Rudolf U, Zoltán N, Zsuzsa J
Experimental Research Dept., Semmelweis University of Medicine, Budapest, Hungary.
Acta Biomed Ateneo Parmense. 1995;66(3-4):75-82.
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.
在本报告中，我们将注意力集中于局部缺血期间及之后以及重复性与单次全脑缺血时的细胞外离子变化。在大脑中动脉闭塞的猫中风模型中，观察到缺血严重程度存在相当大的变异性。这在脑电活动（脑电图）、NAD/NADH荧光反射测定法以及细胞外离子变化中得到了证实。一个显著的现象是，即使在缺血两小时后，钾离子的恢复也相当快，这部分归因于钠钾泵的持续活性。大脑中动脉再灌注后会发生继发性酸中毒，这是乳酸产生过多的结果。这种乳酸性酸中毒肯定会导致后期的形态学损伤。反复的酸中毒损伤（在沙土鼠全脑缺血模型中）也可能是重复性缺血中更严重的形态学和血脑屏障损伤的原因。在许多情况下，解除颈动脉阻塞后酸中毒甚至会更明显。这种继发性酸中毒会导致内皮损伤和血管源性水肿。
