A longitudinal analysis of pulmonary function in rats during a 12 month cigarette smoke exposure

Wright, J. L.; Sun, JP; Vedal, Sverre

doi:10.1183/09031936.97.10051115

Cited by 18 publications

(12 citation statements)

References 17 publications

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“…It is important that in our newly designed BPG, the temperature in the box is actively controlled, thereby rendering it unnecessary to consider changes in temperature. There has been great variation in the reported FRC values, which have ranged from 2.08 to 5.8 ml [10,12,15,[23][24][25]. Our FRC was within the range of those observed in these reports.…”

Section: Frc Measurementsupporting

confidence: 62%

Functional Residual Capacity and Airway Resistance of the Rat Measured with a Heat- and Temperature-Adjusted Body Plethysmograph

2006

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Abstract:The functional residual capacity (FRC) and airway resistance (R aw ) of the rat were measured, using a newly designed body plethysmograph (BPG), the inner environment of which was maintained at body temperature and was water-vapor saturated. The subjects were anesthetized and tracheally intubated male Wistar rats (n = 15). After measuring the FRC and R aw , we analyzed the effects of inhaled methacholine (Mch, 0-8 mg/ml) on R aw .The determined FRC was 5.37 ± 0.22 ml (mean ± SE). An almost linear relationship between box pressure and respiratory flow was obtained when the difference between box-gas temperature and the rectal temperature of the rat was less than 1.0°C. The R aw at FRC was 0.230 ± 0.017 cmH 2 O/ml/s. It increased proportionally with increases in the Mch concentration. When the dynamic changes in R aw were analyzed, the R aw was found to progressively increase during expiration; this increase continued throughout inspiration. Thus in the rat, R aw is not simply a function of changes in lung volume. In conclusion, the humidity-and temperature-adjusted BPG provided an absolute and possibly dynamic value of R aw .

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Section: Frc Measurementsupporting

confidence: 62%

Functional Residual Capacity and Airway Resistance of the Rat Measured with a Heat- and Temperature-Adjusted Body Plethysmograph

2006

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“…Normally lung volumes and airflows increase over time during the growth of rats. The decrease in airflow associated with ageing is only found after 8-12 months in SpragueDawley rats that initially weighed 400-510 g [23]. In the present study, rats weighing 200-250 g, were used and studied over a 3 month period.…”

Section: Discussionmentioning

confidence: 99%

Time-course of functional and pathological changes after a single high acute inhalation of chlorine in rats

Demnati¹,

Fraser²,

Ghezzo³

et al. 1998

Eur Respir J

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Reactive airways dysfunction syndrome (RADS) is an asthma-like condition that follows exposure to very high concentrations of an irritant material. We assessed the time-course of pathophysiological alterations in a model of RADS. Sprague-Dawley rats were exposed to 1,500 parts per million (ppm) of chlorine for 5 min. Lung resistance (RL), responsiveness to inhaled methacholine (MCh), the airway epithelium and bronchoalveolar lavage (BAL) were assessed over a 3 month period after exposure. RL increased significantly up to 3 days after exposure, reaching a maximal change of 110+/-16% from baseline. There was a significant decrease in the concentration of MCh required to increase RL by 0.20 cmH2O x mL(-1) x s from days 1-7 after exposure. In some rats, MCh hyperresponsiveness and RL changes persisted after exposure for as long as 1 and 3 months, respectively. Histological evaluation with morphometric evaluation revealed epithelial flattening, necrosis, increase in smooth muscle mass and evidence of epithelial regeneration. BAL showed an increased number of neutrophils. The timing of maximal abnormality in the appearance of the epithelium (days 1-3) corresponded to that of the maximal functional changes. Acute high chlorine exposure results in functional and pathological abnormalities that resolve in the majority of animals after a variable period; however, these changes can persist in some animals. Functional abnormalities in the initial stages may be related to airway epithelial damage.

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“…After anesthesia, the animals can be (relatively) easily intubated and subsequent measurements obtained (11,140). The obvious advantage of this technique is that it allows the documentation of functional changes over time in the same animal (161).…”

Section: Development (See Elastase Emphysema Model and Genetic And Gementioning

confidence: 99%

Animal models of chronic obstructive pulmonary disease

Wright¹,

Cosio²,

Churg³

2008

American Journal of Physiology-Lung Cellular and Molecular Phys

379

326

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-The mechanisms involved in the genesis of chronic obstructive pulmonary disease (COPD) are poorly defined. This area is complicated and difficult to model because COPD consists of four separate anatomic lesions (emphysema, small airway remodeling, pulmonary hypertension, and chronic bronchitis) and a functional lesion, acute exacerbation; moreover, the disease in humans develops over decades. This review discusses the various animal models that have been used to attempt to recreate human COPD and the advantages and disadvantages of each. None of the models reproduces the exact changes seen in humans, but cigarette smoke-induced disease appears to come the closest, and genetically modified animals also, in some instances, shed light on processes that appear to play a role. chronic obstructive pulmonary disease CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) is an increasingly important cause of morbidity and mortality. COPD is now the fifth leading cause of death worldwide (109), and recent estimates suggest that the prevalence is as high as 9 -10% of adults over age 40 (38, 131). In the developed world, cigarette smoking is by far the most important risk factor for COPD. Exposure to air pollution particles, occupational exposures to dusts and fumes (39), and, in the developing world, exposure to biomass fuels used for cooking is also believed to be etiological agents of COPD (38).There are few animal models of COPD related to air pollution particles, dusts and fumes, and biomass fuels; most COPD models have either used cigarette smoke or other approaches, including genetic modifications to mice, believed to reproduce some of the mechanisms behind cigarette smoke. We have recently reviewed mechanistic studies of smoke-exposed animal models (16). In this paper, we will focus on the pros and cons of different COPD animal models.The first question to ask in this context is what would constitute a perfect model of human COPD. This is not a simple question because human COPD consists of at least four anatomic lesions (further defined below): emphysema, small airway remodeling (including goblet cell metaplasia), chronic bronchitis, and pulmonary hypertension; a given patient may have any or all of these lesions. In addition, COPD patients may develop acute exacerbations that are believed to have an infectious basis. To further complicate matters, no matter which lesions are present, COPD develops and is slowly progressive over many years.Because COPD is closely related to the underlying anatomy of the lung, a good animal model should have pulmonary anatomy similar to that of humans. The fundamental mechanisms behind COPD should be similar in animal models and humans. The ideal model would allow the investigator to produce the various different anatomic lesions just listed, all in a short period of time. Unfortunately, all of the known animal models meet only some of the above criteria, and even another human would probably not meet all of them, because, as noted above, there is considerable human to human variation in th...

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A longitudinal analysis of pulmonary function in rats during a 12 month cigarette smoke exposure

Cited by 18 publications

References 17 publications

Functional Residual Capacity and Airway Resistance of the Rat Measured with a Heat- and Temperature-Adjusted Body Plethysmograph

Functional Residual Capacity and Airway Resistance of the Rat Measured with a Heat- and Temperature-Adjusted Body Plethysmograph

Time-course of functional and pathological changes after a single high acute inhalation of chlorine in rats

Animal models of chronic obstructive pulmonary disease

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