ArticleBMC cardiovascular disorders2025
Why does dexmedetomidine cause bradycardia?
Article in BMC cardiovascular disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Effect of Titrated Dexmedetomidine versus Esmolol on Postoperative Myocardial Injury in High-Risk Patients Undergoing Laparoscopic Colorectal Cancer Surgery: A Randomized Controlled Trial.Drug design, development and therapy · 2026Trial
- Paradoxical reflex bradycardia in paroxysmal sympathetic hyperactivity following traumatic brain injury: a case report.Frontiers in neuroscience · 2026Article
- Overdose Effects of Medetomidine and Fentanyl in Rats: Reflex, Vital and Analgesic Parameters as Predictive Markers.Veterinary medicine (Auckland, N.Z.) · 2026Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aims to investigate the potential mechanism by which dexmedetomidine (Dex) causes bradycardia.
methodsTwenty-four healthy rabbits were divided into 4 groups (n = 6 each): Dex 10 µg/kg group (group D1), Dex 20 µg/kg group (group D2), Dex 40 µg/kg group (group D3) and sham group (group C). Heart rate and frequency of vagal efferent discharge were recorded before and at 0, 0.5, 1, 2, and 10 min after intravenous injection. Then, the action potentials of the sinoatrial (SA) node pacemaker cells were measured after the SA node was exposed to Dex at concentrations of 0.06, 0.6, 6, and 12ng/ml.
resultsThe heart rate obviously decreased, and the vagal efferent discharge increased significantly at 0, 0.5, 1, and 2 min. In addition, these changes showed a dose-dependent effect. Dex exerted a negative chronotropic action on SA node pacemaker cells and could obviously reduce the amplitude of action potential (APA), velocity of diastolic depolarization in phase 4 (VDD), rate of pacemaker firing (RPF), as well as prolong action potential duration (APD) at 90% repolarization (APD
conclusionsDex may induce bradycardia through central and peripheral mechanisms.
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Registered trials
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