{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T01:08:05Z","timestamp":1789780085720,"version":"4.0.1"},"reference-count":38,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[1997,11]]},"abstract":"<jats:p><jats:italic>Background and Purpose<\/jats:italic>Traumatic injury is the leading cause of death for infants and children, and mortality is increased with head injury. Previous studies have shown that pial arteries constricted and that responses to several nitric oxide (NO)\u2013dependent dilator stimuli were blunted after fluid percussion injury (FPI) in newborn pigs. Membrane potential of vascular muscle is a major determinant of vascular tone, and activity of K<jats:sup>+<\/jats:sup>channels is a major regulator of membrane potential. Recent data show that the NO releasers sodium nitroprusside (SNP) and S-nitroso-<jats:italic>N<\/jats:italic>-acetylpenicillamine (SNAP) and 8-bromo-cGMP elicit dilation via ATP-sensitive K<jats:sup>+<\/jats:sup>channel (K<jats:sub>ATP<\/jats:sub>) activation. The present study was designed to investigate the effect of FPI on K<jats:sub>ATP<\/jats:sub>channel function.<\/jats:p><jats:p><jats:italic>Methods<\/jats:italic>Chloralose-anesthetized newborn pigs equipped with a closed cranial window were connected to a percussion device that consisted of a saline-filled cylindrical reservoir and a metal pendulum. Brain injury of moderate severity (1.9 to 2.1 atm) was produced by allowing the pendulum to strike a piston on the cylinder. Pial artery diameter was measured with a video microscaler. Data were analyzed by repeated measures ANOVA. An \u03b1 level of<jats:italic>P<\/jats:italic>&lt;.05 was considered significant.<\/jats:p><jats:p><jats:italic>Results<\/jats:italic>FPI blunted dilation to cromakalim (10<jats:sup>\u22128<\/jats:sup>, 10<jats:sup>\u22126<\/jats:sup>mol\/L), a K<jats:sub>ATP<\/jats:sub>agonist (10\u00b11% and 27\u00b12% versus 3\u00b11% and 7\u00b12% before and after FPI, respectively, n=8). Similarly, FPI blunted dilation to calcitonin gene\u2013related peptide, an endogenous K<jats:sub>ATP<\/jats:sub>activator. FPI also blunted dilator responses to SNP, S-nitroso-<jats:italic>N<\/jats:italic>-acetylpenicillamine, and 8-bromo-cGMP (10<jats:sup>\u22126<\/jats:sup>to 10<jats:sup>\u22128<\/jats:sup>mol\/L) (10\u00b11% and 20\u00b11% versus 2\u00b11% and 8\u00b12% for SNP before and after FPI; 9\u00b11% and 16\u00b11% versus 2\u00b11% and 4\u00b11% for 8-bromo-cGMP before and after FPI, respectively, n=8). In contrast, responses to papaverine and brain natriuretic peptide were unchanged after FPI.<\/jats:p><jats:p><jats:italic>Conclusions<\/jats:italic>These data show that K<jats:sub>ATP<\/jats:sub>channel function is impaired after FPI. Furthermore, these data suggest that impaired function of mechanisms distal to NO synthase contribute to altered cerebral hemodynamics after FPI.<\/jats:p>","DOI":"10.1161\/01.str.28.11.2273","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T20:08:03Z","timestamp":1308341283000},"page":"2273-2280","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":55,"title":["Brain Injury Impairs ATP-Sensitive K<sup>+<\/sup>Channel Function in Piglet Cerebral Arteries"],"prefix":"10.1161","volume":"28","author":[{"given":"William M.","family":"Armstead","sequence":"first","affiliation":[{"name":"From the Departments of Anesthesia and Pharmacology, University of Pennsylvania, and The Children\u2019s Hospital of Philadelphia, Philadelphia, Pa."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-3468(85)80382-1"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.3171\/jns.1987.66.3.0409"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1089\/neu.1994.11.357"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1089\/neu.1994.11.487"},{"key":"e_1_3_2_5_2","first-page":"H1776","volume":"269","year":"1995","unstructured":"Thorogood MC, Armstead WM. 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