Lung Response To Cigarette Smoke Inhalation: An Animal Model

2018 ◽  
pp. 215-229
Author(s):  
Daniel H. Matulionis
Keyword(s):  
Animal Model ◽  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Lung Response

scholarly journals A novel large animal model of smoke inhalation-induced acute respiratory distress syndrome

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Premila D. Leiphrakpam ◽  
Hannah R. Weber ◽  
Andrea McCain ◽  
Roser Romaguera Matas ◽  
Ernesto Martinez Duarte ◽  
...  
Keyword(s):  
Animal Model ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Distress Syndrome ◽  
Inhalation Injury ◽  
Smoke Inhalation ◽  
Large Animal Model ◽  
Large Animal ◽  
X Ray ◽  
Chest X Ray

Abstract Background Acute respiratory distress syndrome (ARDS) is multifactorial and can result from sepsis, trauma, or pneumonia, amongst other primary pathologies. It is one of the major causes of death in critically ill patients with a reported mortality rate up to 45%. The present study focuses on the development of a large animal model of smoke inhalation-induced ARDS in an effort to provide the scientific community with a reliable, reproducible large animal model of isolated toxic inhalation injury-induced ARDS. Methods Animals (n = 21) were exposed to smoke under general anesthesia for 1 to 2 h (median smoke exposure = 0.5 to 1 L of oak wood smoke) after the ultrasound-guided placement of carotid, pulmonary, and femoral artery catheters. Peripheral oxygen saturation (SpO2), vital signs, and ventilator parameters were monitored throughout the procedure. Chest x-ray, carotid, femoral and pulmonary artery blood samples were collected before, during, and after smoke exposure. Animals were euthanized and lung tissue collected for analysis 48 h after smoke inhalation. Results Animals developed ARDS 48 h after smoke inhalation as reflected by a decrease in SpO2 by approximately 31%, PaO2/FiO2 ratio by approximately 208 (50%), and development of bilateral, diffuse infiltrates on chest x-ray. Study animals also demonstrated a significant increase in IL-6 level, lung tissue injury score and wet/dry ratio, as well as changes in other arterial blood gas (ABG) parameters. Conclusions This study reports, for the first time, a novel large animal model of isolated smoke inhalation-induced ARDS without confounding variables such as cutaneous burn injury. Use of this unique model may be of benefit in studying the pathophysiology of inhalation injury or for development of novel therapeutics.

scholarly journals Rat model of smoke inhalation-induced acute lung injury

2021 ◽  
Vol 8 (1) ◽  
pp. e000879
Author(s):  
Premila Devi Leiphrakpam ◽  
Hannah R Weber ◽  
Tobi Ogun ◽  
Keely L Buesing
Keyword(s):  
Animal Model ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Caspase 3 ◽  
Small Animal ◽  
Therapeutic Options ◽  
Smoke Inhalation ◽  
Small Animal Model ◽  
Injury Score ◽  
Confounding Variables

BackgroundAcute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a lethal disease with limited therapeutic options and an unacceptably high mortality rate. Understanding the complex pathophysiological processes involved in the development of ALI/ARDS is critical for developing novel therapeutic strategies. Smoke inhalation (SI) injury is the leading cause of morbidity and mortality in patients with burn-associated ALI/ARDS; however, to our knowledge few reliable, reproducible models are available for pure SI animal model to investigate therapeutic options for ALI/ARDS without the confounding variables introduced by cutaneous burn or other pathology.ObjectiveTo develop a small animal model of pure SI-induced ALI and to use this model for eventual testing of novel therapeutics for ALI.MethodsRats were exposed to smoke using a custom-made smoke generator. Peripheral oxygen saturation (SpO2), heart rate, arterial blood gas, and chest X-ray (CXR) were measured before and after SI. Wet/dry weight (W/D) ratio, lung injury score and immunohistochemical staining of cleaved caspase 3 were performed on harvested lung tissues of healthy and SI animals.ResultsThe current study demonstrates the induction of ALI in rats after SI as reflected by a significant, sustained decrease in SpO2 and the development of diffuse bilateral pulmonary infiltrates on CXR. Lung tissue of animals exposed to SI showed increased inflammation, oedema and apoptosis as reflected by the increase in W/D ratio, injury score and cleaved caspase 3 level of the harvested tissues compared with healthy animals.ConclusionWe have successfully developed a small animal model of pure SI-induced ALI. This model is offered to the scientific community as a reliable model of isolated pulmonary SI-induced injury without the confounding variables of cutaneous injury or other systemic pathology to be used for study of novel therapeutics or other investigation.

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.

Cigarette Smoke–Related Oxidants and the Development of Sub-RPE Deposits in an Experimental Animal Model of Dry AMD

2006 ◽  
Vol 47 (2) ◽  
pp. 729 ◽  
Author(s):  
Diego G. Espinosa-Heidmann ◽  
Ivan J. Suner ◽  
Paola Catanuto ◽  
Eleut P. Hernandez ◽  
Maria E. Marin-Castano ◽  
...  
Keyword(s):  
Animal Model ◽  
Cigarette Smoke ◽  
Experimental Animal ◽  
Experimental Animal Model ◽  
Dry Amd

Murine lung response to kaolin conveyed by cigarette smoke

1988 ◽  
Vol 413 (3) ◽  
pp. 227-237 ◽  
Author(s):  
Daniel H. Matulionis ◽  
obert A. Yokel
Keyword(s):  
Cigarette Smoke ◽  
Murine Lung ◽  
Lung Response

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

Increased Bone Resorption by Long-Term Cigarette Smoke Exposure in Animal Model

2021 ◽  
Author(s):  
Jader Joel Machado Junqueira ◽  
Juliana Dias Lourenço ◽  
Kaique Rodrigues da Silva ◽  
Vanda Jorgetti ◽  
Rodolfo Vieira ◽  
...  
Keyword(s):  
Animal Model ◽  
Bone Resorption ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure

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.

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