-phase stimulation was partially suppressed
either by
DMTU or by Indo but was totally abolished by DMTU + Indo. These
results suggest
that 1) the stimulation of PCs is linked to the gas phase of wood
smoke and 2)
hydroxyl radical, but not cyclooxygenase products, is involved
in the
immediate-phase stimulation, whereas both metabolites are responsible
for
evoking the delayed-phase stimulation.
PMID: 9451614 [PubMed - indexed for MEDLINE]
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