Failure of bumetanide to improve outcome after intracerebral hemorrhage in rat.
Cassandra M Wilkinson; Brittany A Fedor; Jasmine R Aziz; Colby A Nadeau; Paul S Brar; Julia J A Clark; Frederick Colbourne · 2019 · PLoS ONE
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
After intracerebral hemorrhage (ICH), brain edema commonly occurs and can cause death. Along with edema, there are significant alterations in the concentrations of key ions such as sodium, potassium, and chloride, which are essential to brain function. NKCC1, a cation-chloride cotransporter, is upregulated after brain damage, such as traumatic injury and ischemic stroke. NKCC1 brings sodium and chloride into the cell, possibly worsening ion dyshomeostasis. Bumetanide, a specific NKCC1 antagonist, blocks the transport of chloride into cells, and thus should attenuate the increases in chloride,
Abstract by Cassandra M Wilkinson; Brittany A Fedor; Jasmine R Aziz; Colby A Nadeau; Paul S Brar; Julia J A Clark; Frederick Colbourne, PLoS ONE (2019) — licensed CC BY 4.0.
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Metadata source: DOAJ · DOI 10.1371/journal.pone.0210660