Donkin James J, Turner Renee J, Hassan Islam, Vink Robert
Discipline of Pathology, University of Adelaide, Adelaide, South Australia, Australia.
Prog Brain Res. 2007;161:97-109. doi: 10.1016/S0079-6123(06)61007-8.
Recent evidence has suggested that neuropeptides, and in particular substance P (SP), may play a critical role in the development of morphological injury and functional deficits following acute insults to the brain. Few studies, however, have examined the role of SP, and more generally, neurogenic inflammation, in the pathophysiology of traumatic brain injury and stroke. Those studies that have been reported suggest that SP is released following injury to the CNS and facilitates the increased permeability of the blood brain barrier, the development of vasogenic edema and the subsequent cell death and functional deficits that are associated with these events. Inhibition of the SP activity, either through inhibition of the neuropeptide release or the use of SP receptor antagonists, have consistently resulted in profound decreases in edema formation and marked improvements in functional outcome. The current review summarizes the role of SP in acute brain injury, focussing on its properties as a neurotransmitter and the potential for SP to adversely affect outcome.
最近有证据表明，神经肽，尤其是P物质（SP），可能在急性脑损伤后形态学损伤和功能缺陷的发展中起关键作用。然而，很少有研究探讨SP以及更普遍的神经源性炎症在创伤性脑损伤和中风病理生理学中的作用。已报道的那些研究表明，中枢神经系统损伤后会释放SP，并促进血脑屏障通透性增加、血管源性水肿的发展以及随后与这些事件相关的细胞死亡和功能缺陷。通过抑制神经肽释放或使用SP受体拮抗剂来抑制SP活性，始终会导致水肿形成显著减少和功能结局明显改善。本综述总结了SP在急性脑损伤中的作用，重点关注其作为神经递质的特性以及SP对结局产生不利影响的可能性。
