Complex adrenergic and inflammatory mechanisms contribute to phase 2 ventricular arrhythmias in anaesthetized rats


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Abstract

Mandarin translation of abstractBackground and purpose:The mechanisms responsible for phase 2 (infarct-related) ventricular arrhythmias remain unclear. We have investigated the role of α1 and β1 adrenoceptor activation and the interaction of this with infarct neutrophil accumulation, in anaesthetized rats.Experimental approach:Neutrophil-replete Sprague-Dawley rats (n = 8–9 per group) were anaesthetized and randomized to receive vehicle, prazosin (0.5 mg·kg−1 i.v.), atenolol (4 mg·kg−1 i.v.) or their combination prior to left main coronary artery occlusion. A further group was depleted of neutrophils and received both atenolol and prazosin. Coronary ligation in all groups was maintained for 240 min.Key results:Atenolol and prazosin treatment lowered heart rates and blood pressures respectively, but neither agent given alone affected the incidence of phase 2 ventricular tachycardia or fibrillation. However, co-administration of atenolol with prazosin reduced phase 2 ventricular premature beats (log10-transformed totals were 1.25 ± 0.26 vs. 2.43 ± 0.18 in controls; P < 0.05). Neutrophil depletion attenuated this antiarrhythmic effect (log10-transformed total ventricular premature beats were 1.66 ± 0.35; P > 0.05 vs. controls).Conclusions and implications:Phase 2 arrhythmias appear to depend in part on a complex interaction between catecholamines and neutrophils. A model of this interaction is proposed.

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