Pharmacokinetics of Nicotine in Rats after Single-Cigarette Smoke Inhalation

1980 ◽  
Vol 69 (9) ◽  
pp. 1087-1090 ◽  
Author(s):  
K.S. Rotenberg ◽  
R.P. Miller ◽  
J. Adir
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation

scholarly journals Cigarette smoke inhalation aggravates diabetic kidney injury in rats

2019 ◽  
Vol 8 (6) ◽  
pp. 964-971 ◽  
Author(s):  
Songling Jiang ◽  
Do Van Quan ◽  
Jae Hyuck Sung ◽  
Moo-Yeol Lee ◽  
Hunjoo Ha
Keyword(s):  
Kidney Disease ◽  
Cigarette Smoke ◽  
Density Lipoprotein ◽  
Kidney Injury ◽  
Diabetic Rats ◽  
Smoke Inhalation ◽  
Lipoprotein Cholesterol ◽  
Sprague Dawley ◽  
Experimental Conditions ◽  
Diabetic Kidney

Abstract Diabetic kidney disease (DKD) is the leading cause of end-stage kidney disease. Epidemiological studies have demonstrated that cigarette smoke or nicotine is a risk factor for the progression of chronic kidney injury. The present study analyzed the kidney toxicity of cigarette smoke in experimental rats with DKD. Experimental diabetes was induced in 7-week-old Sprague-Dawley rats by a single intraperitoneal injection of streptozotocin (60 mg kg−1). Four weeks after the induction of diabetes, rats were exposed to cigarette smoke (200 μg L−1), 4 h daily, and 5 days per week for 4 weeks. Cigarette smoke did not affect the levels of plasma glucose, hemoglobin A1c, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol or non-esterified fatty acids in both control and diabetic rats under the experimental conditions. Cigarette smoke, however, significantly increased diabetes-induced glomerular hypertrophy and urinary kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) excretion, suggesting exacerbation of diabetic kidney injury. Cigarette smoke promoted macrophage infiltration and fibrosis in the diabetic kidney. As expected, cigarette smoke increased oxidative stress in both control and diabetic rats. These data demonstrated that four weeks of exposure to cigarette smoke aggravated the progression of DKD in rats.

Effects of chronic cigarette smoke inhalation on the development of senile lung in senescence-accelerated mouse

1997 ◽  
Vol 197 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Shinji Teramoto ◽  
Yasuhide Uejima ◽  
Teruaki Oka ◽  
Kazuko Teramoto ◽  
Takeshi Matsuse ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Senescence Accelerated Mouse

Cigarette Smoke Inhalation Studies in Inbred Syrian Hamsters

1974 ◽  
pp. 320-330 ◽  
Author(s):  
Freddy Homburger ◽  
Peter Bernfeld ◽  
A. B. Russfield
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Syrian Hamsters

Cigarette smoke inhalation study for lung tumorigenicity in A/J mice

2010 ◽  
Vol 01 (01) ◽  
Author(s):  
R. B. Lichtner ◽  
B. Friedrichs ◽  
A. Buettner ◽  
F. Van Overveld ◽  
W. Stinn
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Inhalation Study

scholarly journals Oral Leukoplakia and Costochondral Hyperplasia Induced by Diethylnitrosamine in Hamsters Exposed to Cigarette Smoke with or without Dietary Vitamin C

1987 ◽  
Vol 24 (3) ◽  
pp. 257-264 ◽  
Author(s):  
T. Harada ◽  
A. Enomoto ◽  
T. Kitazawa ◽  
K. Maita ◽  
Y. Shirasu
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Vitamin C ◽  
Cigarette Smoke ◽  
Precancerous Lesions ◽  
Costal Cartilage ◽  
Oral Leukoplakia ◽  
Smoke Inhalation ◽  
Dietary Vitamin ◽  
Scanning Electron

Male Syrian golden hamsters receiving 12 weekly subcutaneous injections of diethylnitrosamine (DEN) were subjected to cigarette smoke inhalation and fed a diet with or without 1% vitamin C supplement for a period of 58 weeks. Another group was a sham-smoked control and was not fed vitamin C. Tissues of the oral cavity and costal cartilage were examined by light and/or scanning electron microscopy. Oral leukoplakia and costochondral hyperplasia occurred with high frequency in all groups treated with DEN. Leukoplakic lesions were found in the palate, tongue, and pharynx; the early change was focal erosion with mild epithelial hyperplasia and inflammatory cell infiltration. Advanced lesions had marked mucosal thickening due to acanthosis, parakeratosis, hyperkeratosis, and submucosal infiltration of lymphocytes and plasma cells. Precancerous lesions were noted in tongue and pharynx. Scanning electron microscopy of tongues revealed destruction of filiform papillae. The incidence of leukoplakic lesions was higher in smoke-exposed hamsters than in controls, but the incidence in vitamin C-supplemented hamsters was low when compared with the smoke-exposed hamsters without vitamin C. Costochondral hyperplasia was initiated by thickening of the perichondrium followed by proliferation of chondrocytes. Costochondral hyperplasia appeared earlier, and the incidence was higher in the vitamin C-supplemented hamsters. It could not be determined whether costochondral hyperplasia was the primary lesion induced by DEN or secondary change.

