[Changes of extracellular potassium concentration in the cortex and brain stem during the acute phase of experimental closed head injury (author's transl)].
The high concentration of extracellular potassium ((K+)o) impedes neuronal activity by depolarizing the membrane potential and further causing depolarization block or conduction block, and also causes swelling of astrocytes, which may result in narrowing of extracellular space and affect the diffusion of metabolites. Thus, when high concentration of extracellular potassium prolongs, pathological changes of neurons may ensue. In such state as cerebral ischemia, contusion or spreading depression, marked elevation of extracellular potassium was reported by many authors. In order to reveal the changes of extracellular potassium during the acute phase of closed head injury, following experimental studies were performed. In the first experiment, closed head injury model of the mouse was used. Directly after the impact with 600 g.cm, spontaneous movement of the animal disappeared for about 5-6 minutes often accompanied by immediate epilepsy. In this state, cortical (K+)0 increased from the control level of 4.1 +/- 1.8 mM to 20-30 mM. The elevated (K+)0 recovered gradually within 10-30 minutes. Directly after the same impact, apnea, bradycardia and low voltage EEG also appeared. In the second experiment, closed head injury model of the rat was used. With the impact of 9000 g.cm, the same concussion-like symptoms appeared as those of mice. Directly after the impact, (K+)0 in the cortex and brain stem elevated but the change patterns of cortical (K+)0 and brain stem (K+)0 were different. The different patterns in changes of (K+)0 were classified into four types. Type 1. Both cortical and brain stem (K+)0 elevated significantly immediately after the trauma, and recovered to control level within 30 minutes. Type 2. Both (K+)0 elevated significantly as in type 1 but only brain stem (K+)0 recovered within 30 minutes. Type 3. With the exacerbation of vital signs, both (K+)0 elevated over 50 mM, resulting in the death of the animal. Type 4. Although cortical (K+)0 elevated significantly after the impact, the increase of brain stem (K+)0 was below 10 mM. In type 1,2 and 3, blood pressure always elevated and brady- or apnea appeared immediately after the impact. In type 4, blood pressure after the impact showed to become slightly lower transiently as compared to control blood pressure. In control study, spreading depression was elicited by application of KC1-solution on the cortex. Spreading depression caused the elevation of cortical (K+)0 only, and almost no changes of brain stem (K+)0 were observed. The present study suggested that during the acute phase of closed head injury, diffuse neuronal disturbances involving the brain stem existed. And the elevation of brain stem (K+)0 is an important finding of this study because it may affect the level of consciousness directly by the mechanisms as described above.
D000818:Animals; D001930:Brain Injuries / Q000378:metabolism*; D001933:Brain Stem / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism*; D005110:Extracellular Space / Q000378:metabolism*; D005260:Female; D051379:Mice; D010063:Ovum; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D014949:Wounds, Nonpenetrating / Q000378:metabolism*
D011188:Potassium