{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T04:38:49Z","timestamp":1773290329612,"version":"3.50.1"},"reference-count":22,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[2009,10]]},"abstract":"<jats:p>\n            <jats:bold>\n              <jats:italic>Background and Purpose\u2014<\/jats:italic>\n            <\/jats:bold>\n            The functional role of arteriolo-arteriolar anastomosis (AAA) between the middle cerebral artery (MCA) and anterior cerebral artery in local hemodynamics is unknown, and was investigated here.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Methods\u2014<\/jats:italic>\n            <\/jats:bold>\n            Blood flow in AAAs was examined using fluorescein isothiocyanate\u2013labeled red blood cells (RBCs) as a flow indicator in 16 anesthetized C57BL\/6J mice before and after MCA occlusion up to 7 experimental days.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Results\u2014<\/jats:italic>\n            <\/jats:bold>\n            We observed paradoxical flow in AAAs; labeled RBCs entered from both the MCA and anterior cerebral artery sides and the opposing flows met at a branching T-junction, where the flows combined and passed into a penetrating arteriole. The dually fed T-junction was not fixed in position, but functionally jumped to adjacent T-junctions in response to changing hemodynamic conditions. On MCA occlusion, RBC flow from the MCA side immediately stopped. After a period of \u201chesitation,\u201d blood started to move retrogradely in one of the MCA branches toward the MCA stem. The retrograde blood flow was statistically significantly (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05), serving to feed blood to other MCA branches after a lag period. In capillaries, MCA occlusion induced immediate RBC disappearance in the ischemic core and to a lesser extent in the marginal zone near AAAs. At day 3 after ischemia, we recognized the beginning of remodeling with angiogenesis centering on AAAs.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Conclusions\u2014<\/jats:italic>\n            <\/jats:bold>\n            AAAs appear to play a key role in local hemodynamic homeostasis, both in the normal state and in the development of collateral channels and revascularization during ischemia.\n          <\/jats:p>","DOI":"10.1161\/strokeaha.109.558577","type":"journal-article","created":{"date-parts":[[2009,8,7]],"date-time":"2009-08-07T01:56:44Z","timestamp":1249610204000},"page":"3378-3383","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":51,"title":["Dually Supplied T-Junctions in Arteriolo-Arteriolar Anastomosis in Mice"],"prefix":"10.1161","volume":"40","author":[{"given":"Haruki","family":"Toriumi","sequence":"first","affiliation":[{"name":"From the Departments of Neurology (H.T., J.T., M.T., Y.T., M.U., N.S.) and Preventive Medicine for Cerebrovascular Disease (Y.T.), School of Medicine, Keio University, Tokyo Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jemal","family":"Tatarishvili","sequence":"additional","affiliation":[{"name":"From the Departments of Neurology (H.T., J.T., M.T., Y.T., M.U., N.S.) and Preventive Medicine for Cerebrovascular Disease (Y.T.), School of Medicine, Keio University, Tokyo Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Minoru","family":"Tomita","sequence":"additional","affiliation":[{"name":"From the Departments of Neurology (H.T., J.T., M.T., Y.T., M.U., N.S.) and Preventive Medicine for Cerebrovascular Disease (Y.T.), School of Medicine, Keio University, Tokyo Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yutaka","family":"Tomita","sequence":"additional","affiliation":[{"name":"From the Departments of Neurology (H.T., J.T., M.T., Y.T., M.U., N.S.) and Preventive Medicine for Cerebrovascular Disease (Y.T.), School of Medicine, Keio University, Tokyo Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Miyuki","family":"Unekawa","sequence":"additional","affiliation":[{"name":"From the Departments of Neurology (H.T., J.T., M.T., Y.T., M.U., N.S.) and Preventive Medicine for Cerebrovascular Disease (Y.T.), School of Medicine, Keio University, Tokyo Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Norihiro","family":"Suzuki","sequence":"additional","affiliation":[{"name":"From the Departments of Neurology (H.T., J.T., M.T., Y.T., M.U., N.S.) and Preventive Medicine for Cerebrovascular Disease (Y.T.), School of Medicine, Keio University, Tokyo Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_3_1_2","unstructured":"Mchedlishvili G. Arterial Behavior and Blood Circulation in the Brain. New York: Plenum Press; 1986: 130\u2013135."