ABSTRACT
Effects of histamine and serotonin on strophanthine cardiotoxicity were examined in experiments on 312 cats. It was shown that inflammation mediators exert sympathomimetic action on the myocardium and potentiate strophanthine cardiotoxicity. These effects can be prevented by premedication with the beta-blocker alprenolol, antihistaminic, steroid and non-steroidal anti-inflammatory agents. It was disclosed that premedication with diphenhydramine, analgin and hydrocortisone might correct strophanthine tolerance decreased as a result of coronary artery occlusion. The conclusion is made that inflammation mediators play a role in the genesis of strophanthine hypersensitivity in experimental myocardial infarction.
Subject(s)
Drug Hypersensitivity/etiology , Heart/drug effects , Histamine/pharmacology , Serotonin/pharmacology , Strophanthins/adverse effects , Animals , Anti-Inflammatory Agents/pharmacology , Arrhythmias, Cardiac/chemically induced , Cats , Drug Interactions , Female , Male , Myocardial Infarction/metabolism , Myocardium/metabolismABSTRACT
The effect of various pathogenic factors and drugs on sensitivity to strophanthin and the possibility of pharmacoprophylaxis of toxicosis caused by this cardiotonic agent were studied in acute and chronic experiments on 375 cats. It is shown that impaired blood supply to the myocardium, toxic affection of the liver, sensitization with the cardiac antigen, and the effect of inflammation mediators, mineralocorticoids, and some antianginous agents reduce strophanthin tolerance. The altered sensitivity to strophanthin is successfully corrected with the beta-adrenoblocker alpheprol, hydrocortisone, analgin, dimedrol, and the anesthetic trimecaine.