CORONARY ANAPHYLAXIS INVITRO

The reactivity of isolated coronary arteries and cardiac veins of the calf to selected chemical mediators of anaphylaxis and to sensitizing antigen (horse plasma) was studied. Both the coronary arteries and cardiac veins contracted to bradykinin, 5‐hydroxytryptamine (5‐HT), prostaglandin E2 (PGE2), PGF2α, histamine and carbachol. Isoprenaline and PGE1 relaxed vessels which had been partially contracted by PGF2α, PGE2, histamine, 5‐HT, bradykinin, carbachol or antigen. Horse plasma (antigen) contracted coronary vessels obtained from sensitized calves, but not from control calves. Subsequent antigen ‘challenge’ produced ‘desensitization’ (tachyphylaxis). After 1 or 2 h of rest, the anaphylactic response partially recovered although there was no change in tissue reactivity to the exogenous agonists. Specific doses of atropine, mepyramine (H1‐blocker) and methysergide (5‐HT antagonist) did not modify the anaphylactic reaction in coronary arteries, suggesting a negligible role for these biogenic amines. Compound PRD‐92‐EA (a new anti‐allergic agent) exhibited non‐specific receptor blocking activity towards histamine, 5‐HT and carbachol and inhibited the coronary anaphylactic reaction. 1979 British Pharmacological Society