Romodanov A P, Kop'ev O V, Pedachenko E G, Parkhomets V P, Vasil'eva I G
Zh Vopr Neirokhir Im N N Burdenko. 1990 Nov-Dec(6):10-3.
Advances in the study of the molecular mechanisms of the pathogenesis of closed craniocerebral trauma (CCCT) which was conducted on an experimental model, a clinical equivalent of CCCT, allow one to form a new view of the course of traumatic disease and its division into periods. The data obtained provide evidence that increase of the pathological process in the posttraumatic period is of a skipping and cascade character. The existence of such breaks makes it possible to distinguish periods with consideration for the pathogenetic essence of the pathological changes. 1. The period of intensified metabolic processes, "conflagration of metabolism". 2. The period of development of energy deficit in the nerve tissue. 3. The period of development of cell intoxication processes and secondary structural changes. 4. The period of formation of posttraumatic homeostasis (a) in the regimen of stable homeostasis, (b) in the regimen of stress and subsequent exhaustion of the activity of adaptation systems with the formation of late-term progressive sequelae.
在闭合性颅脑创伤(CCCT)发病机制分子机制研究方面取得的进展是基于实验模型进行的,该模型相当于CCCT的临床情况,这使人们能够对创伤性疾病的病程及其分期形成新的认识。所获得的数据表明,创伤后时期病理过程的加剧具有跳跃性和级联性。这种间断的存在使得根据病理变化的发病本质来区分不同时期成为可能。1. 代谢过程强化期,即“代谢燃烧”期。2. 神经组织能量 deficit 发展期。3. 细胞中毒过程及继发性结构变化发展期。4. 创伤后内环境稳定形成期(a)在稳定内环境稳定状态下,(b)在应激状态及随后适应系统活动耗竭并形成晚期进行性后遗症的状态下。