The role of calcium and cellular membrane dysfunction in experimental trauma and subarachnoid hemorrhage.
Acute subarachnoid hemorrhage (SAH) and intraparenchymal hematoma (IPH) in cats are accompanied by massive cellular depolarization. This depolarization, characterized by potassium (K+) efflux and calcium (Ca++) influx, results in membrane destabilization, osmotic imbalance, and a decrease in electrical conduction. The Ca++ influx appears to initiate a chain reaction that, in some instances, may result in delayed cell destruction. The ionic dysequilibrium probably contributes to both brain engorgement and spasm in large vessels. The cellular depolarization and calcium-induced cell membrane injury at the moment of impact may play a greater role in the pathophysiology of head trauma than previously thought.
D000818:Animals; D001692:Biological Transport; D001930:Brain Injuries / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D002415:Cats; D002462:Cell Membrane / Q000378:metabolism; D002463:Cell Membrane Permeability; D002543:Cerebral Hemorrhage / Q000378:metabolism; D006406:Hematoma / Q000378:metabolism; D008564:Membrane Potentials; D011188:Potassium / Q000378:metabolism; D013345:Subarachnoid Hemorrhage / Q000378:metabolism*
D011188:Potassium; D002118:Calcium