ArticleBritish journal of pharmacology2009
Complex adrenergic and inflammatory mechanisms contribute to phase 2 ventricular arrhythmias in anaesthetized rats.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Role of Oxidative Stress in the Genesis of Ventricular Arrhythmias.International journal of molecular sciences · 2020Review
- A first case report of dapsone inducing recurrent ventricular arrhythmia.European heart journal. Case reports · 2019Article
- Facilitation of ischaemia-induced ventricular fibrillation by catecholamines is mediated by βBritish journal of pharmacology · 2018Article
- Incidence and risk factors of ventricular fibrillation before primary angioplasty in patients with first ST-elevation myocardial infarction: a nationwide study in Denmark.Journal of the American Heart Association · 2015Article
- Feasibility of targeting ischaemia-related ventricular arrhythmias by mimicry of endogenous protection by endocannabinoids.British journal of pharmacology · 2013Article
- Effect of different doses of oxytocin on cardiac electrophysiology and arrhythmias induced by ischemia.Journal of advanced pharmaceutical technology & researchArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeThe mechanisms responsible for phase 2 (infarct-related) ventricular arrhythmias remain unclear. We have investigated the role of alpha(1) and beta(1) 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
resultsAtenolol 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 (log(10)-transformed totals were 1.25 +/- 0.26 vs. 2.43 +/- 0.18 in controls; P < 0.05). Neutrophil depletion attenuated this antiarrhythmic effect (log(10)-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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