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Thromboxane A2 mediated bronchoconstriction in the anesthetized guinea pig.
European Journal of Pharmacology
|May 7, 1982
Summary
Thromboxane A2 (TXA2) inhibitors and receptor antagonists block arachidonic acid-induced bronchoconstriction. These agents also inhibit bradykinin-induced responses, suggesting TXA2 mediation, but do not affect histamine or antigen responses.
Area of Science:
- Pharmacology
- Respiratory Physiology
- Biochemistry
Background:
- Platelet aggregation is inhibited by thromboxane A2 (TXA2) synthetase inhibitors and receptor antagonists.
- The role of TXA2 in bronchoconstriction is not fully understood.
Purpose of the Study:
- To investigate the effects of TXA2 synthetase inhibitor SQ 80,338 and TXA2 receptor antagonist SQ 24,775 on various forms of bronchoconstriction in anesthetized guinea pigs.
Main Methods:
- Administered SQ 80,338 and SQ 24,775 intravenously to guinea pigs.
- Measured pulmonary resistance and dynamic compliance to assess bronchoconstriction.
- Evaluated responses to arachidonic acid, bradykinin, histamine, and antigen.
- Assessed TXA2 release from isolated guinea pig lungs and aortic contraction in response to a TXA2 analog.
Main Results:
- Both SQ 80,338 and SQ 24,775 dose-dependently inhibited arachidonic acid-induced bronchoconstriction.
- SQ 80,338 also inhibited bradykinin-induced bronchoconstriction.
- Neither compound affected histamine- or antigen-induced bronchoconstriction.
- SQ 80,338 inhibited TXA2 release, and SQ 24,775 antagonized TXA2 receptor activity.
Conclusions:
- Arachidonic acid and bradykinin-induced bronchoconstriction are mediated by TXA2 generation.
- Histamine- and antigen-induced bronchoconstriction do not appear to be mediated by TXA2.