ArticleBMC neuroscience2019
Amiodarone exacerbates brain injuries after hypoxic-ischemic insult in mice.
Article in BMC neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Amiodarone Administration during Cardiopulmonary Resuscitation Is Not Associated with Changes in Short-Term Mortality or Neurological Outcomes in Cardiac Arrest Patients with Shockable Rhythms.Journal of clinical medicine · 2024Article
- Identifying Subgroups with Differential Responses to Amiodarone among Cardiac Arrest Patients with a Shockable Rhythm at Hospital Arrival using the Machine Learning Approach.Reviews in cardiovascular medicine · 2024Article
- Understanding the Pathophysiology of Ischemic Stroke: The Basis of Current Therapies and Opportunity for New Ones.Biomolecules · 2024Review
- Influence of pneumoperitoneum and head-down maneuver on the cerebral microvasculature in rabbits.BMC anesthesiology · 2022Article
- A mechanistic model of calcium homeostasis leading to occurrence and propagation of secondary brain injury.Journal of neurophysiology · 2022Article
- Amiodarone Enhances Anticonvulsive Effect of Oxcarbazepine and Pregabalin in the Mouse Maximal Electroshock Model.International journal of molecular sciences · 2021Article
- Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSodium ion transportation plays a crucial role in the pathogenesis of hypoxic-ischemic brain injury. Amiodarone, a Vaughan-Williams class III antiarrhythmic drug, has been widely used to treat life-threatening arrhythmia and cardiac arrest worldwide. In addition to its inhibitory effects on the potassium channel, amiodarone also blocks various sodium ion transporters, including the voltage-gated sodium channel, sodium pump, and Na
resultsCompared with the control group mice, mice that received amiodarone after induction of 40-min hypoxic-ischemic brain injury exhibited lower survival rates over 7 days and worse neurological function. After 25-min hypoxic-ischemic brain injury, amiodarone treated mice exhibited larger infarct volumes (16.0 ± 6.9 vs. 24.2 ± 6.8 mm
conclusionsAmiodarone exacerbated brain injuries and neurological outcomes after hypoxic-ischemic insults. Severe brain sodium accumulation and brain edema were associated with the detrimental effects of amiodarone. Amiodarone at the clinical dose can exacerbate brain injury after hypoxic-ischemic insult by affecting sodium ion transportation and facilitate intracellular sodium accumulation in the brain.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.