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[Airway hyperresponsiveness and airway mucosal permeability]
H Ikeda1, H Nishiyama, T Kaneko
1First Department of Internal Medicine, Yokohama City University School of Medicine.
Nihon Kyobu Shikkan Gakkai Zasshi
|December 1, 1996
Summary
Airway hyperresponsiveness and mucosal permeability changes in guinea pigs were studied. Tachykinins increased permeability, while superoxide dismutase reduced hyperresponsiveness, suggesting different causes for these airway conditions.
Area of Science:
- Respiratory Physiology
- Pharmacology
Background:
- Airway hyperresponsiveness and increased mucosal permeability are key features of airway inflammation.
- Tachykinins and superoxide radicals are implicated in airway pathophysiology.
Purpose of the Study:
- To investigate the roles of tachykinins and superoxide dismutase in ozone-induced airway inflammation, specifically their effects on airway hyperresponsiveness and mucosal permeability.
Main Methods:
- Male Hartley guinea pigs were exposed to ozone to induce airway inflammation.
- Tachykinins (substance P, neurokinin A), selective antagonists (CP-96345, SR-48968), and superoxide dismutase were administered.
- Airway hyperresponsiveness, mucosal permeability, and vascular permeability were measured.
Main Results:
- Ozone-induced airway inflammation increased hyperresponsiveness and mucosal permeability, with a delay in vascular permeability.
- Neurokinin-2 receptor antagonist SR-48968 reduced mucosal permeability but not hyperresponsiveness.
- Substance P and neurokinin A increased mucosal permeability, while superoxide dismutase reduced hyperresponsiveness.
Conclusions:
- The factors influencing airway hyperresponsiveness and mucosal permeability may differ, despite their concurrent increase during inflammation.
- Tachykinins play a role in increasing airway mucosal permeability.
- Superoxide radicals contribute to airway hyperresponsiveness in this model.