{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T19:19:50Z","timestamp":1789154390432,"version":"build-2803163510"},"reference-count":155,"publisher":"Georg Thieme Verlag KG","issue":"04","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Semin Thromb Hemost"],"published-print":{"date-parts":[[2024,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Existing effective treatments for ischemic stroke restore blood supply to the ischemic region using thrombolysis or mechanical removal of clot. However, it is increasingly recognized that successful removal of occlusive thrombus from the large artery\u2014recanalization, may not always be accompanied by successful restoration of blood flow to the downstream tissues\u2014reperfusion. Ultimately, brain tissue survival depends on cerebral perfusion, and a functioning microcirculation. Because capillary diameter is often equal to or smaller than an erythrocyte, microcirculation is largely dependent on erythrocyte rheological (hemorheological) factors such as whole blood viscosity (WBV). Several studies in the past have demonstrated elevated WBV in stroke compared with healthy controls. Also, elevated WBV has shown to be an independent risk factor for stroke. Elevated WBV leads to endothelial dysfunction, decreases nitric oxide-dependent flow-mediated vasodilation, and promotes hemostatic alterations\/thrombosis, all leading to microcirculation sludging. Compromised microcirculation further leads to decreased cerebral perfusion. Hence, modulating WBV through pharmacological agents might be beneficial to improve cerebral perfusion in stroke. This review discusses the effect of elevated WBV on endothelial function, hemostatic alterations, and thrombosis leading to reduced cerebral perfusion in stroke.<\/jats:p>","DOI":"10.1055\/s-0043-1775858","type":"journal-article","created":{"date-parts":[[2023,10,9]],"date-time":"2023-10-09T23:23:26Z","timestamp":1696893806000},"page":"580-591","source":"Crossref","is-referenced-by-count":22,"title":["Whole Blood Viscosity and Cerebral Blood Flow in Acute Ischemic Stroke"],"prefix":"10.1055","volume":"50","author":[{"given":"Prajwal","family":"Gyawali","sequence":"additional","affiliation":[{"name":"Heart and Stroke Program, Hunter Medical Research Institute and School of Health and Medical Sciences, University of Southern Queensland, Toowoomba, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas P.","family":"Lillicrap","sequence":"additional","affiliation":[{"name":"Heart and Stroke Program, Department of Neurology, Hunter Medical Research Institute, John Hunter Hospital, New Lambton Heights, New South Wales, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlos G.","family":"Esperon","sequence":"additional","affiliation":[{"name":"Heart and Stroke Program, Department of Neurology, Hunter Medical Research Institute, John Hunter Hospital, New Lambton Heights, New South Wales, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aseem","family":"Bhattarai","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Institute of Medicine, Kathmandu, Nepal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"Bivard","sequence":"additional","affiliation":[{"name":"Department of Neurology, Royal Melbourne Hospital, Parkville, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neil","family":"Spratt","sequence":"additional","affiliation":[{"name":"Heart and Stroke Program, Department of Neurology, 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