摘要
目的对１０年来有关生物撞击机的研制及撞击伤发生机制的研究作一回顾和系统总结。方法系统整理以往的研究资料，就一些主要问题进行分析总结。结果（１）研制了ＢＩＭ－Ⅰ，Ⅱ，Ⅲ型生物撞击机，可以不同方式、不同速度对不同动物进行撞击实验。（２）建立光弹性模型，探讨了撞击后颅内应力分布过程，证明应力集中区与损伤部位一致。（３）证明循环内皮细胞计数和肌酸磷酸激酶（ＣＫ－ＢＢ）活性测定在脑损伤早期有诊断意义。（４）脑创伤后脑内出现炎症反应，多形核粒细胞（ＰＭＮ）浸入和聚集可能在脑继发损伤中起重要作用。（５）脑创伤后Ｃａ２＋内流增加，尼莫地平可阻止Ｃａ２＋内流，减轻神经细胞损伤。（６）丙酸睾丸酮能促进伤后面神经核内生长相关蛋白（ＧＡＰ４３）的合成，有助于面神经损伤后的修复与再生。（７）胸部撞击伤研究证明，胸部的黏性标准与胸部伤情的相关性最好，变形速度是影响伤情的主要因素。结论撞击伤是交通事故中最常见的伤类，原发损伤是应力传至体内和应力集中于损伤部位的结果。继发性损伤的机制十分复杂，如出现炎症反应，ＣＫ－ＢＢ等许多酶活性增强，细胞内Ｃａ２＋超载等，采取相应的拮抗剂可不同程度地减轻损伤。
Objective Looking back to and systemically summing up the research on the development of biomechanical machines and mechanism on impact injury in the past ten years. Methods Looking up previous technical data on research of impact injury, analyzing and summing up some main results. Results (1)Three types (Ⅰ,Ⅱ,Ⅲ) of biomechanical machines were developed. They may inflict impact injuries on different experimental animals with different ways and speeds. (2) Light-elastic model was established for the research on impacted cerebral injury. The stress distribution in the cranium after impact was observed. It indicted that the stress concentration area was consistent with the injured one. (3)Determination of circulating endothelial cells count and CK-BB activities were useful for the diagnosis of early cerebral injury. (4) There appeared inflammatory response after brain injury. Invasion and accumulation of PMN might play an important role in the development of cerebral secondary injury. (5)There occurred increase of cellular Ca 2+ inflow after injury. Nimodipine might prevent Ca 2+ inflow. (6) Testosterone propionate (TP) accelerated the synthesis of GAP 43 growth related protein and was of benefit to the repair and regeneration of injured facial nerves. (7) It indicated that viscous criterion was closely related to the severity of chest impact injury, and deformation velocity was the most important factor for injuring. Conclusions Impact injury is one of the commonest type of traffic injuries. Primary impact injury is the result of stress propagation and stress concentration in injured regions, while the mechanism of secondary injury is very complicated, such as inflammatory response, increase of activities in some enzymes, such as CK-BB, and overload of cellular Ca 2+ inflow, etc. The damage may be attenuated with some antagonists.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
1999年第4期293-297,共5页
Chinese Journal of Trauma
