Disease-modifying effect of ASP3258, a novel phosphodiesterase type 4 inhibitor, on subchronic cigarette smoke exposure-induced lung injury in guinea pigs

2011 ◽  
Vol 659 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Satoshi Kubo ◽  
Miki Kobayashi ◽  
Masahiro Iwata ◽  
Koichiro Takahashi ◽  
Keiji Miyata ◽  
...  
Keyword(s):  
Lung Injury ◽  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Modifying Effect ◽  
Disease Modifying ◽  
Phosphodiesterase Type

scholarly journals Cigarette Smoke Exposure Worsens Endotoxin-Induced Lung Injury and Pulmonary Edema in Mice

2017 ◽  
Vol 19 (9) ◽  
pp. 1033-1039 ◽  
Author(s):  
Jeffrey E Gotts ◽  
Jason Abbott ◽  
Xiaohui Fang ◽  
Haru Yanagisawa ◽  
Naoki Takasaka ◽  
...  
Keyword(s):  
Lung Injury ◽  
Pulmonary Edema ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
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.

Acute Cigarette Smoke Exposure Causes Lung Injury in Rabbits Treated with Ibuprofen

1987 ◽  
Vol 13 (2) ◽  
pp. 113-126 ◽  
Author(s):  
Mark L. Witten ◽  
Richard J. Lemen ◽  
Stuart F. Quan ◽  
Richard E. Sobonya ◽  
Judith L. Magarelli ◽  
...  
Keyword(s):  
Lung Injury ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
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

Effect of Cigarette Smoke Exposure on Biomarkers of Lung Injury in the Rat

1996 ◽  
Vol 8 (8) ◽  
pp. 803-817 ◽  
Author(s):  
K. Miller ◽  
B. Hudspith ◽  
M. Cunninghame ◽  
C. Prescott ◽  
C. Meredith
Keyword(s):  
Lung Injury ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure
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