Specific airway conductance in guinea pigs: Normal values and histamine induced fall

Agrawal, K. P.

doi:10.1016/0034-5687(81)90085-2

Cited by 87 publications

(38 citation statements)

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“…Measurements of specific airway conductance (SGaw) and airway reactivity to inhaled histamine were made in nonanesthetized, spontaneously breathing animals, using a noninvasive body plethysmographic technique as described previously [6]. Records of airflow changes were measured by using a Hans-Rudolf 0000 pneumatachograph and a transducer (Validyne MP-45Ϯ2 cmH 2 O) connected to an amplifier (Validyne CD12), and box pressure changes were measured by using a transducer (Validyne MP-45Ϯ2 cmH 2 O) connected to an amplifier (Validyne CD15).…”

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confidence: 99%

“…A continuous plot of airflow change versus box pressure change was obtained with airflow on the Yaxis and box pressure on the X-axis. The inspiratory limb of the X-Y plot represented the ratio of flow change to flow-related changes in box pressure and provided the data for computing SGaw [6]. The slope of the rising limb of this X-Y loop was recorded in terms of tan that was obtained by dividing the voltage change on Y-axis by the voltage change on X-axis.…”

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confidence: 99%

“…The slope of the rising limb of this X-Y loop was recorded in terms of tan that was obtained by dividing the voltage change on Y-axis by the voltage change on X-axis. SGaw at functional residual capacity (FRC) was calculated by substituting the value of tan in the following equation [6]:…”

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confidence: 99%

“…Subsequently, starting from 0.02 mg/ml, consecutively doubled concentrations of histamine in PBS were given, measuring the response to each at 30 and 90 s until SGaw fell by Ͼ35% or until a concentration of 2.5 mg/ml was reached. A log dose response curve was plotted, and the concentration of histamine producing a 35% fall in SGaw was calculated (ED 35 histamine) as described by Agrawal [6]. This represented the airway reactivity of the animal.…”

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confidence: 99%

“…The activities of Na ] i was measured by using the fluorescent dye FURA-2AM, as described by Grynkiewicz [15]. Briefly, 2ϫ10 6 Tracheal smooth muscle cells were isolated as described above, and [Ca 2ϩ ] i was estimated in tracheal cell suspension by the same method.…”

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confidence: 99%

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Relationship between Intracellular Calcium and Airway Reactivity in Guinea Pigs.

Jain

Raj²,

Gangal³

et al. 2001

JJP

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The regulation of intracellular calcium may play a crucial role in the pathogenesis of asthma because an increase in [Ca 2ϩ ] i is an essential initiating mechanism of cellular activation in inflammatory cells and in airway smooth muscle [1][2][3][4]. Because of the inaccessibility of tracheal tissue in human subjects, animal models have been used to define the biochemical correlates of airway reactivity. Na -ATPase activities in guinea pigs. Because these enzymes serve to lower the intracellular calcium, it was suggested that the higher activities in the more-reactive animals might reflect a compensatory response to higher [Ca 2ϩ ] i level. However, measurements of intracellular calcium were not made. The present study was carried out to examine the relationship between airway reactivity and intracellular calcium. Japanese Journal of Physiology577Japanese Journal of Physiology, 51, 577-583, 2001 Key words: airway hyperreactivity, intracellular calcium, Na-ATPase, lysophosphatidylcholine.Abstract: The present study was carried out to examine the relationship between intracellular free calcium ion concentrations and its regulatory enzymes, sodium potassium adenosine triphosphatase (Na ϩ ,K ϩ -ATPase) and calcium adenosine triphosphatase (Ca 2ϩ -ATPase), with airway reactivity to inhaled histamine in guinea pigs. Forty-nine guinea pigs were included in this study. Of these, 34 animals responded to histamine bronchoprovocation challenge in vivo with a greater than 35% fall in specific airways conductance and were labeled as "reactive," and the remaining 15 were "nonreactive." The dose of histamine producing a 35% fall in specific airways conductance was labeled as ED 35 SGaw. The animals were then sacrificed, and the following biochemical measurements were carried out: intracellular free calcium ion concentrations [Ca 2ϩ ] i in leukocytes and isolated tracheal smooth muscle cells, activities of Na ] i is an important determinant of airway reactivity. Intracellular calcium levels modulate airway response to histamine with higher levels being associated with greater reactivity. [Japanese Journal of Physiology, 51, 577-583, 2001] Relationship between Intracellular Calcium and Airway Reactivity in Guinea Pigs ] i , intracellular free calcium concentration; SGaw, specific airway conductance; ED 35 histamine, dose of histamine that produced a fall of 35% in SGaw; LPC, lysophosphatidylcholine.

