Abstract:
:BACKGROUND: Nicotine, the active agent in tobacco, is released into the circulation during cigarette smoking. It elevates plasma catecholamines, heart rate, and arterial blood pressure; produces coronary spasm; and increases myocardial work and oxygen demand with concomitant reduction in oxygen supply. This may generate cardiac arrhythmias that might contribute to an increased incidence of sudden death due to smoking. It is hypothesized that acute administration of nicotine will induce cardiac arrhythmias, and this experimental study was planned with an aim to assess arrhythmogenic activity as a result of acute administration of nicotine. METHODS: Nicotine was administered in different doses intravenously in 16 anesthesized dogs, and 52 experiments were carried out at weekly intervals. In each experiment, continuing anesthesia and after nicotine administration. They were scrutinized by two experienced electrocardiographers at intervals of 1, 2, 3, 4, 5, 10, 15, and 30 minutes. RESULTS: Data revealed nonsignificant arrhythmias with doses of 2.5, 5.0, and 10.0 mg/kg of intravenous nicotine. The dose of 50 µg/kg induced supraventricular arrhythmias, atrioventricular junctional arrhythmias, and ventricular arrhythmias. Supraventricular bradycardia in 30 (83%; P <.0001), supraventricular arrhythmia in 30 (83%; P <.0001), sinus arrest in 18 (50%; P <.003), atrial ectopics in 24 (67%; P <.0004), and atrial tachycardia in 98 experiments (25%; P <.021). These results were statistically significant. In 18 experiments, sinus arrest was observed to be missing P waves and QRS complexes for a period corresponding to 4:1-10:1 SA block, lasting 2-6 seconds, within 3 seconds of injection. Occurrence of wandering pacemaker was observed in 6 experiments, atrial flutter in 2, and atrial fibrillation in 2, but these incidents were not significant. Atrioventricular junctional arrhythmias consisted of escape beats in 9 subjects (25%; P <.02), premature contractions in 12 (33%; P <.005), first-degree heart block in 9 (25%; P <.02), second degree heart block in 9 (25%; P <.02) and atrioventricular dissociation in 9 (25%; P <.02). All arrhythmias in this category were significant. Ventricular arrhythmias consisted of ventricular premature contractions that were unifocal in 32 subjects (89%; P <.0001), multifocal in 30 (83%; P <.0001), bigeminy in 28 salvos in 18 (50%; P <.003). Sustained ventricular tachycardia (> 30 beats) in 12 experiments (33%; P <.005) proved significant. The dose of 100 µg/kg induced fatal ventricular flutter and ventricular fibrillation. The dog expired and experiments with that dose were not repeated. CONCLUSION: Data reveal dose-dependent arrhythmogenecity of nicotine in dogs. Smaller doses of nicotine did not produce significant arrhythmias. Higher doses, bioequivalent to smoking two standard cigarettes, may generate cardiac arrhythmias of simple to severe nature. Further work in human beings may confirm whether nicotine in cigarette smoke will generate similar cardiac arrhythmias especially in patients with autonomic imbalance and/or compromised and ischemic myocardium.
journal_name
J Cardiovasc Pharmacol Therjournal_title
Journal of cardiovascular pharmacology and therapeuticsauthors
Mehta MC,Jain AC,Mehta A,Billie Mdoi
10.1177/107424849700200407keywords:
subject
Has Abstractpub_date
1997-10-01 00:00:00pages
291-298issue
4eissn
1074-2484issn
1940-4034pii
S1074248497000278journal_volume
2pub_type
杂志文章abstract:INTRODUCTION:Recent evidence suggests that transcriptional reprogramming is involved in the pathogenesis of cardiac remodeling (cardiomyocyte hypertrophy and fibrosis) and the development of heart failure. 5-Azacytidine (5aza), an inhibitor of DNA methylation approved for hematological malignancies, has previously demo...
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abstract::Dofetilide is a class III antiarrhythmic agent approved by the Food and Drug Administration for the conversion of atrial fibrillation and atrial flutter and maintenance of sinus rhythm in symptomatic patients with persistent arrhythmia. Drug trials showed neutral mortality in post-myocardial infarction patients and th...
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journal_title:Journal of cardiovascular pharmacology and therapeutics
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journal_title:Journal of cardiovascular pharmacology and therapeutics
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journal_title:Journal of cardiovascular pharmacology and therapeutics
pub_type: 杂志文章,随机对照试验
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更新日期:2013-09-01 00:00:00
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journal_title:Journal of cardiovascular pharmacology and therapeutics
pub_type: 杂志文章
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更新日期:1996-07-01 00:00:00
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abstract::BACKGROUND: Digoxin improves baroreflex function and reduces neurohumoral activation in severe heart failure, but it is uncertain how digoxin affects ventricular remodeling and progression to left ventricular dysfunction. In addition, the effect of digoxin in in vitro beta-adrenoceptor density and function, and contra...
journal_title:Journal of cardiovascular pharmacology and therapeutics
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更新日期:1998-10-01 00:00:00
abstract::Pulmonary arterial hypertension (PAH) is a progressive disease, which can be potentially fatal. The management of a complex disease like PAH requires a multidisciplinary approach from a team consisting of physicians, nurses, social workers, and pharmacists. Adherence to PAH-specific therapy is one of the key factors i...
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更新日期:2020-03-01 00:00:00