Actions of prostaglandins (PG) E1, E2, and F2α on the cardiovascular–respiratory systems of anesthetized calves were studied in conjunction with the effects of a series of prostaglandin antagonists on acute systemic anaphylaxis. Meclofenamate, acetylsalicylic acid (ASA), phenylbutazone, and indomethacin, all inhibitors of PG synthesis, were particularly effective in protecting calves from anaphylactic cardiovascular shock. Meclofenamate showed "broad spectrum" antagonism of the mediators of anaphylaxis. Indomthacin and ASA eliminated the biphasic fall in systemic arterial pressure, suggesting that prostaglandins may be involved, together with biogenic amines, in the early stages of anaphylaxis. SC-19220, polyphloretin phosphate, and diethylcarbamazine citrate (DECC) had little or no inhibitory effects against exogenous prostaglandins and afforded only weak protection against systemic anaphylaxis. "Broad spectrum" inhibition of amine and PG receptors, as well as inhibition of slow-reacting substance of anaphylaxis formation and release, may account for part of the protective effects of DECC. A blood-bathed superfusion system suggested participation by PG F2α in bovine anaphylaxis. Cardiovascular–respiratory changes induced by exogenous prostaglandins in calves suggest that PG F2α may be responsible for the transient rise in systemic arterial pressure and increase in pulmonary arterial pressure in anaphylaxis, whereas PG E1 and E2 may be participating in the primary fall in systemic arterial pressure.
Reduction of fertility of mice by the intrauterine injection of prostaglandin antagonists
