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Elastase in hyperpnea-induced guinea pig airway constriction
1Department of Physiology, College of Medicine, National Taiwan University, Taipei. tiger@ha.mc.ntu.edu.tw
European Journal of Pharmacology
|December 1, 1998
Summary
Endogenous elastase contributes to airway constriction during hyperpnea in guinea pigs. An elastase inhibitor, eglin-c, and mast cell degranulation significantly reduced this bronchoconstriction.
Area of Science:
- Respiratory Physiology
- Pulmonary Pharmacology
Background:
- Aerosolized elastase induces airway constriction.
- The role of endogenous elastase in hyperpnea-induced bronchoconstriction is unclear.
Purpose of the Study:
- To investigate the involvement of endogenous elastase in isocapnic hyperpnea-induced airway constriction.
- To assess the efficacy of an elastase inhibitor, eglin-c, in preventing this response.
Main Methods:
- Guinea pigs underwent 15 minutes of isocapnic hyperpnea.
- Airway function was measured using dynamic respiratory compliance and expiratory flow rates.
- Animals were treated with eglin-c (elastase inhibitor) or compound 48/80 (mast cell degranulator).
Main Results:
- Isocapnic hyperpnea caused significant airway constriction, evidenced by decreased dynamic respiratory compliance and expiratory flows.
- Eglin-c treatment significantly attenuated hyperpnea-induced bronchoconstriction.
- Pretreatment with compound 48/80 also reduced airway constriction.
- Eglin-c did not affect pulmonary function during normal ventilation.
Conclusions:
- Endogenous elastase, likely released from mast cells, plays a direct or indirect role in hyperpnea-induced airway constriction.
- Targeting elastase activity may be a therapeutic strategy for conditions involving exercise-induced bronchoconstriction.