Key result
Experimental intraparenchymal hemorrhage caused massive cellular depolarization and rapid K+ release in anatomically intact areas near the hematoma due to mechanical and chemical factors.
In an experimental cat model, intraparenchymal hemorrhage causes immediate massive cellular depolarization and potassium release in adjacent intact tissue, potentially influencing the final degree of cellular damage in head trauma.
A model of intraparenchymal hemorrhage was created in 11 cats. The development of the parenchymal hemorrhage was accompanied by a massive cellular depolarization and K+ release in anatomically intact areas in the vicinity of the hematoma. The K+ clearance was rapid and in most instances total. This initial K+ release was not ischemic in origin but was the result of mechanical and chemical factors of the extravasated blood on cellular membranes. In contrast, an increased water content of the white matter did not affect the cellular function or levels of K+ in the extracellular space of the cerebral cortex in the recording area. The experimental results suggest that K+ release takes place at the onset of trauma in subcritically injured cellular areas in the vicinity of a hemorrhage. The cellular elements undergo massive depolarization which is accompanied by a number of chemical and biochemical changes that lead to cellular swelling. Cellular depolarization and K+ release appear to be the initial response of the central nervous system to trauma. The extent of this response may strongly influence the final degree of cellular damage and, thus, the neurological deficit in patients with head trauma.
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Hubschmann et al. (1983) studied Intraparenchymal hemorrhage / head trauma (n=11). Intraparenchymal hemorrhage model was evaluated on Extracellular cortical potassium (K+) release and cellular depolarization. Experimental intraparenchymal hemorrhage caused massive cellular depolarization and rapid K+ release in anatomically intact areas near the hematoma due to mechanical and chemical factors.
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