Wade J G, Amtorp O, Sorensen S C
Arch Neurol. 1975 Jun;32(6):381-4. doi: 10.1001/archneur.1975.00490480047005.
Rats were subjected to total cerebral ischemia by occluding outflow from the heart. In control experiments and following different periods of ischemia, potassium concentration was measured in cisternal cerebrospinal fluid (CSF). It rose to 19.4 mEq/liter following 16 minutes of ischemia. Changes in cerebrovascular resistance (CVR) were also assessed by measuring the cerebral perfusion rate (CPR). Following two minutes of ischemia, CVR was decreased to half control value. After 8 and 16 minutes of ischemia, CVR was markedly increased, and "no-flow" state was approached after 16 minutes of ischemia. The CVR increased concomitantly with increase in potassium concentration in cisternal CSF. We suggest that the increase in CVR following cerebral ischemia is due to increase in potassium concentration in brain extracellular fluid and is part of a vicious circle that leads to brain death.
通过阻断心脏流出道使大鼠遭受全脑缺血。在对照实验以及不同缺血时间段后，测量脑池脑脊液（CSF）中的钾浓度。缺血16分钟后，钾浓度升至19.4毫当量/升。还通过测量脑灌注率（CPR）来评估脑血管阻力（CVR）的变化。缺血两分钟后，CVR降至对照值的一半。缺血8分钟和16分钟后，CVR显著增加，缺血16分钟后接近“无血流”状态。CVR随着脑池CSF中钾浓度的增加而相应增加。我们认为，脑缺血后CVR的增加是由于脑细胞外液中钾浓度的增加，并且是导致脑死亡的恶性循环的一部分。
