caa a22 4500 477107907 CHVBK 20180405111600.0 cr unu---uuuuu 170330e19960401xx s 000 0 eng 10.1007/BF01420301 doi (NATIONALLICENCE)springer-10.1007/BF01420301 The role of the coagulation cascade in brain edema formation after intracerebral hemorrhage [Elektronische Daten] [K. Lee, A. Betz, S. Kim, R. Keep, J. Hoff] Summary: The coagulation cascade has a potential role in brain edema formation due to intracerebral hemorrhage. In this study blood and other solutions were injected stereotactically into the right basal ganglia in rats. Twenty-four hours following injection, brain water and ion contents were measured to determine the amount of brain edema. Intracerebral blood resulted in an increase in brain water content. The amount of brain edema surrounding the intracerebral hematoma was reduced by a thrombin inhibitor Na-(2-Naphthalenesulfonylglycyl)-4-amidino-DL-phenylalaninepiperidide, (α-NAPAP) infused into the hematoma after the clot had been allowed to solidify. The inhibitor did not alter the actual size of the clot mass. An artificial clot composed of fibrinogen, thrombin, and styrene microspheres also produced brain edema. A fibrin clot led to edema formation even in the absence of mass effect provided by the microspheres. The single component responsible for production of brain edema in all these models was thrombin. The edema was formed in response to a fibrinogen-independent pathway. These results indicate that the coagulation cascade is involved in brain edema that develops adjacent to an intracerebral hematoma. Springer-Verlag, 1996 Brain edema nationallicence brain water nationallicence coagulation cascade nationallicence fibrinogen nationallicence Nα-(2-Naphthalenesulfonylglycyl)-4-amidino-DL-phenylalaninepiperidide nationallicence α-NAPAP nationallicence rat nationallicence thrombin nationallicence Lee K. Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor, MI, USA aut Betz A. Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor, MI, USA aut Kim S. Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor, MI, USA aut Keep R. Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor, MI, USA aut Hoff J. Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor, MI, USA aut Acta Neurochirurgica Springer-Verlag 138/4(1996-04-01), 396-401 0001-6268 138:4<396 1996 138 701 https://doi.org/10.1007/BF01420301 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF01420301 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Lee K. Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor, MI, USA aut NATIONALLICENCE 700 1- Betz A. Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor, MI, USA aut NATIONALLICENCE 700 1- Kim S. Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor, MI, USA aut NATIONALLICENCE 700 1- Keep R. Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor, MI, USA aut NATIONALLICENCE 700 1- Hoff J. Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor, MI, USA aut NATIONALLICENCE 773 0- Acta Neurochirurgica Springer-Verlag 138/4(1996-04-01), 396-401 0001-6268 138:4<396 1996 138 701 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer