scholarly journals Acute cigarette smoke inhalation blunts lung responsiveness to methacholine and allergen in rabbit: differentiation of central and peripheral effects

2010 ◽  
Vol 299 (2) ◽  
pp. L242-L251 ◽  
Author(s):  
Liisa Porra ◽  
Ferenc Peták ◽  
Satu Strengell ◽  
Kimmo Neitola ◽  
Tibor Z. Janosi ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Airway Responsiveness ◽  
Smoke Inhalation ◽  
Acute Exposure ◽  
Tobacco Smoke Exposure ◽  
Short Term ◽  
Peripheral Airway ◽  
Airway Response ◽  
Central Airway ◽  
Mainstream Cigarette Smoke

Despite the prevalence of active smoking in asthmatics, data on the short-term effect of acute mainstream tobacco smoke exposure on airway responsiveness are very scarce. The aim of this study was to assess the immediate effect of acute exposure to mainstream cigarette smoke on airway reactivity to subsequent nonspecific and allergenic challenges in healthy control ( n = 5) and ovalbumin-sensitized rabbits ( n = 6). We combined low-frequency forced oscillations and synchrotron radiation CT imaging to differentiate central airway and peripheral airway and lung parenchymal components of the response to airway provocation. Acute exposure to smoke generated by four successive cigarettes (CS) strongly inhibited the central airway response to subsequent IV methacholine (MCh) challenge. In the sensitized animals, although the response to ovalbumin was also inhibited in the central airways, mainstream CS did not blunt the peripheral airway response in this group. In additional groups of experiments, exposure to HEPA-filtered CS ( n = 6) similarly inhibited the MCh response, whereas CO (10,000 ppm for 4 min, n = 6) or nitric oxide inhalation instead of CS (240 ppm, 4 × 7 min, n = 5) failed to blunt nonspecific airway responsiveness. Pretreatment with α-chymotrypsin to inhibit endogenous VIP before CS exposure had no effect ( n = 4). Based on these observations, the gas phase of mainstream cigarette smoke may contain one or more short-term inhibitory components acting primarily on central airways and inhibiting the response to both specific and nonspecific airway provocation, but not on the lung periphery where both lung mechanical parameters, and synchrotron-imaging derived parameters, showed large changes in response to allergen challenge in sensitized animals.

scholarly journals Cigarette smoke inhalation and the acute airway response.

Thorax ◽  
1980 ◽  
Vol 35 (4) ◽  
pp. 246-254 ◽  
Author(s):  
T Higenbottam ◽  
C Feyeraband ◽  
T J Clark
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Airway Response

Enhanced Pulmonary Epithelial Replication and Axial Airway Mucosubstance Changes in F344 Rats Exposed Short-Term to Mainstream Cigarette Smoke

1999 ◽  
Vol 161 (2) ◽  
pp. 171-179 ◽  
Author(s):  
T.H. March ◽  
L.M. Kolar ◽  
E.B. Barr ◽  
G.L. Finch ◽  
M.G. Ménache ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Short Term ◽  
F344 Rats ◽  
Mainstream Cigarette Smoke

Short term model of COPD acute exacerbation combining cigarette smoke inhalation and Influenza A virus infection in mice.

2019 ◽  
Author(s):  
Maximiliano Ruben Ferrero ◽  
Cristiana Couto Garcia ◽  
Julian Torres ◽  
Tatiana Paula Ferreira ◽  
Ana Carolina Arantes ◽  
...  
Keyword(s):  
Virus Infection ◽  
Acute Exacerbation ◽  
Cigarette Smoke ◽  
Influenza A Virus ◽  
Influenza A ◽  
Smoke Inhalation ◽  
Short Term ◽  
Term Model ◽  
Influenza A Virus Infection

scholarly journals Towards the validation of a lung tumorigenesis model with mainstream cigarette smoke inhalation using the A/J mouse

Toxicology ◽  
2013 ◽  
Vol 305 ◽  
pp. 49-64 ◽  
Author(s):  
Walter Stinn ◽  
An Berges ◽  
Kris Meurrens ◽  
Ansgar Buettner ◽  
Stephan Gebel ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Smoke Inhalation ◽  
Lung Tumorigenesis ◽  
Mainstream Cigarette Smoke

