Comparative 13-week cigarette smoke inhalation study in Sprague–Dawley rats: Evaluation of cigarettes with two banded cigarette paper technologies

2007 ◽  
Vol 45 (6) ◽  
pp. 1076-1090 ◽  
Author(s):  
Eugenia H. Theophilus ◽  
W. Keith Shreve ◽  
Paul H. Ayres ◽  
Charles D. Garner ◽  
Deborah H. Pence ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Sprague Dawley ◽  
Inhalation Study ◽  
Sprague Dawley Rats ◽  
Cigarette Paper

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.

Toxicity of aerosols of propylene glycol, vegetable glycerin and nicotine in Sprague-Dawley rats in a 90-d OECD 413 sub-chronic inhalation study

2016 ◽  
Vol 258 ◽  
pp. S201
Author(s):  
B. Phillips ◽  
D. Sharma ◽  
D. Sciuscio ◽  
E. Veljkovic ◽  
S. Lebrun ◽  
...  
Keyword(s):  
Propylene Glycol ◽  
Sprague Dawley ◽  
Inhalation Study ◽  
Sprague Dawley Rats

Endothelin-A receptor antagonist BQ-610 blocks cigarette smoke-induced mitogenesis in rat airways and vessels

1997 ◽  
Vol 272 (4) ◽  
pp. L614-L618 ◽  
Author(s):  
F. Dadmanesh ◽  
J. L. Wright
Keyword(s):  
Cell Proliferation ◽  
Cigarette Smoke ◽  
Airway Epithelial ◽  
Sprague Dawley ◽  
Cell Nuclei ◽  
Sprague Dawley Rats ◽  
Endothelin A ◽  
Bq 610 ◽  
Air Control ◽  
Wall Components

To ascertain whether endothelin may play a role in cigarette smoke-induced cell proliferation in the airways and arterial vasculature of the lung, we exposed groups of seven Sprague-Dawley rats to either room air (control) plus saline infusion, an intravenous infusion of the selective endothelin A antagonist BQ-610 (control BQ-610), the smoke of 10 cigarettes (smoke only), or the smoke of 10 cigarettes after intravenous BQ-610 infusion (smoke + BQ-610). Cell proliferation was quantified by determining the percentage of cell nuclei labeled by 5-bromo-2'-deoxyuridine. We separately evaluated the cells in the epithelium and wall components of the bronchioles, and endothelium and wall components of the peribronchiolar and perialveolar ductular arteries. We found that cigarette smoke produced significant cell proliferation in the airway epithelium and wall, in the peribronchiolar arterial endothelial compartment, and in both the endothelial and wall compartments of the perialveolar ductular arteries. Pretreatment with BQ-610 reduced the peribronchiolar arterial endothelial and the perialveolar ductular arterial wall proliferation to control lev- els and reduced but did not totally abrogate the smoke-in- duced proliferation of the airway epithelial, airway wall, and perialveolar ductular arterial endothelial compartments. We conclude that cigarette smoke-induced cell proliferation of the airways and pulmonary arterial vessels is at least partially mediated through stimulation of the endothelin-A receptors.

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 Effect of Cigarette Smoke on Bronchial Reactivity

1995 ◽  
Vol 2 (4) ◽  
pp. 231-235
Author(s):  
JL Wright ◽  
J-P Sun ◽  
S Vedal ◽  
A Churg
Keyword(s):  
Pulmonary Function ◽  
Cigarette Smoke ◽  
Pulmonary Function Tests ◽  
Lung Compliance ◽  
Forced Expiratory Volume ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Different Strains

OBJECTIVE: To compare the effects of a brief low level exposure to cigarette smoke in rats with known low (Sprague-Dawley) and high (Fisher) airway responsiveness, to test the hypothesis that airways reactivity influences the severity or duration of pulmonary function alterations after cigarette smoke exposure.METHODS: Baseline pulmonary function tests and methacholine dose response tests were conducted in 10 Sprague-Dawley and 10 Fisher rats. On the following day, the animals were reanaesthetized, and breathed for 1 min from a 2 L chamber into which 25 mL of fresh cigarette smoke had been injected, followed by a second set of pulmonary function and methacholine response tests; a final set was performed two weeks later.RESULTS: Sprague-Dawley rats were larger, with larger lung volumes, compliance and flow rates, but Fisher rats showed a fourfold higher airway reactivity. Although neither resistance nor response to methacholine changed in either strain of animal, Sprague-Dawley rats showed an increase in residual volume post smoke, which was not sustained over two weeks, and sustained small increases in vital capacity, total lung capacity and static lung compliance, with a sustained decrease in forced expiratory volume in 0.1 s, while Fisher rats showed only a small sustained increase in functional residual capacity.CONCLUSIONS: Although there are marked differences in pulmonary function between the two different strains of rats, increased airways responsiveness per se does not make the animal more sensitive to the acute effects of cigarette smoke, and the effects of cigarette smoke on pulmonary function are not necessarily related to increased airway resistance. Pulmonary function alterations seen after brief cigarette smoke exposure may be sustained for a relatively long period of time.

