Abstract
To study the role of thromboxane (Tx) A 2 in Forssman systemic shock (FSS) in guinea pig, the effect of (E)-3-[p(1H-Imidazol-1-ylmethyl) phenyl]-2-propenoic acid hydrochloride (OKY-046), a specific Tx A 2 synthetase inhibitor, was studied. OKY-046 administered intravenously clearly prolonged survival time and protected against fatal shock. In shocked animals, definite decreases in serum complement hemolytic activity (CH50), leucocyte counts and platelet counts and an increase in lactate dehydrogenase (LDH) activity were observed. In addition, a significant increase of Tx B 2 and incoagulability of blood were observed after shock. Whereas OKY-046 had no effect on the decreases in CH 50, platelet counts and leucocyte counts, it inhibited the increase of Tx B 2 and increased the amount of 6-keto PG F 1α. When Forssman antibody (half a lethal dose) was injected, a diphasic increase in airway resistance was observed. OKY-046 inhibited this diphasic increase in airway resistance. These data suggest a pathophysiological role for Tx A 2 in FSS. OKY-046 inhibited the Forssman antibody induced respiratory disorders probably due to the inhibition of Tx A 2 synthesis after shock.
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