[Structural changes in tracheal epithelium in environmental smoke exposed rats--experimental studies].
2
Citation
0
Reference
20
Related Paper
Citation Trend
Abstract:
It has been already proved in many experimental studies that tobacco smoke has multiple toxic effects on respiratory tract cells. Alterations in cilliary epithelium of rats trachea after short exposition to high tobacco smoke concentrations in inhaled air were been determined in current study. Morphological evaluation revealed in lining epithelium decrease in number of cilliary cells and increase in number of goblet cells. The mucous membrane was thickened and infiltrated with inflammatory cells.Keywords:
Respiratory tract
Mucous membrane
Cite
Coal dust
Cite
Citations (0)
Rats were exposed to the smoke of non-filter cigarettes for various periods of time. The weight gain of the exposed animals was markedly less than that of controls, and they revealed signs of irritation of the respiratory mucous membrane. The frequency of ciliary beat and the rate of mucous flow in the bronchial tree of the exposed rats were not significantly altered. However, patches were observed in the tracheobronchial epithelium of these animals in which mucociliary mechanism was abnormal. Also numerous areas of ciliary inactivity were present. These alterations in mucociliary function were very similar to those found in bronchitis.
Mucociliary clearance
Respiratory tract
Mucous membrane
Respiratory Mucosa
Cite
Citations (14)
Cite
Citations (0)
Cite
Citations (0)
Objective
To investigate the effect of toxic smoke on the heart, lung, liver and kidney of male rats after combustion of non-metal material in military airtight cabins.
Methods
36 male SD rats were randomly divided into control group and five smoke inhaled groups (1, 6, 24, 72 h and 7 d post-exposure) with 6 rats in each group. The control group inhaled fresh air and smoke inhalation groups were continuously exposed in smoke for 10 min, and the pathological changes of heart, lung, liver and kidney in each group were observed.
Results
Varying degrees of injury can be observed in heart, lung, trachea, liver, kidney of rats after smoke inhalation at different time points and smoke particles were observed to deposit extensively in the tissues above. The degree of damage at 24 h post-exposure was the most serious and the process of injury coexisted with proliferation after 24 h post-exposure. All the observation above suggests that smoke inhalation can lead to a certain degree of damage on heart, lung, trachea, liver and kidney, and the process of self-repairing could be coexisted after smoke exposure. Damage to the myocardium: particulate matter deposition, myocyte swelling, local dissolution and necrosis. Damage to the lung tissue: diffuse hyperemia of the pulmonary interstitium, infiltration of inflammatory cells and erythrocyte exudation in the alveoli. Damage to the trachea: edema of epithelial cells, partial cilium exfoliation, and separation of local epithelial cells from cartilage. Damage to the liver: particulate matter deposition, hepatocyte cytoplasm loosening, and varying degrees of edema and vacuolation. Damage to the kidney: the damage of the glomerular vascular endothelial cells, the interstitial space of the renal tubules and the deposition of smoke particles in the lumen.
Conclusion
Smoke particles resulting from combustion of nonmetal materials in military airtight cabins can deposit in tissues of heart, lung, liver, kidney and other major organs through the blood circulation after inhalation and lead to morphological pathological changes of tissues in above organs.
Key words:
smoke inhalation injury; pathology; military airtight cabin; rats, Sprague-Dawley; Systemic toxicity
Infiltration (HVAC)
Inhalation exposure
Cite
Citations (0)
We examined the effect of polluted roadside air on the pathogenesis of chronic respiratory diseases, by exposing rats directly to roadside air in Kawasaki City. Five-week-old Wistar rats were assigned to be exposed to either roadside air (containing 55.7 ppb NO2 and 62.7 microg/m(3) suspended particulate matter [SPM]; roadside-air group) or filtered air (containing 5.1 ppb NO2 and 14.3 microg/m(3) SPM; filtered-air group), prepared by eliminating dust and emission gas from the polluted roadside air, for a period of 60 consecutive wk. The morphological changes over time in the respiratory tissue of these animals were observed by light microscopy and electron microscopy at 24, 48, and 60 wk of exposure. In addition to the general microscopic findings, other features observed for included the proliferation of goblet cells producing mucus in the airways, acidification of neutral mucous granules in these goblet cells, the behavior of inflammatory cells such as alveolar macrophages, mast cells, and plasma cells, and the number of alveolar holes, known to be a primary indicator of early alveolar destruction. Focal anthracosis, acidified mucus in the goblet cells, and infiltration to the submucosa by inflammatory cells were observed in the lungs of the animals after 60 wk of exposure to polluted roadside air. However, these inflammatory changes were weak. No remarkable differences in the number of alveolar holes were noted between the two experimental groups. These findings suggest that the effects of roadside air on the respiratory tissue in rats may not be as severe as would be expected under these experimental conditions.
Infiltration (HVAC)
Submucosa
Cite
Citations (9)
This research aimed to study on the microscopic changes of lungs in male rat that exposured to cigarette smoke. A factorial CRD with periode of treatment and sample collection was applied in this study. An exposure of cigarette smoke was carried out at 10 cigarettes/rat/day for 2.5 hours in an smoking chamber. Group N is untreated animals. Group 20d is exposed animals with cigarette smoke for 20 days consectitively and released from the cigarette smoke exposure for 20 days. Group 40d is exposed animals for 40 days and released from the cigarette smoke for 40 days. Group 60d is exposed animals for 60 days similar as above. Data collection was carried out twice : after exposure and after redeasing the cigarette smoke exposure. The parameters of observation microscopic analysis of lungs included weight wet of lung and change of lung histopathologic.The results show decreased weight wet of lung, increased number of blackish particulate deposits in the cytoplasm of alveoli at 40d and 60d considered as tar deposit, an increased activity of inflammatory cells of male rats after exposing which were unable to recover after releasing of cigarette smoke exposure.
tar (computing)
Adult male
Cite
Citations (1)
Alveolar macrophage
Histopathology
Bronchiole
Metaplasia
Tobacco smoke
Cite
Citations (14)
Section:ChooseTop of pageAbstract <
Cite
Citations (49)
Journal Article Action of Intensive Cigarette Smoke Inhalations on the Rat Lung. Role of Particulate and Gaseous Cofactors Get access L. Le Bouffant, L. Le Bouffant 3Centre d'Etudes et Recherches des Charbonnages de France, BP No. 2, 60550 Verneuil en Halatte, France. Search for other works by this author on: Oxford Academic PubMed Google Scholar J. C. Martin, J. C. Martin 3Centre d'Etudes et Recherches des Charbonnages de France, BP No. 2, 60550 Verneuil en Halatte, France. Search for other works by this author on: Oxford Academic PubMed Google Scholar H. Daniel, H. Daniel 3Centre d'Etudes et Recherches des Charbonnages de France, BP No. 2, 60550 Verneuil en Halatte, France. Search for other works by this author on: Oxford Academic PubMed Google Scholar J. P. Henin, J. P. Henin 3Centre d'Etudes et Recherches des Charbonnages de France, BP No. 2, 60550 Verneuil en Halatte, France. Search for other works by this author on: Oxford Academic PubMed Google Scholar C. Normand C. Normand 3Centre d'Etudes et Recherches des Charbonnages de France, BP No. 2, 60550 Verneuil en Halatte, France. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 64, Issue 2, February 1980, Pages 273–284, https://doi.org/10.1093/jnci/64.2.273 Published: 01 February 1980 Article history Received: 12 July 1978 Revision received: 12 June 1979 Accepted: 30 June 1979 Published: 01 February 1980
Acrolein
Metaplasia
tar (computing)
Cite
Citations (20)