Johnson T D
Department of Anesthesiology, Baylor College of Medicine, Houston, TX, USA.
Prog Drug Res. 1998;50:193-258. doi: 10.1007/978-3-0348-8833-2_5.
It has been well established that alterations in polyamine metabolism are associated with animal models of global ischemia. Recently, this has been extended to include models of focal ischemia and traumatic brain injury. There is much evidence to support the idea that polyamines may play a multifaceted detrimental role following ischemia reperfusion. Due to the deficit of knowledge about their physiology in the CNS, the link between ischemia-induced alterations in polyamine metabolism and neuronal injury remains to be substantiated. With the recent revelation that polyamines are major intracellular modulators of inward rectifier potassium channels and certain types of NMDA and AMPA receptors, the long wait for the physiologic relevance of these ubiquitous compounds may be in sight. Therefore, it is now conceivable that the alterations in polyamines could have major effects on ion homeostasis in the CNS, especially potassium, and thus account for the observed injury after cerebral ischemia.
多胺代谢的改变与全脑缺血的动物模型相关，这一点已经得到充分证实。最近，这一关联已扩展到包括局灶性缺血和创伤性脑损伤模型。有大量证据支持多胺在缺血再灌注后可能发挥多方面有害作用的观点。由于对其在中枢神经系统中的生理学认识不足，缺血诱导的多胺代谢改变与神经元损伤之间的联系仍有待证实。随着最近发现多胺是内向整流钾通道以及某些类型的NMDA和AMPA受体的主要细胞内调节剂，对这些普遍存在的化合物生理相关性的漫长等待可能即将结束。因此，现在可以想象，多胺的改变可能对中枢神经系统中的离子稳态，尤其是钾离子稳态产生重大影响，从而解释脑缺血后观察到的损伤。
