Orfeo T, Doherty J M, Adey G, Penar P L, Shatos M A
Department of Surgery, University of Vermont College of Medicine, Burlington.
J Trauma. 1994 Sep;37(3):347-57. doi: 10.1097/00005373-199409000-00003.
The delivery of a blow to the head represents a transfer of energy, part of which manifests itself as a short-lived pressure change within the skull. An in vitro model was developed to test whether cerebral endothelial cell hemostatic function is altered with exposure to this type of pressure event. Human cerebral microvascular endothelium (HCME) cells were subjected to rapid (2-5 msec) changes in pressure (delta atmosphere = 1.2-10), the sublethal range defined (delta atmosphere < or = 6.5), and the nonthrombogenic status of sublethally percussed HCME cells assessed using the adherence of alpha-thrombin activated platelets as an indicator. The HCME cells had lost their normal capacity to suppress adherence of activated platelets when evaluated 1 hour or 24 hours after percussion. Adherence of activated platelets to percussed HCME cells was blocked by the addition of PGI2, an inhibitor of platelet adherence, when evaluated at 1 hour but not 24 hours after percussion, indicating that percussed HCME cells were undergoing further derangement of their nonthrombogenic mechanisms. Percussed HCME cells cultured for 24 hours in medium containing scavengers of oxygen free radicals recovered their capacity to block platelet adherence. We conclude that sublethal percussion immediately compromises the nonthrombogenic character of HCME cells and initiates the development of a persisting prothrombotic state in HCME cells. This derangement appears linked to increased production of reactive oxygen species by percussed HCME cells.
头部受到撞击会导致能量转移，其中一部分能量会在颅骨内表现为短暂的压力变化。我们建立了一个体外模型，以测试暴露于这种压力事件时，脑内皮细胞的止血功能是否会发生改变。将人脑血管内皮（HCME）细胞置于压力快速（2 - 5毫秒）变化（气压变化 = 1.2 - 10）的环境中，确定亚致死范围（气压变化≤6.5），并以α-凝血酶激活的血小板的黏附作为指标，评估亚致死撞击后HCME细胞的非血栓形成状态。在撞击后1小时或24小时进行评估时，HCME细胞失去了抑制活化血小板黏附的正常能力。在撞击后1小时进行评估时，添加血小板黏附抑制剂前列环素（PGI2）可阻止活化血小板与撞击后的HCME细胞黏附，但在撞击后24小时进行评估时则无效，这表明撞击后的HCME细胞的非血栓形成机制正在进一步紊乱。在含有氧自由基清除剂的培养基中培养24小时的撞击后HCME细胞恢复了阻止血小板黏附的能力。我们得出结论，亚致死撞击会立即损害HCME细胞的非血栓形成特性，并引发HCME细胞持续的促血栓形成状态的发展。这种紊乱似乎与撞击后的HCME细胞产生活性氧增加有关。
