{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T07:42:17Z","timestamp":1777794137509,"version":"3.51.4"},"reference-count":48,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2016,7,21]],"date-time":"2016-07-21T00:00:00Z","timestamp":1469059200000},"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":[[2017,2]]},"abstract":"<jats:p>Intracranial hypertension is a common final pathway in many acute neurological conditions. However, the cerebral haemodynamic response to acute intracranial hypertension is poorly understood. We assessed cerebral haemodynamics (arterial blood pressure, intracranial pressure, laser Doppler flowmetry, basilar artery Doppler flow velocity, and vascular wall tension) in 27 basilar artery-dependent rabbits during experimental (artificial CSF infusion) intracranial hypertension. From baseline (\u223c9 mmHg; SE 1.5) to moderate intracranial pressure (\u223c41 mmHg; SE 2.2), mean flow velocity remained unchanged (47 to 45\u2009cm\/s; p\u2009=\u20090.38), arterial blood pressure increased (88.8 to 94.2 mmHg; p\u2009&lt;\u20090.01), whereas laser Doppler flowmetry and wall tension decreased (laser Doppler flowmetry 100 to 39.1% p\u2009&lt;\u20090.001; wall tension 19.3 to 9.8 mmHg, p\u2009&lt;\u20090.001). From moderate to high intracranial pressure (\u223c75 mmHg; SE 3.7), both mean flow velocity and laser Doppler flowmetry decreased (45 to 31.3\u2009cm\/s p\u2009&lt;\u20090.001, laser Doppler flowmetry 39.1 to 13.3%, p\u2009&lt;\u20090.001), arterial blood pressure increased still further (94.2 to 114.5 mmHg; p\u2009&lt;\u20090.001), while wall tension was unchanged (9.7 to 9.6 mmHg; p\u2009=\u20090.35).This animal model of acute intracranial hypertension demonstrated two intracranial pressure-dependent cerebroprotective mechanisms: with moderate increases in intracranial pressure, wall tension decreased, and arterial blood pressure increased, while with severe increases in intracranial pressure, an arterial blood pressure increase predominated. Clinical monitoring of such phenomena could help individualise the management of neurocritical patients.<\/jats:p>","DOI":"10.1177\/0271678x16639060","type":"journal-article","created":{"date-parts":[[2016,3,18]],"date-time":"2016-03-18T22:09:39Z","timestamp":1458338979000},"page":"694-705","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":28,"title":["Cerebral haemodynamics during experimental intracranial hypertension"],"prefix":"10.1177","volume":"37","author":[{"given":"Joseph","family":"Donnelly","sequence":"first","affiliation":[{"name":"Brain Physics Laboratory, Division of Neurosurgery, Department of Clinical Neurosciences, Cambridge Biomedical Campus, University of Cambridge, Cambridge, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marek","family":"Czosnyka","sequence":"additional","affiliation":[{"name":"Brain Physics Laboratory, Division of Neurosurgery, Department of Clinical 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