Changes in extracellular potassium concentration in cortex and brain stem during the acute phase of experimental closed head injury

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Abstract
A high K+ concentration ([K+]o) in brain tissue impedes neuronal activity, as observed in spreading cortical depression. Experimental studies were performed on mice and rats to determine the role of changes of [K+]o in cerebral concussion. In the 1st experiment a 600 g-cm impact was delivered to the vertex of the mouse skull. This impact induced arrest of spontaneous movement for 465 .+-. 55.9 s (mean .+-. SD), accompanied by apnea, bradycardia and low-voltage EEG recordings. The injury was frequently followed immediately by epilepsy. This impact induced an increase of cortical [K+]o from the control level of 4.1 .+-. 1.8 mM to 20-30 mM, with gradual recovery within 30 min to the control level. In the 2nd experiment an impact of 9000 g-cm was delivered to the midline parieto-occipital area of the rat and produced concussion-like phenomena similar to those elicited in mice. This level of trauma induced a significant increase of cortical [K+]o from the control level of 4.2 .+-. 0.8 mM to 20-50 mM in all of the rats, and also a significant increase of brainstem [K+]o from 3.9 .+-. 0.6 to 20-30 mM in 73% of the rats. In these rats the impact also induced apnea and a transient elevation of blood pressure, and resulted in low-voltage EEG recordings. In 23% of the rats in which [K+]o changes in the brainstem were not significant, the impact caused a transient reduction of blood pressure. An increase of [K+]o in the cerebral cortex and in the brainstem is an important element in the phenomenon of concussion.