Glibenclamide pretreatment attenuates early hematoma expansion of warfarin-associated intracerebral hemorrhage in rats by alleviating perihematomal blood-brain barrier dysfunction.

Background: Hematoma expansion is a determinant of poor outcome of intracerebral hemorrhage but occurs frequently, especially in warfarin-associated intracerebral hemorrhage (W-ICH). In the present study, we employ the warfarin-associated intracerebral hemorrhage (W-ICH) rat model, to explore the efficacy and potential mechanism of glibenclamide pretreatment on hematoma expansion after intracerebral hemorrhage, hoping to provide proof of concept that glibenclamide in stroke primary and secondary prevention is also potentially beneficial for intracerebral hemorrhage patients at early stage.

Methods: In the present study, we tested whether glibenclamide, a common hypoglycemic drug, could attenuate hematoma expansion in a rat model of W-ICH.

The Role of Neutrophil Extracellular Traps in Early Microthrombosis and Brain Injury After Subarachnoid Hemorrhage in Mice.

Microthrombosis plays an important role in secondary brain injury after experimental subarachnoid hemorrhage (SAH), but the specific mechanism of microthrombosis remains unclear. The purpose of this study was to investigate the role of neutrophil extracellular traps (NETs) in microthrombosis after SAH. SAH was induced in male C57BL/6 mice using an endovascular perforation technique.

The role of cell-free DNA in fibrinolysis for intraventricular hemorrhage.

Objective: Tissue plasminogen activator (tPA) fibrinolysis did not improve functional outcomes of patients with intraventricular hemorrhage (IVH), largely because of the unsatisfactory clot clearance. The presence of neutrophil extracellular traps (NETs) within the clot has been confirmed to impair tPA fibrinolysis, but the mechanism has been unclear. The authors hypothesized that cell-free DNA (cfDNA), the main framework of NETs, might be the important reason for the fibrinolysis resistance, and they validated the hypothesis, hoping to provide a new target to promote intraventricular fibrinolysis.