Role in kinin in rat epinephrine pulmonary edema (REPE)

High doses (10-40 micrograms/Kg, i.v.), of epinephrine evoke conspicuous consumption of circulatory rat kininogen (Kg), an effect not observed in animals pre-treated with either soybean trypsin inhibitor (SBTI, 10 mg/Kg, i.v.), Trasylol (1000 KIU/Kg, i.v.) or Aspirin (10 mg/Kg). Kg consumption by epinephrine is accompanied by a raise in rat plasma TAME-esterase attributed to the activation of plasma kallikrein by pro-kininogenase generated in circulatory basophils or mast cells exposed to epinephrine. The severe pulmonary edema observed in rats given epinephrine, is very markedly reduced in animals pre-treated with either SBTI, Trasylol or Aspirin at doses which inhibit Kg consumption by the catecholamine. Indomethacin (1-10 mg/kg) did not reduce REPE nor inhibit Kg loss. These results indicate that while kinin released via the action of epinephrine-activated basophils and/or mast cells, could play a major role in REPE, the same cannot be suggested for prostaglandins, whose eventual formation in the epinephrine-treated lung, would be expected to be fully prevented by Indomethacin. Since Aspirin, known as a less effective inhibitor of PG formation than Indomethacin, was nevertheless a highly effective inhibitor of both REPE and Kg consumption, an explanation for the action of Aspirin not involving the lung PG system, is clearly called for.