We have several ongoing projects in the study subarachnoid hemorrhage (SAH).
Using a modified endovascular filament puncture model of SAH devoid of ischemic injury, we have shown that glibenclamide exerts salutatory anti-inflammatory effects, likely unrelated to blockade of the SUR1/TRPM4 channel.
We have since identified a potent inflammatory mediator that binds to glibenclamide in-vitro, and further investigations are underway.
Additionally, we published an extensive review of the potential use of unfractionated heparin in the context of SAH.
Using a novel stereotactic-guided injection model of SAH and have recently shown that heparin indeed significantly reduces multiple measures of neuroinflammation and cell apoptosis.
Further experiments are planned to compare glibenclamide-treated cohorts to heparin-treated cohorts, along with long-term complex neurobehavioral analysis.
- Heparin Reduces Neuroinflammation and Transsynaptic Neuronal Apoptosis in a Model of Subarachnoid Hemorrhage
- Unfractionated heparin: multitargeted therapy for delayed neurological deficits induced bysubarachnoid hemorrhage
- Glibenclamide reduces inflammation, vasogenic edema, and caspase-3 activation after subarachnoid hemorrhage