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Failure of allopurinol and a spin trapping agent N‐t‐butyl‐α‐phenyl nitrone to modify significantly ischaemia and reperfusion‐induced arrhythmias
Author(s) -
Parratt James R.,
Wainwright Cherry L.
Publication year - 1987
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1987.tb08982.x
Subject(s) - allopurinol , free radical scavenger , ischemia , xanthine oxidase , medicine , nitrone , radical , ventricular fibrillation , cardiology , anesthesia , pharmacology , chemistry , oxidative stress , enzyme , biochemistry , cycloaddition , catalysis
1 The possible role of free radicals in the genesis of occlusion and reperfusion‐induced arrhythmias was studied by determining the effects of the xanthine oxidase inhibitor allopurinol (400 mg p.o. 24 h before experimentation + 25 mg kg −1 i.v.) and the free radical scavenger N‐t‐butyl‐α‐phenyl nitrone (PBN; 50 mg kg −1 i.v.) on these arrhythmias in chloralose anaesthetized greyhounds. 2 Neither of the drugs had any major effects on haemodynamic variables, although allopurinol caused a significant increase in heart rate. 3 The mean number of extrasystoles observed during ischaemia in dogs given allopurinol or PBN was not significantly different from those seen in controls. Further, the incidence of ventricular fibrillation during either occlusion or reperfusion was unchanged by either drug and there was thus no improvement in survival. 4 These results suggest that, in this model of myocardial ischaemia and reperfusion, free radicals may not play a major role in the genesis of life‐threatening arrhythmias.