Toxicological assessment of the mainstream aerosol of a carbon heated tobacco product in Sprague-Dawley rats; a 90-day sub-chronic inhalation study

2017 ◽  
Vol 280 ◽  
pp. S144
Author(s):  
Blaine Phillips ◽  
Jenny Ho ◽  
Davide Sciuscio ◽  
Emilija Veljkovic ◽  
Stefan Lebrun ◽  
...  
Keyword(s):  
Tobacco Product ◽  
Sprague Dawley ◽  
Inhalation Study ◽  
Toxicological Assessment ◽  
Sprague Dawley Rats

scholarly journals Effects of cigarette smoke on Haemophilus influenzae-induced otitis media in a rat model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sung-Won Choi ◽  
Sunmi Choi ◽  
Eun-Jin Kang ◽  
Hyun Min Lee ◽  
Se-Joon Oh ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Haemophilus Influenzae ◽  
Cigarette Smoke ◽  
Otitis Media ◽  
Inflammatory Reaction ◽  
Rat Model ◽  
The Other ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Group Control

AbstractExposure to cigarette smoke (CS) is a factor that could delay or worsen the recovery of otitis media (OM) by causing inflammatory swelling of the Eustachian tube (ET). However, despite the suggested relationship, little is known about the association between OM and CS. Therefore, we aimed to evaluate the effects of CS on the development, progression, and recovery of OM, as well as the histological and molecular changes caused by CS exposure, by using a rat model of OM infected with non-typeable Haemophilus influenzae (NTHi). Eighty Sprague–Dawley rats with normal middle ears (MEs) were divided into four groups (n = 20 rats/group): control, CS, OM, and CS + OM. The CS and CS + OM groups were exposed to CS for 2 weeks. The inflammatory reaction to NTHi was more intense and lasted longer in the CS + OM group than in the other groups. Goblet cell proliferation and mucus secretion in the ET were more significant in the CS and CS + OM groups than in the other groups. These findings suggested that because CS directly affects the ET and ME mucosa, bacterial OM can become more severe and may resolve more slowly in the presence of CS exposure rather than in its absence.

scholarly journals Rosuvastatin Attenuated Elastic Fiber Degradation in Chronic Obstructive Pulmonary Disease Sprague-Dawley Rats

2019 ◽  
Vol 30 (3) ◽  
pp. 175
Author(s):  
Rahmaningsih Mara Sabirin ◽  
Prasetyastuti ◽  
Denny Agustiningsih
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Cigarette Smoke ◽  
Elastic Fiber ◽  
Degradation Process ◽  
Chronic Obstructive ◽  
Sprague Dawley ◽  
Obstructive Pulmonary Disease ◽  
Fiber Degradation ◽  
Sprague Dawley Rats

<p>Chronic obstructive pulmonary disease (COPD) is an incurable disease which causes disability and death. The main pathogenesis of COPD is oxidative stress due to cigarette smoke which initiates various reactions and lead to lung elastic fibers destruction. Statins are known to have antioxidant effects and reduce mortality in COPD. We studied the effects of cigarette smoke exposure cessation and rosuvastatin on oxidative stress and the level of elastic fiber destruction in COPD model rats. Thirty 10-week old male Sprague-Dawley rats were divided into 2 groups: Control (n=6, did not received fumigation nor treatment) and Smoking (n=24, received fumigation for 70 days) groups. Afterwards, the smoking group was divided into 4 groups: Sham, R2, R5,R10, and received 0.9% NaCl, 2.5, 5 and 10 mg/kg/day of rosuvastatin, respectively. Examination of malondialdehyde (MDA) and desmosine serum were conducted to measure oxidative stress and elastic fiber degradation level, respectively. After smoke exposure, MDA and desmosine levels of COPD rats were found to be significantly higher (p=0.000 and 0.000) than controls. The MDA level in Sham, R2, R5 and R10 groups decreased significantly after therapy (p=0.000; 0.033; 0.015; 0.002). However, the post-treatment desmosine level was increase significantly in Sham and R2 groups (p=0.006 dan 0.012) and insignificantly (p=0.117 dan 0.278) in the R5 and R10 groups. It can be concluded that the cessation of exposure to cigarette smoke can reduce oxidative stress, but not elastic degradation process. The administration of rosuvastatin of 5 or 10 mg/kg/day attenuated elastic degradation process.</p>

Sign in / Sign up

Export Citation Format

Share Document