Acute effect of cigarette smoke on cytoplasmic motility of alveolar macrophages in dogs

1989 ◽  
Vol 66 (3) ◽  
pp. 1172-1178 ◽  
Author(s):  
M. Yamaya ◽  
K. Zayasu ◽  
K. Sekizawa ◽  
K. Yamauchi ◽  
S. Shimura ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Alveolar Macrophages ◽  
Lower Lobe ◽  
The Body ◽  
Sensory Nerves ◽  
Smoke Inhalation ◽  
Base Line ◽  
Particle Rotation ◽  
Lobe Bronchus

To study effects of cigarette smoke on the cytoplasmic motility (CM) of alveolar macrophages (AM), we measured remanent field strength (RFS) in dogs in vivo. Four days after instillation of ferrimagnetic particles (Fe3O4, 3 mg/kg) into the right lower lobe bronchus, RFS was measured at the body surface immediately after magnetization of the Fe3O4 particles by an externally applied magnetic field. RFS decreased with time due to particle rotation (relaxation), which is thought to be inversely related to CM of AM (J. Appl. Physiol. 55: 1196–1202, 1983). The initial relaxation curve was fitted to an exponential function. The relaxation rate (lambda 0) increased during cigarette smoke inhalation and returned to base-line values within 15 min. With the inhalation of the smoke of up to five cigarettes, peak lambda 0 was increased; with a further increase in the number of cigarettes, the effect of cigarette smoke decreased or disappeared. Nicotine injection and acetylcholine inhalation increased respiratory resistance to a degree similar to that observed with cigarette smoke but did not change lambda 0. However, either substance P (SP) or capsaicin injection increased lambda 0 in a fashion similar to that noted with cigarette smoke inhalation. Repeated administration of SP produced a significant tachyphylaxis of the effect, and capsaicin did not increase lambda 0 after the cigarette smoke-induced tachyphylaxis of the effect. Colchicine inhibited the cigarette smoke-induced increase in lambda 0. These results suggest that cigarette smoke increases CM of AM, probably through the release of tachykinins including SP from sensory nerves in the lung.

The Effects of Cigarette Smoke on Porcine Airway Epithelium

1998 ◽  
Vol 4 (S2) ◽  
pp. 1076-1077
Author(s):  
Darrell D. Morgan ◽  
Anthony G. Moss
Keyword(s):  
Endoplasmic Reticulum ◽  
Cigarette Smoke ◽  
Airway Epithelium ◽  
Laser Scanning ◽  
Beat Frequency ◽  
Airway Epithelial Cells ◽  
Smoke Inhalation ◽  
Ultrastructural Changes ◽  
Epithelial Tissue ◽  
Periodic Movement

Cephalad pulmonary mucociliary clearance driven by cilia of the ciliated airway epithelium provides probably the most important line of defense against inhaled toxins and particulate material for organs of the thoracic cavity. We demonstrate the reorganization of the cytoskeleton and the endoplasmic reticulum of airway epithelial cells upon cigarette smoke inhalation by employing DIC, LSCM, TEM and widefield fluorescence microscopy and have correlated this reorganization to changes in ciliary beat frequency (CBF) via FFT analysis. Neonatal pigs were used to provided healthy tracheal epithelial tissue. Exposure to cigarette smoke causes rapid ultrastructural changes including: ciliary distortion and detachment, ciliary abscission and severe alteration in endoplasmic reticulum structure suggesting profound disruption of essential membrane-cytoskeletal linkages.To examine changes in CBF we describe a simple approach, using a laser scanning confocal microscope (LSCM) and an analog-to-digital computer converter/analyzer for the acquisition of data from biological systems that undergo rapid periodic movement, such as ciliary motion.

Inhalation toxicity studies on cigarette smoke III. Tobacco smoke inhalation dosimetry study on rats

Toxicology ◽  
1976 ◽  
Vol 6 (2) ◽  
pp. 207-217 ◽  
Author(s):  
R. Binns ◽  
J.L. Beven ◽  
Lynda V. Wilton ◽  
W.G.D. Lugton
Keyword(s):  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Smoke Inhalation ◽  
Inhalation Toxicity ◽  
Toxicity Studies

Investigations on the Effects of Chronic Cigarette-Smoke Inhalation in Syrian Golden Hamsters

1973 ◽  
Vol 51 (6) ◽  
pp. 1781-1832 ◽  
Author(s):  
W. Dontenwill ◽  
H. -J. Chevalier ◽  
H. -P. Harke ◽  
U. Lafrenz ◽  
G. Reckzeh ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Golden Hamsters ◽  
Syrian Golden Hamsters
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