Research

Subarachnoid hemorrhage (SAH) occurs most commonly when an aneurysm in the brain ruptures, spilling blood into the cerebrospinal fluid.

We study two major side effects of this event: (1) development of a syndrome of progressive strokes 1-2 weeks after the hemorrhage (cerebral vasospasm), and (2) acute dysfunction of the heart (neurocardiomyopathy) that occurs in up to 50% of patients after SAH.

We found that elevated percentages of neutrophils in the cerebrospinal fluid (CSF) are associated with cerebral vasospasm. Our data suggest that selected molecular inflammatory mediators including chemokines play a role in attracting neutrophils to the CSF.

With our collaborators, we also correlated the neutrophil-derived reactive oxidant species hypochlorous acid with cerebral vasospasm in patients. In our model of SAH, we have shown that vasospasm is associated with an infiltration of neutrophils in the brain and can be ameliorated by neutrophil depletion. Future studies are aimed at determining the specific mediators of neutrophil extravasation in SAH patients.

We have developed a model of cardiac damage after SAH that will allow us to investigate the pathways responsible for this phenomenon. We recently found that depletion of neutrophils prior to SAH decreases the severity of cardiac damage.

Studies are now under way to determine neutrophil effector mechanisms that may be responsible for cardiac damage after SAH.