In utero exposure to mainstream cigarette smoke alters neonatal pulmonary signaling networks and postnatal lung function

Pneumologie ◽  
2013 ◽  
Vol 67 (12) ◽  
Author(s):  
S Dehmel ◽  
P Nathan ◽  
K Milger ◽  
R Prungnaud ◽  
R Imker ◽  
...  
Keyword(s):  
Lung Function ◽  
Cigarette Smoke ◽  
In Utero ◽  
Signaling Networks ◽  
In Utero Exposure ◽  
Mainstream Cigarette Smoke

Effects of stem wire, expansion wire and flake wire on 3 harmful components in mainstream cigarette smoke

2014 ◽  
Vol 39 (1) ◽  
pp. 23-25
Author(s):  
Cheng-long XU ◽  
Zhao-peng SONG ◽  
Ya DAI ◽  
Kuo-yan MA ◽  
Wen-chao WANG ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Mainstream Cigarette Smoke

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.

The Effect of Smoke Inhalation on Lung Function and Airway Responsiveness in Wildland Fire Fighters

1992 ◽  
Vol 146 (6) ◽  
pp. 1469-1473 ◽  
Author(s):  
Diane Liu ◽  
Ira B. Tager ◽  
John R. Balmes ◽  
Robert J. Harrison
Keyword(s):  
Lung Function ◽  
Wildland Fire ◽  
Airway Responsiveness ◽  
Smoke Inhalation ◽  
Fire Fighters

Comparison of Oxidative Effects of Electronic Cigarette and Tobacco Smoke Exposure Performed Experimentally

2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Electronic Cigarette ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Exposure Group ◽  
Oxidative Effects

<b><i>Objective:</i></b> Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. <b><i>Method:</i></b> We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (<i>N</i> = 8); the electronic cigarette group (<i>N</i> = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (<i>N</i> = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. <b><i>Results:</i></b> Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (<i>p</i> &#x3c; 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (<i>p</i> &#x3c; 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (<i>p</i> &#x3c; 0.000). <b><i>Conclusion:</i></b> Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.

Positive Expiratory Pressure: A Potential Therapy to Mitigate Acute Bronchoconstriction in the Asthma of Obesity

2021 ◽  
Author(s):  
Swati a. Bhatawadekar ◽  
Anne E. Dixon ◽  
Ubong Peters ◽  
Nirav Daphtary ◽  
Kevin Hodgdon ◽  
...  
Keyword(s):  
Airway Resistance ◽  
Late Onset ◽  
Rescue Therapy ◽  
Pharmacologic Therapy ◽  
Airway Closure ◽  
Airway Narrowing ◽  
Asthma Patients ◽  
Peripheral Airway ◽  
Central Airway ◽  
Positive Expiratory Pressure

Late-onset non-allergic (LONA) asthma in obesity is characterized by increased peripheral airway closure secondary to abnormally collapsible airways. We hypothesized that positive expiratory pressure (PEP) would mitigate the tendency to airway closure during bronchoconstriction, potentially serving as rescue therapy for LONA asthma of obesity. The PC20 dose of methacholine was determined in 18 obese participants with LONA asthma. At each of 4 subsequent visits, we used oscillometry to measure input respiratory impedance (Zrs) over 8 minutes; participants received their PC20 concentration of methacholine aerosol during the first 4.5 minutes. PEP combinations of either 0 or 10 cmH2O either during and/or after the methacholine delivery were applied, randomized between visits. Parameters characterizing respiratory system mechanics were extracted from the Zrs spectra. In 18 LONA asthma patients (14 females, BMI: 39.6±3.4 kg/m2), 10 cmH2O PEP during methacholine reduced elevations in the central airway resistance, peripheral airway resistance and elastance, and breathing frequency was also reduced. During the 3.5 min following methacholine delivery, PEP of 10 cmH2O reduced Ax and peripheral elastance compared to no PEP. PEP mitigates the onset of airway narrowing brought on by methacholine challenge, and airway closure once it is established. PEP thus might serve as a non-pharmacologic therapy to manage acute airway narrowing for obese LONA asthma.

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