Enhancement by prostacyclin of the contractility of the guinea-pig airways smooth muscle.

Aerosolized prostacyclin (PGI2) potentiated the increase in pulmonary resistance to inflation induced by serotonin, prostaglandin F2 alpha (PGF2 alpha), acetylcholine and histamine in the guinea-pig. This was not due to a reflex, nor to further production of PG cyclooxygenase derivatives. PGI2 and PGF2 alpha induced contraction of the parenchyma lung strip of the guinea-pig, which could be inhibited by polyphloretin phosphate and by PGE1. Since PGF2 alpha failed to potentiate the bronchial responses to acetylcholine, histamine or serotonin, under conditions where PGI2 was effective, the in vitro similarities between the two PGs cannot explain the in vivo results. The ability of PGI2 to potentiate bronchial responses was not shared by the other PGs. Since the latter are either bronchoconstrictor agents by themselves (PGF2 alpha and PGD2), or bronchodilators (PGE1, PGE2), our hypothesis is that PGI2 potentiates the responses of the bronchi to various agonists by a mechanism similar to that which accounts for the potentiation of acute inflammation and pain by PGE1 and PGE2, the latter being ineffective in enhancing the bronchial responses because of the associated bronchodilator activity.