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Leukocyte plugging and cortical capillary flow after subarachnoid hemorrhage

Background It is believed that increased intracranial pressure immediately after subarachnoid hemorrhage (SAH) causes extensive brain ischemia and results in worsening clinical status. Arterial flow to the cerebral surfaces is clinically well maintained during clipping surgery regardless of the seve...

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Published in:Acta neurochirurgica 2016-06, Vol.158 (6), p.1057-1067
Main Authors: Ishikawa, Mami, Kajimura, Mayumi, Morikawa, Takayuki, Tsukada, Kosuke, Tsuji, Toshiyuki, Kusaka, Gen, Tanaka, Yuichi, Suematsu, Makoto
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container_end_page 1067
container_issue 6
container_start_page 1057
container_title Acta neurochirurgica
container_volume 158
creator Ishikawa, Mami
Kajimura, Mayumi
Morikawa, Takayuki
Tsukada, Kosuke
Tsuji, Toshiyuki
Kusaka, Gen
Tanaka, Yuichi
Suematsu, Makoto
description Background It is believed that increased intracranial pressure immediately after subarachnoid hemorrhage (SAH) causes extensive brain ischemia and results in worsening clinical status. Arterial flow to the cerebral surfaces is clinically well maintained during clipping surgery regardless of the severity of the World Federation of Neurological Societies grade after SAH. To explore what kinds of changes occur in the cortical microcirculation, not at the cerebral surface, we examined cortical microcirculation after SAH using two-photon laser scanning microscopy (TPLSM). Methods SAH was induced in mice with an endovascular perforation model. Following continuous injection of rhodamine 6G, velocities of labeled platelets and leukocytes and unlabeled red blood cells (RBCs) were measured in the cortical capillaries 60 min after SAH with a line-scan method using TPLSM, and the data were compared to a sham group and P-selectin monoclonal antibody-treated group. Results Velocities of leukocytes, platelets, and RBCs in capillaries decreased significantly 60 min after SAH. Rolling and adherent leukocytes suddenly prevented other blood cells from flowing in the capillaries. Flowing blood cells also decreased significantly in each capillary after SAH. This no-reflow phenomenon induced by plugging leukocytes was often observed in the SAH group but not in the sham group. The decreased velocities of blood cells were reversed by pretreatment with the monoclonal antibody of P-selection, an adhesion molecule expressed on the surfaces of both endothelial cells and platelets. Conclusions SAH caused sudden worsening of cortical microcirculation at the onset. Leukocyte plugging in capillaries is one of the reasons why cortical microcirculation is aggravated after SAH.
doi_str_mv 10.1007/s00701-016-2792-6
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Arterial flow to the cerebral surfaces is clinically well maintained during clipping surgery regardless of the severity of the World Federation of Neurological Societies grade after SAH. To explore what kinds of changes occur in the cortical microcirculation, not at the cerebral surface, we examined cortical microcirculation after SAH using two-photon laser scanning microscopy (TPLSM). Methods SAH was induced in mice with an endovascular perforation model. Following continuous injection of rhodamine 6G, velocities of labeled platelets and leukocytes and unlabeled red blood cells (RBCs) were measured in the cortical capillaries 60 min after SAH with a line-scan method using TPLSM, and the data were compared to a sham group and P-selectin monoclonal antibody-treated group. Results Velocities of leukocytes, platelets, and RBCs in capillaries decreased significantly 60 min after SAH. Rolling and adherent leukocytes suddenly prevented other blood cells from flowing in the capillaries. Flowing blood cells also decreased significantly in each capillary after SAH. This no-reflow phenomenon induced by plugging leukocytes was often observed in the SAH group but not in the sham group. The decreased velocities of blood cells were reversed by pretreatment with the monoclonal antibody of P-selection, an adhesion molecule expressed on the surfaces of both endothelial cells and platelets. Conclusions SAH caused sudden worsening of cortical microcirculation at the onset. Leukocyte plugging in capillaries is one of the reasons why cortical microcirculation is aggravated after SAH.