{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T07:43:10Z","timestamp":1777794190094,"version":"3.51.4"},"reference-count":51,"publisher":"SAGE Publications","issue":"6","license":[{"start":{"date-parts":[[2020,10,7]],"date-time":"2020-10-07T00:00:00Z","timestamp":1602028800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2021,6]]},"abstract":"<jats:p>\n                    Glibenclamide inhibits sulfonylurea receptor (SUR), which regulates several ion channels including SUR1-transient receptor potential melastatin 4 (SUR1-TRPM4) channel and ATP-sensitive potassium (K\n                    <jats:sub>ATP<\/jats:sub>\n                    ) channel. Stroke upregulates SURl-TRPM4 channel, which causes a rapid edema formation and brain swelling. Glibenclamide may antagonize the formation of cerebral edema during stroke. Preclinical studies showed that glibenclamide inhibits K\n                    <jats:sub>ATP<\/jats:sub>\n                    channel-induced vasodilation without altering the basal vascular tone. The in vivo human cerebrovascular effects of glibenclamide have not previously been investigated.\n                  <\/jats:p>\n                  <jats:p>\n                    In a randomized, double-blind, placebo-controlled, three-way cross-over study, we used advanced 3 T MRI methods to investigate the effects of glibenclamide and K\n                    <jats:sub>ATP<\/jats:sub>\n                    channel opener levcromakalim on mean global cerebral blood flow (CBF) and intra- and extracranial artery circumferences in 15 healthy volunteers. Glibenclamide administration did not alter the mean global CBF and the basal vascular tone. Following levcromakalim infusion, we observed a 14% increase of the mean global CBF and an 8% increase of middle cerebral artery (MCA) circumference, and glibenclamide did not attenuate levcromakalim-induced vascular changes. Collectively, the findings demonstrate the vital role of K\n                    <jats:sub>ATP<\/jats:sub>\n                    channels in cerebrovascular hemodynamic and indicate that glibenclamide does not inhibit the protective effects of K\n                    <jats:sub>ATP<\/jats:sub>\n                    channel activation during hypoxia and ischemia-induced brain injury.\n                  <\/jats:p>","DOI":"10.1177\/0271678x20959294","type":"journal-article","created":{"date-parts":[[2020,10,8]],"date-time":"2020-10-08T02:07:51Z","timestamp":1602122871000},"page":"1328-1337","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":18,"title":["Cerebrovascular effects of glibenclamide investigated using high-resolution magnetic resonance imaging in healthy volunteers"],"prefix":"10.1177","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1118-9665","authenticated-orcid":false,"given":"Mohammad 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