Mami Ishikawa1,2, Mayumi Kajimura3, Takayuki Morikawa3,4, Kosuke Tsukada5, Toshiyuki Tsuji3, Gen Kusaka6, Yuichi Tanaka6, Makoto Suematsu3. 1. Department of Neurosurgery, Saitama Medical Center, Jichi Medical University, 1-847 Amanumacho Omiya-ku, Saitama-city, Saitama, 330-8503, Japan. m.ishikawa@jichi.ac.jp. 2. Department of Biochemistry School of Medicine, Keio University, Tokyo, Japan. m.ishikawa@jichi.ac.jp. 3. Department of Biochemistry School of Medicine, Keio University, Tokyo, Japan. 4. Department of Stem Cell Biology, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan. 5. Graduate School of Science and Technology, Keio University, Kanagawa, Japan. 6. Department of Neurosurgery, Saitama Medical Center, Jichi Medical University, 1-847 Amanumacho Omiya-ku, Saitama-city, Saitama, 330-8503, Japan.
Abstract
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.
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.
Entities:
Keywords:
Cerebral microcirculation; Line scan; No reflow; P-selectin; Two photon
Authors: Jean C Cruz Hernández; Oliver Bracko; Nozomi Nishimura; Chris B Schaffer; Calvin J Kersbergen; Victorine Muse; Mohammad Haft-Javaherian; Maxime Berg; Laibaik Park; Lindsay K Vinarcsik; Iryna Ivasyk; Daniel A Rivera; Yiming Kang; Marta Cortes-Canteli; Myriam Peyrounette; Vincent Doyeux; Amy Smith; Joan Zhou; Gabriel Otte; Jeffrey D Beverly; Elizabeth Davenport; Yohan Davit; Charles P Lin; Sidney Strickland; Costantino Iadecola; Sylvie Lorthois Journal: Nat Neurosci Date: 2019-02-11 Impact factor: 24.884