Secondary Bleeding During Acute Experimental Intracerebral Hemorrhage.
Secondary Bleeding During Acute Experimental Intracerebral Hemorrhage.
复制标题
急性实验性脑出血期间的继发性出血。
DOI：
10.1161/strokeaha.118.021732
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发表时间：
2019
期刊：
影响因子：
8.3
通讯作者：
Ayata,Cenk
中科院分区：
文献类型：
--
作者：
Schlunk,Frieder;Böhm,Maximilian;Boulouis,Gregoire;Qin,Tao;Arbel,Michal;Tamim,Isra;Fischer,Paul;Bacskai,BrianJ;Frosch,MatthewP;Endres,Matthias;Greenberg,StevenM;Ayata,Cenk
Background and PurposeMechanisms contributing to acute hematoma growth in intracerebral hemorrhage are not well understood. Neuropathological studies suggest that the initial hematoma may create mass effect that can tear vessels in the vicinity by shearing, causing further bleeding and hematoma growth.MethodsTo test this in mice, we simulated initial intracerebral hemorrhage by intrastriatal injection of a liquid polymer that coagulates upon contact with tissue and measured the presence and volume of bleeding secondary to the mass effect using Hemoglobin ELISA 15 minutes after injection.ResultsSecondary hemorrhage occurred in a volume-dependent (4, 7.5, or 15 μL of polymer) and rate-dependent (0.05, 0.5, or 5 μL/s) manner. Anticoagulation (warfarin or dabigatran) exacerbated the secondary hemorrhage volume. In a second model of hematoma expansion, we confirmed that intrastriatal whole blood injection (15 μL, 0.5 μL/s) also caused secondary bleeding, using acute Evans blue extravasation as a surrogate. Anticoagulation once again exacerbated secondary hemorrhage after intrastriatal whole blood injection. Secondary hemorrhage directly and significantly correlated with arterial blood pressures in both nonanticoagulated and anticoagulated mice, when modulated by phenylephrine or labetalol.ConclusionsOur study provides the first proof of concept for secondary vessel rupture and bleeding as a potential mechanism for intracerebral hematoma growth.
