{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T07:42:08Z","timestamp":1777794128670,"version":"3.51.4"},"reference-count":34,"publisher":"SAGE Publications","issue":"7","license":[{"start":{"date-parts":[[2016,4,6]],"date-time":"2016-04-06T00:00:00Z","timestamp":1459900800000},"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":[[2016,7]]},"abstract":"<jats:p>\n                    Transient global cerebral ischemia is often followed by delayed disturbances of cerebral blood flow, contributing to neuronal injury. The pathophysiological processes underlying such disturbances are incompletely understood. Here, using an established model of transient global cerebral ischemia, we identify dramatically impaired neurovascular coupling following ischemia. This impairment results from the loss of functional inward rectifier potassium (K\n                    <jats:sub>IR<\/jats:sub>\n                    ) channels in the smooth muscle of parenchymal arterioles. Therapeutic strategies aimed at protecting or restoring cerebrovascular K\n                    <jats:sub>IR<\/jats:sub>\n                    channel function may therefore improve outcomes following ischemia.\n                  <\/jats:p>","DOI":"10.1177\/0271678x16638350","type":"journal-article","created":{"date-parts":[[2016,4,7]],"date-time":"2016-04-07T01:18:06Z","timestamp":1459991886000},"page":"1195-1201","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":27,"title":["Uncoupling of neurovascular communication after transient global cerebral ischemia is caused by impaired parenchymal smooth muscle K\n                    <sub>ir<\/sub>\n                    channel function"],"prefix":"10.1177","volume":"36","author":[{"given":"Gro Klitgaard","family":"Povlsen","sequence":"first","affiliation":[{"name":"Department of Pharmacology, College of Medicine, University of Vermont, Burlington, Vermont, USA"},{"name":"Department of Clinical Experimental Research, Glostrup Research Institute, Glostrup University Hospital, Glostrup, Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas A","family":"Longden","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, College of Medicine, University of Vermont, Burlington, Vermont, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Adrian D","family":"Bonev","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, College of Medicine, University of Vermont, Burlington, Vermont, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David C","family":"Hill-Eubanks","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark T","family":"Nelson","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, College of Medicine, University of Vermont, Burlington, Vermont, 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