Cerebral metabolism in ischaemia: neurochemical basis for therapy.
Cerebral metabolism in ischaemia: neurochemical basis for therapy.
复制标题
缺血时的脑代谢：治疗的神经化学基础。
DOI：
10.1093/bja/57.1.47
复制
发表时间：
1985
影响因子：
9.8
通讯作者：
Wieloch,T
中科院分区：
文献类型：
--
作者：
Siesjö,BK;Wieloch,T
缺血性脑损伤的密度，如果发生，与脑缺血的严重程度和持续时间有关，这似乎是显而易见的假设。因此，只有缺血的持续时间才能决定缺血是否完全，即营养性血流是否完全停止。然而，由于几个原因，这些假设只是部分正确的。首先，有证据表明，除非脑血流量（CBF）降至某一阈值以下，否则即使缺血时间延长，神经元损伤也不会发生。其次，在某些情况下，短暂的缺血可能会造成出乎意料的广泛损害。例如，这可能发生在缺血后脑灌注压恢复不足的情况下，在这种情况下，缺血延长到再循环期。另一个继发性损伤的可能原因是缺血后癫痫发作。第三，现在很清楚，对于给定的缺血密度和持续时间，结果主要取决于对衰竭循环的脑代谢反应。因此，尽管缺血是一种脑循环疾病，但其对组织的影响是由细胞和亚细胞水平的神经化学事件决定的。
It seems obvious to assume that the density of ischaemic brain damage, if incurred, is related to both the severity and duration of cerebral ischaemia. As a corollary, only the duration of ischaemia should determine the outcome if ischaemia is complete, that is, if nutritional blood flow has ceased completely. However, such postulates are only partly true, for several reasons.First, evidence exists that unless cerebral blood flow (CBF) is decreased below a certain threshold value, neuronal damage will not develop, even if ischaemia is prolonged. Second, under certain circumstances, brief periods of ischaemia may cause surprisingly extensive damage. This may, for example, occur with inadequate restoration of postischaemic cerebral perfusion pressure, a condition in which ischaemia is extended into the recirculation period. Another possible cause of secondary damage is post-ischaemic seizure activity. Third, it is now clear that, for a given density and duration of ischaemia, the outcome depends critically on the cerebral metabolic reaction to the failing circulation. Thus, although ischaemia is a disease of the cerebral circulation, its impact on the tissue is determined by neurochemical events at the cellular and subcellular level.