scholarly journals Effect of a mucoactive compound (CO 1408) on airway hyperreactivity and inflammation induced by passive cigarette smoke exposure in guinea-pigs

1994 ◽  
Vol 7 (4) ◽  
pp. 693-697 ◽  
Author(s):  
A. Hernandez ◽  
L. Daffonchio ◽  
L. Brandolini ◽  
G. Zuccari
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Smoke Exposure ◽  
Airway Hyperreactivity ◽  
Cigarette Smoke Exposure

Passive cigarette smoke exposure induces airway hyperreactivity to histamine but not to acetylcholine in guinea-pigs

1990 ◽  
Vol 3 (3) ◽  
pp. 145-150 ◽  
Author(s):  
C. Omini ◽  
A. Hernandez ◽  
G. Zuccari ◽  
G. Clavenna ◽  
L. Daffonchio
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Smoke Exposure ◽  
Airway Hyperreactivity ◽  
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.

The effect of carvacrol on systemic inflammation in guinea pigs model of COPD induced by cigarette smoke exposure

2015 ◽  
Vol 67 (1) ◽  
pp. 140-145 ◽  
Author(s):  
Leila Gholami Mahtaj ◽  
Azadeh Feizpour ◽  
Majid Kianmehr ◽  
Mohammad Soukhtanloo ◽  
Mohammad Hossein Boskabady
Keyword(s):  
Cigarette Smoke ◽  
Systemic Inflammation ◽  
Guinea Pigs ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure

Cigarette smoke exposure potentiates bleomycin-induced lung fibrosis in guinea pigs

2003 ◽  
Vol 285 (4) ◽  
pp. L949-L956 ◽  
Author(s):  
José Cisneros-Lira ◽  
Miguel Gaxiola ◽  
Carlos Ramos ◽  
Moisés Selman ◽  
Annie Pardo
Keyword(s):  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Guinea Pigs ◽  
Lung Fibrosis ◽  
Smooth Muscle Actin ◽  
Smoke Exposure ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Fibroblast Proliferation

The role of tobacco smoking in the development and outcome of pulmonary fibrosis is uncertain. To approach the effects of cigarette smoke on bleomycin-induced lung fibrosis, we studied five groups of guinea pigs: 1) controls, 2) instilled with bleomycin (B), 3) exposed to tobacco smoke for 6 wk (TS), 4) bleomycin instillation plus tobacco smoke exposure for 6 wk (B+TS), and 5) tobacco smoke exposure for 6 wk and bleomycin after smoking (TS/B). Guinea pigs receiving bleomycin and tobacco smoke exposure exhibited higher fibrotic lesions including a significant increase in the number of positive α-smooth muscle actin cells compared with bleomycin alone (B+TS, 3.4 ± 1.2%; TS/B, 3.7 ± 1.5%; B, 2.3 ± 1.5%; P < 0.01). However, only the TS/B group reached a significant increase in lung collagen compared with the bleomycin group (TS/B, 3.5 ± 0.7; B ± TS, 2.9 ± 0.4; B, 2.4 ± 0.2 mg hydroxyproline/lung; P < 0.01). Bronchoalveolar lavage (BAL) from TS/B showed an increased number of eosinophils and higher levels of IL-4 and tissue inhibitor of metalloproteinase-2 ( P < 0.01 for all comparisons) and induced a significant increase in fibroblast proliferation ( P < 0.05). Importantly, smoke exposure alone induced an increase in BAL neutrophils, matrix metalloproteinase-9, and fibroblast proliferation compared with controls, suggesting that tobacco smoke creates a profibrotic milieu that may contribute to the increased bleomycin-induced fibrosis.

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