TY - JOUR
T1 - Hyperventilation-induced airway injury and vascular leakage in dogs
T2 - Effects of α1-adrenergic agonists
AU - Freed, Arthur N.
AU - Taskar, Varsha
AU - Schofield, Brian
AU - Omori, Chiharu
PY - 1997/12
Y1 - 1997/12
N2 - α1-Adrenergic agonists inhibit hyperventilation-induced bronchoconstriction (HIB) in dogs. We tested the hypothesis that α-agonists inhibit HIB by reducing bronchovascular leakage and edema that theoretically could cause airway obstruction. Peripheral airways were isolated by using a bronchoscope; pretreated with either methoxamine (Mx), norepinephrine (NE), or saline aerosol; and then exposed to a 2,000 ml/min dry-air challenge (DAC) for 2 min. Colloidal carbon was injected before DAC and used to quantify bronchovascular permeability. Mx-, NE-, and vehicle-treated airways were prepared for morphometric analysis within 1 h after DAC. Light microscopy revealed that the 2-min DAC produced minimal bronchovascular leakage and little epithelial damage. However, pretreatment with either Mx or NE significantly enhanced dry air-induced bronchovascular hyperpermeability and mucosal injury. The increased damage associated with these α1-agonists implicates a protective role for the bronchial circulation. The fact that α1-agonists inhibit HIB suggests that neither dry air-induced leakage nor injury directly contributes to the development of airway obstruction. In addition, our data suggest that α-agonists attenuate HIB in part by augmenting hyperventilation-induced bronchovascular leakage and by replacing airway water lost during a DAC.
AB - α1-Adrenergic agonists inhibit hyperventilation-induced bronchoconstriction (HIB) in dogs. We tested the hypothesis that α-agonists inhibit HIB by reducing bronchovascular leakage and edema that theoretically could cause airway obstruction. Peripheral airways were isolated by using a bronchoscope; pretreated with either methoxamine (Mx), norepinephrine (NE), or saline aerosol; and then exposed to a 2,000 ml/min dry-air challenge (DAC) for 2 min. Colloidal carbon was injected before DAC and used to quantify bronchovascular permeability. Mx-, NE-, and vehicle-treated airways were prepared for morphometric analysis within 1 h after DAC. Light microscopy revealed that the 2-min DAC produced minimal bronchovascular leakage and little epithelial damage. However, pretreatment with either Mx or NE significantly enhanced dry air-induced bronchovascular hyperpermeability and mucosal injury. The increased damage associated with these α1-agonists implicates a protective role for the bronchial circulation. The fact that α1-agonists inhibit HIB suggests that neither dry air-induced leakage nor injury directly contributes to the development of airway obstruction. In addition, our data suggest that α-agonists attenuate HIB in part by augmenting hyperventilation-induced bronchovascular leakage and by replacing airway water lost during a DAC.
KW - Bronchovascular permeability
KW - Exercise-induced asthma
KW - Goblet cells
KW - Hyperventilation-induced bronchoconstriction
KW - Mast cells
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U2 - 10.1152/jappl.1997.83.6.1884
DO - 10.1152/jappl.1997.83.6.1884
M3 - Article
C2 - 9390959
AN - SCOPUS:0031453027
SN - 8750-7587
VL - 83
SP - 1884
EP - 1889
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
IS - 6
ER -