Stewart R H
Vet Clin North Am Equine Pract. 1987 Aug;3(2):371-7. doi: 10.1016/s0749-0739(17)30679-x.
Traumatic injury to the central nervous system causes immediate damage and sets in motion a complex series of pathophysiologic events that result in further neuronal injury. This secondary damage seems to be related to changes in blood flow and pressure on a systemic, regional, and microvascular level. Currently, there is evidence that these changes are, in part, mediated by endogenous opioids and arachidonic acid metabolites, namely thromboxane A2. Medical management is generally designed to intervene at one or more stages in this secondary cascade of events. Further research should lead us to better understanding of the mechanisms involved in trauma to the central nervous system and, subsequently, more specific and effective treatments.
中枢神经系统的创伤性损伤会造成即时损害，并引发一系列复杂的病理生理事件，进而导致进一步的神经元损伤。这种继发性损伤似乎与全身、局部和微血管水平上的血流及压力变化有关。目前，有证据表明这些变化部分是由内源性阿片类物质和花生四烯酸代谢产物（即血栓素A2）介导的。药物治疗通常旨在干预这一继发性事件级联反应的一个或多个阶段。进一步的研究应能使我们更好地理解中枢神经系统创伤所涉及的机制，从而带来更具针对性和更有效的治疗方法。
