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Persistent airway hyperresponsiveness after neonatal viral bronchiolitis in rats
R Sorkness1, R F Lemanske, W L Castleman
1Department of Medicine, School of Medicine, University of Wisconsin, Madison 53706.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|January 11, 1991
Summary
Neonatal Sendai virus infection in rats causes lasting lung function changes and increased airway hyperresponsiveness. This animal model may help study human airway diseases like bronchiolitis.
Area of Science:
- Pulmonology
- Virology
- Immunology
Background:
- Infant bronchiolitis linked to long-term small airway changes and hyperresponsiveness.
- Sendai virus infection in neonatal rats causes lung changes and inflammation.
Purpose of the Study:
- Evaluate pulmonary mechanics, gas exchange, and airway responsiveness in rats post-Sendai virus infection.
- Determine if neonatal Sendai virus infection leads to persistent lung function alterations.
Main Methods:
- Infection of neonatal rats with Sendai virus.
- Assessment of pulmonary mechanics, gas exchange (arterial PO2, PCO2), and airway responsiveness to methacholine at 7 and 13-16 weeks post-infection.
Main Results:
- Virus-infected rats showed lower arterial PO2 and higher total lung resistance.
- Significantly increased airway sensitivity to methacholine in infected rats compared to controls.
- Both groups showed decreased airway sensitivity with age.
Conclusions:
- Neonatal Sendai virus infection induces persistent alterations in rat lung function and airway responsiveness.
- This model is valuable for studying airway inflammation, lung morphology, and hyperresponsiveness.
- Findings may be relevant to human infant airway diseases.