Medical Effects: Respiratory Responses to Smoke Inhalation

Three Abstracts:

Hum Pathol 1982 Apr;13(4):355-64

Pulmonary responses to smoke inhalation: morphologic changes in rabbits exposed to pine wood smoke.

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

Wood smoke-induced airway hyperreactivity in guinea pigs: time course, and role of leukotrienes and hydroxyl radical.

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

Stimulation of vagal pulmonary C fibers by inhaled wood smoke in rats.

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]

new: Temporary and spatial deposition of aerosol particles in the upper human airways during breathing cycle
A. Moskal, L. Gradon
pp 1525-1539
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