Acute systemic anaphylaxis in the calf

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Bronchial arteries from sensitized calves contracted on antigenic challenge in the absence and presence of selected anti-allergic drugs and autonomic agents in vitro. Anaphylactic reactivity was inhibited by tripelennamine, isoprenaline and aminophylline, and potentiated by indomethacin and dopamine. Disodium cromoglycate, compound FPL 55712 and ketanserin failed to inhibit anaphylactic contraction.

mentioning

confidence: 99%

“…Methods Male Jersey calves (1-3 months old) were sensitized to horse serum as previously described (Eyre, Lewis & Wells, 1973). Calves were anaesthetized and killed with sodium pentobarbitone (100 mgkg-1).…”

mentioning

confidence: 99%

Anaphylactic contraction (Schultz‐Dale reaction) of the bovine bronchial artery in vitro

Alexander

Eyre

Gordon

1983

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“…Activated kallikrein has been implicated in peripheral vascular changes in both P. knowlesi and B. bovis infections . Eyre & Lewis (1972) and Eyre, Lewis & Wells (1973) suggested that kinins contribute significantly to the profound hypotension observed during bovine anaphylactic shock. It is likely that the increased liberation of kinins plays a significant part in the hypotension during B. bovis infections.…”

Section: Discussionmentioning

confidence: 99%

KININ, KININOGEN AND KININASE LEVELS DURING ACUTE Babesia bovis (=B. argentina) INFECTION OF CATTLE

Wright

1977

1Kinin levels began rising on day 3 after infection of cattle with Babesia bovis (=B. argentina) and attained a maximum value of 98% above preinfection levels by day 7. 2 Kininogen levels began falling on day 3 and reached minimum levels of 83% below preinfection levels on day 8. 3 Changes in both kinin and kininogen levels on day 3 coincided with the detection of low levels of parasites, and with a fall in packed cell volume. 4 Plasma kininase levels rose significantly 6 to 9 days after infection. Preparations of lysed and sonicated uninfected and infected red cells contained kininase activity, the respective red cell preparations being 23.9 and 11.4 times more active per mg protein than uninfected red cell preparations. The effect of pH, and the inhibitors disodium edetate, 1,10 phenanthroline and aprotinin on normal and infected plasma and on the various red cell preparations suggested that the rise in plasma kininase levels during infection was probably at least partly due to parasite products. SThese results are discussed in relation to previous data showing that both kallikrein activation and the onset of hypotension also occur on or about day 3.

“…After a further three to four weeks the ponies were anaesthetized with 25 mg/kg pentobarbitone sodium, given intravenously, and anaesthesia was maintained with supplementary pentobarbitone. With the animals in right lateral recumbency, blood pressures were recorded and measured in the left common carotid artery, the pulmonary artery and abdominal vena cava, as previously described in calves Eyre, Lewis & Wells, 1973). Respiratory ventilation volume was also monitored as before.…”

Section: Methodsmentioning

confidence: 99%

Acute systemic anaphylaxis in the horse

Eyre

Lewis

1973

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Summary Histamine in small doses caused systemic depressor responses in horses, whereas greater doses caused biphasic effects. All doses of 5‐hydroxytryptamine (5‐HT) were pressor and all doses of bradykinin depressor. All three active substances raised pulmonary artery pressure and lowered central venous pressure. 5‐HT reduced ventilation volume. Histamine caused brief apnoea followed by hyperpnoea only. Acute anaphylaxis in the horse was accompanied by a severe systemic arterial depressor response, a pressor response in the pulmonary artery and vena cava, and alternating phases of apnoea and dyspnoea. During anaphylaxis, profound haemoconcentration, leucopoenia, thrombo‐cytopoenia and hyperkalaemia were in evidence. Early during anaphylactic shock (2 to 4 min) there were profound increases in plasma histamine (five to six‐fold) and plasma kinin activity (four to five‐fold). Plasma 5‐HT concentrations were reduced initially but recovered. Later in anaphylaxis (10 to 20 min) whole blood histamine concentration fell significantly. This coincided with the most profound period of leucopoenia. No significant differences were observed in histamine concentration in any of five tissues between six ponies subjected to anaphylaxis and six controls. Mast cell numbers were not reduced but mast cells were more metachromatic (pink) and there was spilling of mast cell granules. Gross pathological changes were noted mainly in the lungs which were extensively oedematous and congested. Inflamed, congested and oedematous areas in the large colon and caecum were seen, and the kidneys, spleen and liver were engorged. Alveolar emphysema, peribroncheolar oedema (containing mononuclear cells and neutrophils) were recorded. Alveoli contained erythrocytes.