Ion and metabolic disturbances after global and focal cerebral ischemia

We focus our attention in this presentation to the extracellular ionic changes during and after local ischemia and in repetitive versus single global ischemia. In the cat stroke model of MCA occlusion a considerable variability in the severity of ischemia was observed. This was demonstrated in electrical activity (ECoG), NAD/NADH fluoro-reflectometry and extracellular ionic changes. A striking experience was, that the K+ recovery is rather fast even after two hours of ischemia, and this is partly due to maintained activity of the sodium-potassium pump. After the MCA release a secondary acidosis occurs, which is the result of excess lactic acid production. This lactacidosis is certainly contributes to the late morphological damage. The repeated acidotic insult (in gerbil model of global cerebral ischemia) could be the cause of the more severe morphological and blood-brain-barrier damage in the repetitive ischemia too. The acidosis in many cases is even more pronounced after relieving the carotid arteries. This secondary acidosis causes endothelial damage and vasogenic oedema.