Circulation Research, Vol 36, 520-528, Copyright © 1975 by American Heart Association
ARTICLES |
N Capurro and R Levi
The purpose of this investigation was to define and quantitatively evaluate cardiac anaphylaxis in vivo. Guinea pigs, passively sensitized with graded amounts of rabbit antipenicilloyl antibody, were anesthetized, ventilated, and challenged intravenously with a constant amount of antigen (anaphylaxis in vivo). In other experiments, guinea pig hearts were excised, perfused in a Langendorff apparatus, and challenged (analphylaxis in vitro). During in vivo anaphylaxis, sinus rate increased 10-30 beats/min, conduction arrhythmias occurred in 15 of 22 experiments, and ventricular fibrillation was seen in 8 of 22 experiments. Tachycardia and arrhythmias began approximately 20 seconds after antigen administration and were accompanied, but not preceded, by respiratory and pressor changes. During in vitro anaphylaxis, sinus rate increased 70-110 beats/min, coronary flow rate decreased 2-22%, conduction arrhythmias occurred in 21 of 31 experiments, and ventricular ectopic activity was seen in 13 of 31 experiments. Tachycardia and arrhythmias began approximately 15 seconds after antigen administration. Sinus tachycardia, atrioventricular conduction block, increased ventricular automaticity, and histamine release were characteristic features of cardiac anaphylaxis in vivo and in vitro. Both in vivo and in vitro, the intensity of the cardiac reaction depended on the amount of antibody used in passive sensitization. Our results clearly indicate that the heart reacts as a target organ in systemic anaphylaxis of the guinea pig.
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