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Relationship between Intracellular Calcium and Airway Reactivity in Guinea Pigs.

Jain

Raj²,

Gangal³

et al. 2001

JJP

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The role of inflammatory mediators in airway edema and obstruction produced in guinea pigs exposed to inhaled endotoxin or cotton dusts

Gordon

1990

American J Industrial Med

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Endotoxin is present in significant quantities in several organic dusts [Dutkiewicz;1986;Lundholm et al., 1986] and is thought to play a role in some of the pulmonary effects of inhaled organic dusts, including cotton dust. Inhaled endotoxin and cotton dust are known to cause airway obstruction as well as peripheral lung injury.The purpose of the present study was to examine the effects of inhaled endo toxin on the conducting airways and to determine what role airway inflammation might play in the airway obstruction produced by endotoxin. Therefore, the effects of single and repeated exposures to endotoxin or cotton dust on airway edema, airway conductance, and the influx of inflammatory cells were examined in awake guinea pigs. Specific airway conductance (SGaw) was measured before and during exposure in awake, spontaneously breathing guinea pigs by the method of Agrawal [1981], and airway edema was measured by quantifying the extravasation of protein-bound Evans blue dye in the trachea and the mainstem and hilar bronchi. A single 3-hour exposure to 6.1 or 71.7 μg/m 3 endotoxin produced a dose-related decrease in SGaw by the end of exposure (22% and 34%, respectively). No significant decrease in SGaw was observed in control animals exposed to isotonic, pyrogen-free saline. The airway obstruction produced by inhaled endotoxin was accompanied by a dose-dependent increase in protein extravasation in the trachea, mainstem bronchi, and extrapulmonary hilar bronchi. Mean dye extravasation was increased by 106% and 314% in the mainstem bronchi, and by 124% and 247% in the hilar bronchi of animals exposed to the low and high doses of endotoxin, respectively. In the trachea, dye extravasation was significantly increased only in the high-dose endotoxin animals (136%). Expo sure to cotton dust (32 mg/m 3 ) with a comparable airborne endotoxin concentration (5.1 μg/m 3 ) produced a similar 43% decrease in SGaw. Airway edema was also observed after exposure to cotton dust. To study the hypothesis that airway edema may contribute to the airflow obstruction caused by inhaled endotoxin, animals were

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Effect of four‐week repeated inhalation exposure to unconjugated azodicarbonamide on specific and non‐specific airway sensitivity of the guinea pig

Gerlach

Medinsky

Hobbs

et al. 1989

J of Applied Toxicology

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Reports of respiratory problems among industrial workers exposed repeatedly by inhalation to azodicarbonamide (ADA) raised concern that ADA might be a pulmonary sensitizer. We used a non-invasive method for measuring specific airway conductance to evaluate the potential for repeated inhalation of unconjugated ADA to cause specific or non-specific pulmonary sensitization in the guinea pig. Two groups of male Hartley guinea pigs were exposed 6 h/day, 5 days/week for 4 weeks to aerosolized ADA at 51 or 200 mg/m3, or to filtered air as controls. One group was tested for specific sensitization to ADA by measuring specific airway conductance during inhalation challenge with ADA before and on the third day after the 4-week ADA exposure. The ADA concentrations for the challenges were identical to the repeated exposure concentrations (51 or 200 mg/m3, 200 mg/m3 for controls). The other group was tested for non-specific airway sensitization by inhalation challenge with aerosolized histamine before and after the 4-week ADA exposure. Histamine was administered in stepwise increasing concentrations to elicit an airway response in each guinea pig. Skin tests for immunological responses to ADA, body weight and histopathology of the respiratory tract and skin test sites were also evaluated. The 4-week exposure to ADA did not result in either specific or non-specific airway sensitization. The ADA exposure did not induce positive skin reactions, influence body weight or cause histopathological responses. These results indicate that ADA, acting alone (i.e. not conjugated to a protein), is not a pulmonary sensitizer in the guinea pig exposed repeatedly for 4 weeks and challenged to simulate a 'Monday morning' exposure.

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Specific airway conductance in guinea pigs: Normal values and histamine induced fall

Cited by 87 publications

References 5 publications

Relationship between Intracellular Calcium and Airway Reactivity in Guinea Pigs.

Relationship between Intracellular Calcium and Airway Reactivity in Guinea Pigs.

The role of inflammatory mediators in airway edema and obstruction produced in guinea pigs exposed to inhaled endotoxin or cotton dusts

Effect of four‐week repeated inhalation exposure to unconjugated azodicarbonamide on specific and non‐specific airway sensitivity of the guinea pig

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