Evidence for direct impairment of neuronal function by subarachnoid metabolites following SAH.

Abstract

Dysfunction of neuronal signal processing and transmission occurs after subarachnoid hemorrhage (SAH) and contributes to the high morbidity and mortality of this pathology. The underlying mechanisms include early brain injury due to elevation of the intracranial pressure, disruption of the blood-brain barrier, brain edema, reduction of cerebral blood flow, and neuronal cell death. Direct influence of subarachnoid blood metabolites on neuronal signaling should be considered. After SAH, some metabolites were shown to directly induce disruption of neuronal integrity and neuronal signaling, whereas the effects of other metabolites on neurotoxicity and neuronal signaling have not yet been investigated. Therefore, this mini-review will discuss recent evidence for a direct influence of subarachnoid blood and its metabolites on neuronal function.