Eleff S M, Maruki Y, Monsein L H, Traystman R J, Bryan R N, Koehler R C
Department of Anesthesiology, Johns Hopkins Medical Institutions, Baltimore, Md.
Stroke. 1991 Feb;22(2):233-41. doi: 10.1161/01.str.22.2.233.
We tested the hypotheses that with the onset of cerebral ischemia, massive cellular sodium influx does not occur until adenosine triphosphate is fully depleted and that on reperfusion, neuronal sodium efflux does not occur until adenosine triphosphate is fully restored. We examined the temporal relationships among transcellular sodium, energy metabolism, and intracellular pH with sodium and phosphorus magnetic resonance spectroscopy in a new, hemodynamically stable, brain stem-sparing model of reversible, complete cerebral ischemia in eight anesthetized dogs. Inflation of a neck tourniquet after placement of glue at the tip of the basilar artery resulted in decreased blood flow to the cerebrum from 29 +/- 5 to 0.3 +/- 0.5 ml/min/100 g. Medullary blood flow was not significantly affected, and arterial blood pressure was unchanged. Sodium signal intensity decreased and did not lag behind the fall in adenosine triphosphate. After 12 minutes of ischemia, reperfusion resulted in a more rapid recovery of sodium intensity (12.4 +/- 4.8 minutes) than either adenosine triphosphate (16.5 +/- 3.7 minutes) or intracellular pH (38.9 +/- 1.8 minutes). Because intracellular sodium has a weaker signal than extracellular sodium, the decreased sodium intensity is interpreted as sodium influx and indicates that sodium influx does not require full depletion of adenosine triphosphate. Rapid recovery of sodium intensity during early reperfusion may represent sodium efflux, although increased plasma volume and sodium uptake from plasma may also contribute. If our interpretation of the sodium signal is correct, delayed recovery of adenosine triphosphate may be due to the utilization of adenosine triphosphate for the restoration of transcellular sodium gradient.
在脑缺血发作时，大量细胞内钠流入直到三磷酸腺苷完全耗尽才会发生；而在再灌注时，神经元钠流出直到三磷酸腺苷完全恢复才会发生。我们在一种新的、血流动力学稳定的、保留脑干的可逆性完全脑缺血模型中，对八只麻醉犬进行了钠和磷磁共振波谱分析，以研究跨细胞钠、能量代谢和细胞内pH之间的时间关系。在基底动脉尖端放置胶水后，充气颈部止血带导致大脑血流量从29±5降至0.3±0.5 ml/min/100 g。延髓血流量未受显著影响，动脉血压未变。钠信号强度下降，且不滞后于三磷酸腺苷的下降。缺血12分钟后，再灌注导致钠强度的恢复比三磷酸腺苷（16.5±3.7分钟）或细胞内pH（38.9±1.8分钟）更快（12.4±4.8分钟）。由于细胞内钠的信号比细胞外钠弱，钠强度的下降被解释为钠流入，这表明钠流入并不需要三磷酸腺苷完全耗尽。早期再灌注期间钠强度的快速恢复可能代表钠流出，尽管血浆容量增加和从血浆中摄取钠也可能起作用。如果我们对钠信号的解释正确，三磷酸腺苷的延迟恢复可能是由于三磷酸腺苷用于恢复跨细胞钠梯度。
