Marmarou A
Richard Roland Reynolds Neurosurgical Research Laboratories, Medical College of Virginia, Richmond.
J Neurotrauma. 1992 May;9 Suppl 2:S551-62.
Brain tissue acidosis is considered to play a role in the complex sequence of events following traumatic brain injury. This report reviews the experimental and clinical research conducted at the Medical College of Virginia to help clarify the extent of metabolic derangement that occurs and to evaluate the effect of treatment. Experimental injury models in ventilated animals showed that trauma produces a mild brain tissue acidosis that recovers within hours of injury. Hypoxia combined with trauma produces a relative ischemia and exacerbates the acidosis, which eventually resolves with resuscitation. Other studies revealed that CSF lactate measurements should be interpreted with caution, particularly in patients with subarachnoid hemorrhage. The results of two randomized clinical trials testing therapeutic effects of sustained hyperventilation and treatment with tromethamine (THAM) are discussed.
脑组织酸中毒被认为在创伤性脑损伤后的一系列复杂事件中起作用。本报告回顾了弗吉尼亚医学院进行的实验和临床研究，以帮助阐明所发生的代谢紊乱程度，并评估治疗效果。对通气动物的实验性损伤模型显示，创伤会导致轻度脑组织酸中毒，在损伤后数小时内恢复。缺氧与创伤相结合会导致相对缺血并加重酸中毒，最终随着复苏而缓解。其他研究表明，脑脊液乳酸测量结果应谨慎解读，尤其是对于蛛网膜下腔出血患者。文中讨论了两项测试持续过度通气和用三羟甲基氨基甲烷（THAM）治疗的治疗效果的随机临床试验结果。
