Hossmann K A, Ophoff B G, Csiba L, Paschen W
Max-Planck Institute for Neurological Research, Department of Experimental Neurology, Cologne, FRG.
Neurochem Pathol. 1988 Jul-Dec;9:127-37. doi: 10.1007/BF03160358.
Following prolonged cerebral ischemia, primary electrophysiological recovery may be followed by secondary deterioration of the recovery process. It has been suggested that the secondary deterioration is caused by "late" cytotoxic brain edema. To test this hypothesis, adult normothermic cats were submitted to 1 h complete cerebral ischemia followed by 3 and 6 h recirculation, respectively. Postischemic recovery of energy metabolism was imaged by ATP-induced bioluminescence, and regional tissue pH and electrolyte content was measured in regions with and without metabolic recovery. In areas with postischemic restitution of metabolic activity, sodium gradually rose from 338 +/- 17 to 488 +/- 28 mumol/g protein and calcium from 8.81 +/- 0.35 to 18.24 +/- 0.97 mumol/g protein. Tissue potassium content decreased from 761 +/- 12 to 676 +/- 19 mumol/g protein and magnesium from 46.8 +/- 0.8 to 36.3 +/- 1.1 mumol/g protein. Tissue pH rose from 7.09 +/- 0.04 to 7.31 +/- 0.13 and 7.26 +/- 0.17 after 3 and 6 h recirculation, respectively. In areas without metabolic recovery, electrolyte disturbances were even more pronounced and pH--after transient alkalization--fell to 6.82 +/- 0.12. These data demonstrate that during the later phase of postischemic recirculation, progressive disturbances of electrolyte homeostasis create a preedematous situation that has to be considered for preventing delayed postischemic complications.
在长时间脑缺血后，最初的电生理恢复之后可能会出现恢复过程的继发性恶化。有人提出继发性恶化是由“迟发性”细胞毒性脑水肿引起的。为了验证这一假设，将成年正常体温的猫分别进行1小时的完全脑缺血，然后再灌注3小时和6小时。通过ATP诱导的生物发光对缺血后能量代谢的恢复进行成像，并在有和没有代谢恢复的区域测量局部组织pH值和电解质含量。在缺血后代谢活动恢复的区域，钠含量从338±17逐渐升至488±28 μmol/g蛋白质，钙含量从8.81±0.35升至18.24±0.97 μmol/g蛋白质。组织钾含量从761±12降至676±19 μmol/g蛋白质，镁含量从46.8±0.8降至36.3±1.1 μmol/g蛋白质。再灌注3小时和6小时后，组织pH值分别从7.09±0.04升至7.31±0.13和7.26±0.17。在没有代谢恢复的区域，电解质紊乱更为明显，pH值在短暂碱化后降至6.82±0.12。这些数据表明，在缺血后再灌注的后期，电解质稳态的渐进性紊乱会导致一种水肿前期状态，在预防缺血后延迟并发症时必须考虑到这一点。
