{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T21:32:13Z","timestamp":1787002333766,"version":"build-2736575974"},"reference-count":27,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2010,10,27]],"date-time":"2010-10-27T00:00:00Z","timestamp":1288137600000},"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":[[2011,4]]},"abstract":"<jats:p>\n                    The adipocytokine leptin has distinct functions regulating vascular tone, inflammation, and collateral artery growth. Arteriogenesis is an inflammatory process and provides a mechanism to overcome the effects of vascular obstruction. We, therefore, tested the effects of leptin in hypoperfused rat brain (three-vessel occlusion). Systemic leptin administration for 1 week after occlusion surgery increased cerebral hemodynamic reserve similar to granulocyte\u2013macrophage colony-stimulating factor (GM-CSF), as indicated by improved CO\n                    <jats:sub>2<\/jats:sub>\n                    reactivity (vehicle 0.53%\u00b10.26% versus leptin 1.05%\u00b10.6% per mm Hg arterial pCO\n                    <jats:sub>2<\/jats:sub>\n                    , P&lt;0.05). Infusion of microspheres under maximal vasodilation failed to show a positive effect of leptin on cerebral perfusion (vehicle 64.9%\u00b14.5% versus leptin 66.3%\u00b17.0%, occluded\/nonoccluded hemisphere). Acute treatment with GM-CSF led to a significant increased CO\n                    <jats:sub>2<\/jats:sub>\n                    reactivity and cerebral perfusion (79.2%\u00b18.1% versus 64.9%\u00b14.5%, P&lt;0.05). Vasoconstrictive response of isolated rat carotid artery rings, after phenylephrine was attenuated at 24 hours following preincubation with leptin, was unaffected by removal of endothelium but abrogated by coculture with N-(omega)-nitro-l-arginine methylester, pointing toward an inducible nitric oxide synthase-mediated mechanism. In chronic cerebral hypoperfusion, acute leptin treatment restored the hemodynamic reserve of the cerebral vasculature through its effects on vascular tone, while leaving vascular outward remodeling unaffected. Our results, for the first time, reveal a protective role of leptin on vascular function in hemodynamically compromised brain tissue.\n                  <\/jats:p>","DOI":"10.1038\/jcbfm.2010.192","type":"journal-article","created":{"date-parts":[[2010,10,27]],"date-time":"2010-10-27T04:07:30Z","timestamp":1288152450000},"page":"1085-1092","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":18,"title":["Leptin Augments Cerebral Hemodynamic Reserve after Three-Vessel Occlusion: Distinct Effects on Cerebrovascular Tone and Proliferation in a Nonlethal Model of Hypoperfused Rat Brain"],"prefix":"10.1177","volume":"31","author":[{"given":"Hans-Joerg","family":"Busch","sequence":"first","affiliation":[{"name":"Department of Cardiology and Angiology, Albert Ludwigs University, Freiburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephan H","family":"Schirmer","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Academic Medical Center, Amsterdam, The Netherlands"},{"name":"Department of Cardiology, Angiology and Intensive Care Medicine, Saarland University, Homburg\/Saar, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marco","family":"Jost","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Angiology, Albert Ludwigs University, Freiburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sylvia","family":"van Stijn","sequence":"additional","affiliation":[{"name":"Department of Pharmacology & Pharmacotherapy, Academic Medical Center, Amsterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephan L M","family":"Peters","sequence":"additional","affiliation":[{"name":"Department of Pharmacology & Pharmacotherapy, Academic Medical Center, Amsterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan J","family":"Piek","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Academic Medical Center, Amsterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christoph","family":"Bode","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Angiology, Albert Ludwigs University, Freiburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivo R","family":"Buschmann","sequence":"additional","affiliation":[{"name":"Research Group for Experimental and Clinical Arteriogenesis, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guenter","family":"Mies","sequence":"additional","affiliation":[{"name":"Max Planck Institute for Neurological Research, Cologne, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2010,10,27]]},"reference":[{"key":"bibr1-jcbfm.2010.192","doi-asserted-by":"publisher","DOI":"10.1002\/hep.20965"},{"key":"bibr2-jcbfm.2010.192","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000252068.89775.ee"},{"key":"bibr3-jcbfm.2010.192","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.83.10.1059"},{"key":"bibr4-jcbfm.2010.192","doi-asserted-by":"publisher","DOI":"10.1097\/01.WCB.0000057741.00152.E4"},{"key":"bibr5-jcbfm.2010.192","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000074209.17561.99"},{"key":"bibr6-jcbfm.2010.192","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1092100211"},{"key":"bibr7-jcbfm.2010.192","first-page":"183","volume":"28","author":"Coyle P","year":"1991","journal-title":"Blood 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