Reaginic (type 1 anaphylactic) antibodies produced by calves in response to Hypoderma larvae.

Reaginic antibody production by Hypoderma lineatum and H bovis larval antigens were evaluated in three calves using passive cutaneous anaphylaxis (PCA). Two calves were sensitised with soluble extract of H lineatum larvae and a third was injected with 43 hatching H bovis larvae. Blood serum taken from the calves was injected intradermally in 0.1 ml volumes into three test calves. Sera from the calves sensitised with hypoderma extract produced positive PCA reactions in all three calves with maximum titres of 1:8. Sera from the calf injected with living larvae caused positive PCA reactions in two of the three test calves, the maximum titre being 1:4. The results indicate that the calves produced reaginic antibody to H bovis and H lineatum, although serum concentrations of the antibody were relatively low.

Reversed response to histamine following local anaphylaxis in blood-perfused calf trachea in situ.

Tracheas of calves were perfused via the tracheal artery in situ. An endotracheal tube recorded tracheal muscle contractions. Carbachol, histamine or antigen caused tracheal vascular depressor responses. Carbachol caused contraction; histamine, 2-methylhistamine and antigen relaxed the tracheal muscle. Following antigen challenge, vascular responses remained unchanged; however endotracheal relaxations to histamine were reversed (i.e. contractions). Allergenic 'challenge' impairs H2-receptors (airway relaxation), thus diminishing a compensatory mechanism which may relate to hyperresponsiveness characteristic of asthma.

Cholinergic modulation of anaphylactic dopamine release from calf lung.

Dopamine was released by specific antigen from sensitized calf lung in vitro. Dopamine release was potentiated by carbachol and inhibited by atropine. Nicotine enhanced dopamine release and this action was enhanced by tubocurarine. It is suggested that anaphylactic dopamine release is modulated by a vagal (muscarinic) mechanism in calf lung.

Anaphylactic hypersensitivity in sheep lung in vitro: (vascular Schultz-Dale response and bioamine liberation).

Two aspects of anaphylactic hypersensitivity in sheep lung were studied. Isolated pulmonary vein constricted in response to histamine, acetylcholine, dopamine and bradykinin, whereas serotonin or specific antigen in sensitized tissue caused relaxation of the vessel. Tryptaminergic antagonists did not inhibit vessel relaxation caused by either serotonin or antigen. Antigenic challenge of chopped sheep lung caused significant liberation of serotonin and dopamine but not of histamine. It is suggested that anaphylactic release of serotonin may counteract the inflammatory response in sheep lung; which may explain the relative resistance of sheep to pulmonary hypersensitivity and tryptamine toxicity compared with other species.

Chemical mediators of anaphylaxis (histamine, 5-HT, and SRS-A) released from horse lung and leukocytes in vitro.

Horses were sensitized to bovine plasma in Freund's complete adjuvant. Leukocytes, separated from venous blood, yielded histamine upon incubation with bovine plasma. Ioslated lung fragments incubated with bovine plasma liberated histamine and 5-HT, but not SRS-A. Pulmonary veins obtained from the same animals contracted to histamine, 5-HT and to antigen (Schultz-Dale reaction). Histamine and 5-HT probably contribute to immediate-type hypersensitivity in horses whereas the role of SRS-A is not proved.

Protection by acetylsalicylic acid and other agents in experimental acute interstitial pneumonia of calves.

In experimental acute interstitial pneumonia caused by Ascaris suum, therapy with aspirin (acetylsalicylic acid) provided symptomatic control of the condition, reducing or abolishing the characteristic "setback". Treatment with antihistamines or antiserotonin agents caused no observable clinical improvements.