ArticleResuscitation plus2021
Effect of the KCa3.1 blocker, senicapoc, on cerebral edema and cardiovascular function after cardiac arrest - A randomized experimental rat study.
Article in Resuscitation plus, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 2 citations in OpenAlex.
- Decoding post-myocardial infarction coronary microvascular dysfunction: The SP1-driven STAT3/KCa3.1/eNOS protective mechanism.CytoJournal · 2025Article
- Resuscitation plus - Initial successes and future direction.Resuscitation plus · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimFormation of cerebral edema and cardiovascular dysfunction may worsen brain injury following cardiac arrest. We hypothesized that administration of the intermediate calcium-activated potassium (KCa3.1) channel blocker, senicapoc, would reduce cerebral edema and augment mean arterial pressure in the early post-resuscitation period.
methodMale Sprague-Dawley rats, aged 11-15 weeks, were utilized in the study. Rats were exposed to 8 min of asphyxial cardiac arrest. Shortly after resuscitation, rats were randomized to receive either vehicle or senicapoc (10 mg/kg) intravenously. The primary outcome was cerebral wet to dry weight ratio 4 h after resuscitation. Secondary outcomes included mean arterial pressure, cardiac output, norepinephrine dose, inflammatory cytokines and neuron specific enolase levels. Additionally, a sub-study was conducted to validate intravenous administration of senicapoc.
resultsThe sub-study revealed that senicapoc-treated rats maintained a significantly higher mean arterial pressure during administration of SKA-31 (a KCa3.1 channel opener).The plasma concentration of senicapoc was 1060 ± 303 ng/ml 4 h after administration. Senicapoc did not reduce cerebral edema or augment mean arterial pressure 4 h after resuscitation. Likewise, cardiac function and norepinephrine dose did not vary between groups. Inflammatory cytokines and neuron specific enolase levels increased in both groups after resuscitation with no difference between groups. Senicapoc enhanced the PaO
conclusionSenicapoc was successfully administered intravenously after resuscitation, but did not reduce cerebral edema or increase mean arterial pressure in the early post-resuscitation period.
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Registered trials
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