Bronchoconstriction induced by hyperventilation with humidified warm air in ovalbumin-sensitized Brown Norway rats

Chun-Chun Hsu, Chayse B Martin, Lu-Yuan Lee

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

Previous investigators reported that hyperventilation with hot humid air caused bronchoconstriction in asthmatic patients (Am Rev Resp Dis 131: 357–361, 1985). This study was carried out to further investigate this response in an animal model of allergic asthma. Our results showed: 1) In Brown-Norway rats actively sensitized by chronic inhalation of ovalbumin (Ova) aerosol, isocapnic hyperventilation with humidified warm air (HWA) for 2 min induced an increase in tracheal temperature (Ttr) to a peak of 40.6 ± 0.3°C and an immediate and sustained (> 10 min) increase in RL (from 0.12 ± 0.01 to 0.21 ± 0.02 cmH2O/ml/s; n=7, P<0.01). In sharp contrast, the HWA challenge produced the same increase in Ttr, but did not generate any increase in RL in matching control rats (n=7, P>0.05). 2) The responses in RL were reproducible in both groups when the same HWA challenge was repeated 60–90 min later (n=4). 3) This bronchoconstrictive effect was temperature dependent; a smaller increase in peak Ttr (39.9 ± 0.2°C) generated a smaller, but significant increase in RL in sensitized rats: from 0.12 ± 0.01 to 0.19 ± 0.03 cmH2O/ml/s (n=3, P<0.05). In conclusion, an increase in airway temperature within the normal physiological range triggered bronchoconstriction in sensitized rats, but not in control rats. Chronic airway inflammation in sensitized animals is likely a major contributing factor in causing this response. (NIH grant HL96914, fellowship NSC98-2917-I-038-101)
Original languageEnglish
Title of host publicationEnglish
Pages864.15-864.15
Publication statusPublished - Apr 1 2011
Externally publishedYes

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Bronchoconstriction
Hyperventilation
Ovalbumin
Air
Temperature
Organized Financing
Aerosols
Inhalation
Reference Values
Asthma
Animal Models
Research Personnel
Inflammation

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Bronchoconstriction induced by hyperventilation with humidified warm air in ovalbumin-sensitized Brown Norway rats. / Hsu, Chun-Chun; Martin, Chayse B; Lee, Lu-Yuan.

English. 2011. p. 864.15-864.15.

Research output: Chapter in Book/Report/Conference proceedingConference contribution

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abstract = "Previous investigators reported that hyperventilation with hot humid air caused bronchoconstriction in asthmatic patients (Am Rev Resp Dis 131: 357–361, 1985). This study was carried out to further investigate this response in an animal model of allergic asthma. Our results showed: 1) In Brown-Norway rats actively sensitized by chronic inhalation of ovalbumin (Ova) aerosol, isocapnic hyperventilation with humidified warm air (HWA) for 2 min induced an increase in tracheal temperature (Ttr) to a peak of 40.6 ± 0.3°C and an immediate and sustained (> 10 min) increase in RL (from 0.12 ± 0.01 to 0.21 ± 0.02 cmH2O/ml/s; n=7, P<0.01). In sharp contrast, the HWA challenge produced the same increase in Ttr, but did not generate any increase in RL in matching control rats (n=7, P>0.05). 2) The responses in RL were reproducible in both groups when the same HWA challenge was repeated 60–90 min later (n=4). 3) This bronchoconstrictive effect was temperature dependent; a smaller increase in peak Ttr (39.9 ± 0.2°C) generated a smaller, but significant increase in RL in sensitized rats: from 0.12 ± 0.01 to 0.19 ± 0.03 cmH2O/ml/s (n=3, P<0.05). In conclusion, an increase in airway temperature within the normal physiological range triggered bronchoconstriction in sensitized rats, but not in control rats. Chronic airway inflammation in sensitized animals is likely a major contributing factor in causing this response. (NIH grant HL96914, fellowship NSC98-2917-I-038-101)",
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N2 - Previous investigators reported that hyperventilation with hot humid air caused bronchoconstriction in asthmatic patients (Am Rev Resp Dis 131: 357–361, 1985). This study was carried out to further investigate this response in an animal model of allergic asthma. Our results showed: 1) In Brown-Norway rats actively sensitized by chronic inhalation of ovalbumin (Ova) aerosol, isocapnic hyperventilation with humidified warm air (HWA) for 2 min induced an increase in tracheal temperature (Ttr) to a peak of 40.6 ± 0.3°C and an immediate and sustained (> 10 min) increase in RL (from 0.12 ± 0.01 to 0.21 ± 0.02 cmH2O/ml/s; n=7, P<0.01). In sharp contrast, the HWA challenge produced the same increase in Ttr, but did not generate any increase in RL in matching control rats (n=7, P>0.05). 2) The responses in RL were reproducible in both groups when the same HWA challenge was repeated 60–90 min later (n=4). 3) This bronchoconstrictive effect was temperature dependent; a smaller increase in peak Ttr (39.9 ± 0.2°C) generated a smaller, but significant increase in RL in sensitized rats: from 0.12 ± 0.01 to 0.19 ± 0.03 cmH2O/ml/s (n=3, P<0.05). In conclusion, an increase in airway temperature within the normal physiological range triggered bronchoconstriction in sensitized rats, but not in control rats. Chronic airway inflammation in sensitized animals is likely a major contributing factor in causing this response. (NIH grant HL96914, fellowship NSC98-2917-I-038-101)

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