},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1092030309"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.str.0000086465.41263.06"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.me.04.020153.001241"},{"key":"e_1_3_3_5_2","first-page":"548","volume":"104","year":"1987","unstructured":"Gannushkina IV, Baranchikova MV, Shinkarenko VS, Komm SG. Status of the \u201cdead point\u201d of blood flow in anastomoses of superficial cerebral arteries as affected by an acute increase of blood pressure. Biull Eksp Biol Med. 1987; 104: 548\u2013552.","journal-title":"Biull Eksp Biol Med"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1097\/00004647-199908000-00005"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1080\/10739680701567089"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jcbfm.9600077"},{"key":"e_1_3_3_9_2","first-page":"17","volume":"1","year":"2007","unstructured":"Tomita M. Blood flow control in the brain: possible biphasic mechanism of functional hyperemia (review). Asian Biomedicine. 2007; 1: 17\u201331.","journal-title":"Asian Biomedicine"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1981.6"},{"key":"e_1_3_3_11_2","unstructured":"Tomita M. Basic mechanisms of brain ischemia (Minireview on microcirculation) Capillo-venous flow disturbances in brain ischemia. In: Erdo F ed. Recent Advances and New Strategies in Stroke Research Transworld Research Network 37\/661 (2) Port P.O. Trivandrum-695 023 India: Kerala; 2008: 91\u2013112."},{"key":"e_1_3_3_12_2","unstructured":"Tomita M. Microcirculatory stasis in the brain (Presidential Address). In: Tomita M Mchedlishvili G Rosenblum WI Heiss W-D Fukuuchi Y eds. Microcirculatory Stasis in the Brain Amsterdam: Excerpta Medica ICS 1031; 1993: 1\u20137."},{"key":"e_1_3_3_13_2","unstructured":"Chien S. Present state of blood rheology. In: Messmer K Schmid-Sch\u00f6nbein H eds. Hemodilution Basel: Kager; 1972: 1\u201345."},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.1990.00530110107027"},{"key":"e_1_3_3_15_2","unstructured":"Mchedlishvili G Tomita M Schmid-Sch\u00f6nbein GW. Hemorrheology in microcirculation: Pathological changes (Internet Virtual Symposium The 7th Tbilisi Symposium) Keio J Med. 2000;49(Suppl 3):1\u201382 (Available from http:\/\/mtomita.jp\/content.htm)."},{"key":"e_1_3_3_16_2","unstructured":"Tomita M. Increased intracranial pressure and brain edema. In: Kalimo H. ed. Pathology & Genetics Structure and functions of CNS blood vessels Cerebrovascular Diseases ISN Book Series Basel: ISN Neuropath Press; 2005: 39\u201349."},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1097\/00001756-199911080-00002"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.16.2.3975958"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.15.2.6701929"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1016\/0022-510X(69)90078-1"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.2008.166"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1097\/00004647-199910000-00005"}],"container-title":["Stroke"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/full\/10.1161\/STROKEAHA.109.558577","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,13]],"date-time":"2024-05-13T13:02:00Z","timestamp":1715605320000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/STROKEAHA.109.558577"}},"subtitle":["Key to Local Hemodynamic Homeostasis in Normal and Ischemic States?"],"short-title":[],"issued":{"date-parts":[[2009,10]]},"references-count":22,"journal-issue":{"issue":"10","published-print":{"date-parts":[[2009,10]]}},"alternative-id":["10.1161\/STROKEAHA.109.558577"],"URL":"https:\/\/doi.org\/10.1161\/strokeaha.109.558577","relation":{},"ISSN":["0039-2499","1524-4628"],"issn-type":[{"value":"0039-2499","type":"print"},{"value":"1524-4628","type":"electronic"}],"subject":[],"published":{"date-parts":[[2009,10]]},"assertion":[{"value":"2009-05-25","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2009-06-16","order":1,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2009-08-06","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}