Scanning electron microscopic findings in respiratory nasal mucosa following cigarette smoke exposure in rats

2003 ◽  
Vol 185 (3) ◽  
pp. 207-210 ◽  
Author(s):  
Cahide Ortuğ
Author(s):  
M.D. Graham

The recent development of the scanning electron microscope has added great impetus to the study of ultrastructural details of normal human ossicles. A thorough description of the ultrastructure of the human ossicles is required in order to determine changes associated with disease processes following medical or surgical treatment.Human stapes crura were obtained at the time of surgery for clinical otosclerosis and from human cadaver material. The specimens to be examined by the scanning electron microscope were fixed immediately in the operating room in a cold phosphate buffered 2% gluteraldehyde solution, washed with Ringers, post fixed in cold 1% osmic acid and dehydrated in graded alcohol. Specimens were transferred from alcohol to a series of increasing concentrations of ethyl alcohol and amyl acetate. The tissue was then critical point dried, secured to aluminum stubs and coated with gold, approximately 150A thick on a rotating stage in a vacuum evaporator. The specimens were then studied with the Kent-Cambridge S4-10 Scanning Electron Microscope at an accelerating voltage of 20KV.


1989 ◽  
Vol 66 (5) ◽  
pp. 2109-2116 ◽  
Author(s):  
A. R. Burns ◽  
S. P. Hosford ◽  
L. A. Dunn ◽  
D. C. Walker ◽  
J. C. Hogg

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.


1999 ◽  
Vol 67 (1) ◽  
pp. 85-88 ◽  
Author(s):  
Mohammad Bashar Izzat ◽  
Anthony P.C Yim ◽  
Kenny C.H Ho ◽  
Carmen S.Y Chan ◽  
David Yew ◽  
...  

1989 ◽  
Vol 26 (4) ◽  
pp. 279-281
Author(s):  
Eiji HATANO ◽  
Hiroshi MUNESHIGE ◽  
Kouhei FUKUHARA ◽  
Atsusi SEWAKE ◽  
Yoshiki HASE ◽  
...  

1991 ◽  
Vol 44 (10) ◽  
pp. 1010-1013
Author(s):  
YOSHIKO UCHIDA ◽  
HIRONARI TAKEUCHI ◽  
YOSHIAKI ANDO ◽  
TADAO KOTANI ◽  
YOSHIAKI NUMATA ◽  
...  

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