Cortical cellular response in acute subarachnoid hemorrhage.
Acute subarachnoid hemorrhage (SAH) over the cerebral cortex causes single or multiple waves of cellular depolarization, which may occur in a self-propagating, reverberating fashion. This process is characterized by a massive K+ release and transient depression in electrocortical activity. The K+ levels in the extracellular space reach magnitudes known to substantially affect the membrane potentials of neurons and glia, and may cause a release of neurotransmitters from depolarized presynaptic terminals. The release of K+ may be the initial step in the development of cellular edema and, together with a multitude of other chemical and biochemical changes taking place at the cellular level, may underlie the loss of autoregulation. Cortical cells rather than blood vessels are the primary targets in the initial stages of SAH, and ischemia does not play a causal role in the pathogenesis of cellular dysfunction during this stage.
D000818:Animals; D001769:Blood; D002545:Brain Ischemia / Q000378:metabolism; D002415:Cats; D002463:Cell Membrane Permeability; D002540:Cerebral Cortex / Q000378:metabolism / Q000503:physiopathology*; D013181:Cortical Spreading Depression; D004195:Disease Models, Animal; D004569:Electroencephalography; D018377:Neurotransmitter Agents / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D013345:Subarachnoid Hemorrhage / Q000378:metabolism / Q000503:physiopathology*; D014882:Water-Electrolyte Balance
D018377:Neurotransmitter Agents; D011188:Potassium