6533b7d3fe1ef96bd1260c85

RESEARCH PRODUCT

The Cerebral Thrombin System Is Activated after Intracerebral Hemorrhage and Contributes to Secondary Lesion Growth and Poor Neurological Outcome in C57Bl/6 Mice

Christina F. VogelaarOliver KempskiLouise TaylorEva GresserDaniel JussenDaniel JussenBeat AlessandriNicole RiedeHarald KrenzlinFlorian Ringel

subject

MaleC57BL/6030506 rehabilitationPathologymedicine.medical_specialtyPathogenesisMice03 medical and health sciences0302 clinical medicineThrombinAnimalsMedicineFactor IIaBlood CoagulationCells CulturedCerebral HemorrhageNeuronsIntracerebral hemorrhagebiologybusiness.industryThrombinbiology.organism_classificationmedicine.diseaseMice Inbred C57BLCoagulationCerebrovascular CirculationSecondary LesionNeurology (clinical)0305 other medical sciencebusiness030217 neurology & neurosurgerycirculatory and respiratory physiologymedicine.drug

description

With increasing evidence for the existence of a cerebral thrombin system, coagulation factor IIa (thrombin) is suspected to influence the pathogenesis of secondary injury progression after intracerebral hemorrhage (ICH). We hypothesized that mechanisms associated with local volume expansion after ICH, rather than blood constituents, activate the cerebral thrombin system and are responsible for detrimental neurological outcome. To test this hypothesis, we examine the local thrombin expression after ICH in a C57BL/6N mouse model in the presence and absence of blood constituents. ICH was established using stereotaxic orthotopic injection of utologous blood (

yearjournalcountryeditionlanguage
2020-06-15Journal of Neurotrauma
https://doi.org/10.1089/neu.2019.6582