ArticleNaunyn-Schmiedeberg's archives of pharmacology2020
Chloroform is a potent activator of cardiac and neuronal Kir3 channels.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2020. 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.
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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.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Evaluation of public awareness and performance toward the safe use of household disinfectants-cleaners to prevent COVID-19 in the Emirate of Abu Dhabi.Frontiers in public health · 2023Article
- Hyperpolarization Induced by Lipopolysaccharides but Not by Chloroform Is Inhibited by Doxapram, an Inhibitor of Two-P-Domain KInternational journal of molecular sciences · 2022Article
- Advances in Targeting GIRK Channels in Disease.Trends in pharmacological sciences · 2021Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chloroform has been used over decades in anesthesia before it was replaced by other volatile anesthetics like halothane or sevoflurane. Some of the reasons were inadmissible side effects of chloroform like bradycardia or neural illness. In the present study, we identified members of the G protein-activated inwardly rectifying potassium channel family (Kir3) expressed in Xenopus oocytes as potential common molecular targets for both the neural and cardiac effects of chloroform. Millimolar concentration currents representing a 1:10000 dilution of commercially available chloroform were used in laboratories that augment neuronal Kir3.1/3.2 currents as well as cardiac Kir3.1/3.4. This effect was selective and only observed in currents from Kir3 subunits but not in currents from Kir2 subunits. Augmentation of atrial Kir3.1/3.4 currents leads to an effective drop of the heart rate and a reduction in contraction force in isolated mouse atria.
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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.