Does the cigarette smoke exposure lead to histopathological alterations in olfactory epithelium? An electron microscopic study on a rat model

2017 ◽  
Author(s):  
Elvan Şahin Özbek
Keyword(s):  
Cigarette Smoke ◽  
Microscopic Study ◽  
Olfactory Epithelium ◽  
Electron Microscopic Study ◽  
Rat Model ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Electron Microscopic ◽  
Histopathological Alterations

scholarly journals A Rat Model to Determine the Biomedical Consequences of Concurrent Ethanol Ingestion and Cigarette Smoke Exposure

2004 ◽  
Vol 28 (7) ◽  
pp. 1120-1128 ◽  
Author(s):  
Martha J. Gentry-Nielsen ◽  
Elizabeth Vander Top ◽  
Mary U. Snitily ◽  
Carol A. Casey ◽  
Laurel C. Preheim
Keyword(s):  
Cigarette Smoke ◽  
Rat Model ◽  
Smoke Exposure ◽  
Ethanol Ingestion ◽  
Cigarette Smoke Exposure

Respiratory epithelial permeability after cigarette smoke exposure in guinea pigs

1989 ◽  
Vol 66 (5) ◽  
pp. 2109-2116 ◽  
Author(s):  
A. R. Burns ◽  
S. P. Hosford ◽  
L. A. Dunn ◽  
D. C. Walker ◽  
J. C. Hogg
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Alveolar Epithelium ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Gel Chromatography ◽  
Type I ◽  
Electron Microscopic ◽  
Type I Cells ◽  
I Cells

The purpose of this study was to determine the pathology of cigarette smoke-increased permeability at the bronchioalveolar junction of the guinea pig. After exposure to either smoke or room air, guinea pigs were anesthetized and fluorescein isothiocyanate-dextran (FITC-D, mol wt 10,000) was aerosolized into their lungs. Blood samples taken through a carotid arterial cannula were analyzed by gel chromatography and spectrofluorometry for the presence of FITC-D. The results confirmed that, after smoke exposure, increased amounts of intact FITC-D molecules with a reported Einstein-Stokes radius of 22.2 A crossed the respiratory epithelium into the vascular space. Transmission electron-microscopic studies showed that the FITC-D diffused across damaged type I pneumocyte membranes and cytoplasm to reach the basal lamina and entered the alveolar capillaries through endothelial tight junctions. Damage to the alveolar epithelium was more frequent for the smoke-exposed animals than the room air-exposed animals (P less than 0.05). We conclude that smoke exposure damages type I cells and that inhaled FITC-D crosses the epithelial barrier at damaged type I cells of the bronchioloalveolar junctions.

scholarly journals Effect of Simvastatin on 5-HT and 5-HTT in a Rat Model of Pulmonary Artery Hypertension

2015 ◽  
Vol 37 (5) ◽  
pp. 1712-1724 ◽  
Author(s):  
Xue Jiang ◽  
LinDong Yuan ◽  
Peng Li ◽  
Jia Wang ◽  
Pengyu Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Pulmonary Artery ◽  
Cigarette Smoke ◽  
Rat Model ◽  
Structural Damage ◽  
Inflammatory Cells ◽  
Pulmonary Artery Hypertension ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Mean Pulmonary Arterial Pressure

Background/Aims: To investigaterole of serotonin (5-HT) and serotonin transporter (5-HTT) in a rat model of cigarette smoke-induced pulmonary artery hypertension (PAH) and the effect of statins on regulating 5HT and 5-HTT. Methods: A rat model of COPD comorbid with PAH was established by cigarette smoke exposure with or without simvastatin administration. The smoking and the simvastatin plus smoking groups were exposed to cigarette smoke daily, and the latter received simvastatin at 5mg/kg, once a day. After 16 weeks of cigarette smoke exposure, body weight and mean pulmonary arterial pressure (mPAP) were measured, bronchoalveolar lavage (BAL) was performed, and lung tissues and blood samples were collected to determine cardiopulmonary pathology, physiological indices, blood levelof 5-HT and expression of 5-HTT in the lung. Results: In addition to alveolar structural damage (COPD-like injury), chronic cigarette smoke exposure lead to pulmonary artery remodeling and PAH as evidenced by significant elevation of mPAP, RVHI, WT%and WA%. Cigarette smoke exposure resulted in significant reduction in animal body weight, and simvastatin significantly prevented smoke-induced weight loss. The number of inflammatory cells in BALF was dramatically increased in smoke exposed rats, and simvastatin dampened the number of leukocytes, neutrophils, lymphocytes, and macrophages. In addition, circulating 5-HTand expression of 5-HTT in the lung were significantly increased in the smoked rats compared to control rats, and it was significantly reduced by simvastatin. Alteration of BALF inflammatory cells, 5-HT and 5-HTT was significantly correlated with changes of mPAP, RVHI, WT% and WA%. Conclusions: Cigarette smoke exposure could result in not only COPD, but also PAH, which may attribute to the alteration of blood 5-HT and lung tissue 5-HTT. Simvastatin could significantly inhibited 5-HT and 5-HTT expression, and by which mechanism, it may protect animals from development of PAH.

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