</description><identifier>ISSN: 0001-6268</identifier><identifier>EISSN: 0942-0940</identifier><identifier>DOI: 10.1007/s00701-016-2792-6</identifier><identifier>PMID: 27040552</identifier><language>eng</language><publisher>Vienna: Springer Vienna</publisher><subject>Animals ; Blood Flow Velocity ; Cerebrovascular Circulation ; Experimental Research - Vascular ; Interventional Radiology ; Leukocytes - pathology ; Male ; Medicine ; Medicine &amp; Public Health ; Mice ; Microcirculation ; Minimally Invasive Surgery ; Neurology ; Neuroradiology ; Neurosurgery ; Subarachnoid Hemorrhage - blood ; Subarachnoid Hemorrhage - physiopathology ; Surgical Orthopedics</subject><ispartof>Acta neurochirurgica, 2016-06, Vol.158 (6), p.1057-1067</ispartof><rights>Springer-Verlag Wien 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-f918ca63822b8a553cbfb57654de9e9269afa954700443db29b5a54427324cb83</citedby><cites>FETCH-LOGICAL-c471t-f918ca63822b8a553cbfb57654de9e9269afa954700443db29b5a54427324cb83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27040552$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ishikawa, Mami</creatorcontrib><creatorcontrib>Kajimura, Mayumi</creatorcontrib><creatorcontrib>Morikawa, Takayuki</creatorcontrib><creatorcontrib>Tsukada, Kosuke</creatorcontrib><creatorcontrib>Tsuji, Toshiyuki</creatorcontrib><creatorcontrib>Kusaka, Gen</creatorcontrib><creatorcontrib>Tanaka, Yuichi</creatorcontrib><creatorcontrib>Suematsu, Makoto</creatorcontrib><title>Leukocyte plugging and cortical capillary flow after subarachnoid hemorrhage</title><title>Acta neurochirurgica</title><addtitle>Acta Neurochir</addtitle><addtitle>Acta Neurochir (Wien)</addtitle><description>Background It is believed that increased intracranial pressure immediately after subarachnoid hemorrhage (SAH) causes extensive brain ischemia and results in worsening clinical status. Arterial flow to the cerebral surfaces is clinically well maintained during clipping surgery regardless of the severity of the World Federation of Neurological Societies grade after SAH. To explore what kinds of changes occur in the cortical microcirculation, not at the cerebral surface, we examined cortical microcirculation after SAH using two-photon laser scanning microscopy (TPLSM). Methods SAH was induced in mice with an endovascular perforation model. Following continuous injection of rhodamine 6G, velocities of labeled platelets and leukocytes and unlabeled red blood cells (RBCs) were measured in the cortical capillaries 60 min after SAH with a line-scan method using TPLSM, and the data were compared to a sham group and P-selectin monoclonal antibody-treated group. Results Velocities of leukocytes, platelets, and RBCs in capillaries decreased significantly 60 min after SAH. Rolling and adherent leukocytes suddenly prevented other blood cells from flowing in the capillaries. Flowing blood cells also decreased significantly in each capillary after SAH. This no-reflow phenomenon induced by plugging leukocytes was often observed in the SAH group but not in the sham group. The decreased velocities of blood cells were reversed by pretreatment with the monoclonal antibody of P-selection, an adhesion molecule expressed on the surfaces of both endothelial cells and platelets. Conclusions SAH caused sudden worsening of cortical microcirculation at the onset. 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Arterial flow to the cerebral surfaces is clinically well maintained during clipping surgery regardless of the severity of the World Federation of Neurological Societies grade after SAH. To explore what kinds of changes occur in the cortical microcirculation, not at the cerebral surface, we examined cortical microcirculation after SAH using two-photon laser scanning microscopy (TPLSM). Methods SAH was induced in mice with an endovascular perforation model. Following continuous injection of rhodamine 6G, velocities of labeled platelets and leukocytes and unlabeled red blood cells (RBCs) were measured in the cortical capillaries 60 min after SAH with a line-scan method using TPLSM, and the data were compared to a sham group and P-selectin monoclonal antibody-treated group. Results Velocities of leukocytes, platelets, and RBCs in capillaries decreased significantly 60 min after SAH. Rolling and adherent leukocytes suddenly prevented other blood cells from flowing in the capillaries. Flowing blood cells also decreased significantly in each capillary after SAH. This no-reflow phenomenon induced by plugging leukocytes was often observed in the SAH group but not in the sham group. The decreased velocities of blood cells were reversed by pretreatment with the monoclonal antibody of P-selection, an adhesion molecule expressed on the surfaces of both endothelial cells and platelets. Conclusions SAH caused sudden worsening of cortical microcirculation at the onset. Leukocyte plugging in capillaries is one of the reasons why cortical microcirculation is aggravated after SAH.</abstract><cop>Vienna</cop><pub>Springer Vienna</pub><pmid>27040552</pmid><doi>10.1007/s00701-016-2792-6</doi><tpages>11</tpages></addata></record>
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subjects Animals
Blood Flow Velocity
Cerebrovascular Circulation
Experimental Research - Vascular
Interventional Radiology
Leukocytes - pathology
Male
Medicine
Medicine & Public Health
Mice
Microcirculation
Minimally Invasive Surgery
Neurology
Neuroradiology
Neurosurgery
Subarachnoid Hemorrhage - blood
Subarachnoid Hemorrhage - physiopathology
Surgical Orthopedics
title Leukocyte plugging and cortical capillary flow after subarachnoid hemorrhage
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