RELEASE OF INFLAMMATORY MEDIATORS FROM GUINEA-PIG TRACHEA BY ELECTRICAL-FIELD STIMULATION - LACK OF NEURONAL INVOLVEMENT

Electrical field stimulation (EFS; 5-10 V, 1 ms, 20 Hz for 1 min) of i solated guinea pig trachea resulted in a rapid increase in tone that i s blocked by either atropine or tetrodotoxin (TTX). EFS of tracheal sp irals also caused large increases in the release of certain prostanoid s with release of prostaglandin (PG)D-2, PGE(2) and PGF(2 alpha) (16.5 -, 3.0- and 4.1-fold, respectively). In contrast to the smooth muscle response, however, EFS-induced release of prostanoids was not signific antly altered in the presence of TTX. Removal of the epithelium reduce d the amount of prostanoids released by EFS. Thus, EFS-induced product ion of PGD(2), PGE(2) and PGF(2 alpha) was significantly reduced by ab out 30%, 70% and 80% in epithelium-denuded tissues, respectively. Dire ct vagal stimulation caused a rapid contraction of the trachealis but failed to elicit increases in the release of histamine or arachidonic acid metabolites. Furthermore, the selective stimulant of C-type senso ry fibers capsaicin (3 mu M) or exogenously applied substance P (1 mu M) or neurokinin A (1 mu M) failed to induce histamine, leukotriene or prostanoid release from guinea pig tracheal rings. Although, the mech anism involved in stimulation of arachidonic acid metabolism by EFS is unclear, this effect in part involves the epithelium but apparently i s not mediated by airway elements sensitive to TTX, direct vagal stimu lation or tachykinins.