Yoshida K, Marmarou A
Division of Neurosurgery, Medical College of Virginia, Richmond.
J Neurosurg. 1991 Jan;74(1):87-96. doi: 10.3171/jns.1991.74.1.0087.
The metabolic brain acidosis after trauma has been thought to be harmful and to contribute to neurological deterioration. Amelioration of the brain acidosis either by systemic buffering agents or by hyperventilation has been proposed as a method of treatment. The objective of this study was to explore with magnetic resonance (MR) spectroscopy the metabolic changes in brain that occur with the use of hyperventilation, THAM (tromethamine; tris[hydroxymethyl]aminomethane), and a combination (THAM and hyperventilation) therapy in experimental fluid-percussion injury. Brain lactate, brain pH, inorganic phosphate (Pi), and adenosine triphosphate levels were measured by 1H and 31P MR spectroscopy. Arterial and cerebrovenous lactate and water content in brain tissue was determined in 29 cats using the specific gravimetric technique. Following injury, the phosphocreatine (PCr)/Pi ratio, which is an index of cerebral energy depletion, decreased to 76% in four untreated animals, to 79% in 11 THAM-treated animals, to 68% in seven animals receiving hyperventilation, and to 66% in seven animals with combination THAM and hyperventilation therapy. The PCr/Pi ratio returned to a normal level in 8 hours in animals treated with THAM and THAM in combination with hyperventilation. The brain lactate index increased to 157% in the hyperventilation group after trauma. In cats receiving THAM plus hyperventilation, the brain lactate index was reduced to 142%, while the minimum rise of 126% was associated with treatment of THAM alone. In the THAM-treatment and combination-treatment groups, the water content of the white and gray matter was significantly decreased compared with that in untreated cat brains. Prolonged hyperventilation provided relative ischemia in brain tissue and promoted more production of brain lactate, no recovery of the PCr/Pi ratio, and no decrease in brain edema. On the other hand, administration of THAM decreased production of brain lactate and brain edema and promoted the recovery of cerebral energy dysfunction. It was found that THAM ameliorates the deleterious effects of hyperventilation by minimizing energy disturbance and that it also decreases brain edema. The authors conclude that THAM may be effective in reducing brain tissue acidosis and helpful as a metabolic stabilizing agent following severe head injury.
创伤后的代谢性脑酸中毒被认为是有害的，并会导致神经功能恶化。有人提出通过全身缓冲剂或过度通气来改善脑酸中毒，作为一种治疗方法。本研究的目的是利用磁共振（MR）波谱技术，探讨在实验性液体冲击伤中，过度通气、THAM（三羟甲基氨基甲烷）以及联合治疗（THAM与过度通气）对脑代谢变化的影响。通过1H和31P MR波谱测量脑乳酸、脑pH值、无机磷酸盐（Pi）和三磷酸腺苷水平。采用特定的重量法测定了29只猫的动脉血和脑静脉血乳酸以及脑组织含水量。受伤后，作为脑能量消耗指标的磷酸肌酸（PCr）/Pi比值，在4只未治疗的动物中降至76%，在11只接受THAM治疗的动物中降至79%，在7只接受过度通气的动物中降至68%，在7只接受THAM与过度通气联合治疗的动物中降至66%。接受THAM治疗以及THAM与过度通气联合治疗的动物，其PCr/Pi比值在8小时内恢复到正常水平。创伤后，过度通气组的脑乳酸指数增加到157%。在接受THAM加过度通气的猫中，脑乳酸指数降至142%，而单独使用THAM治疗时，脑乳酸指数最低升至126%。在THAM治疗组和联合治疗组中，与未治疗的猫脑相比，白质和灰质的含水量显著降低。长时间过度通气会导致脑组织相对缺血，促进脑乳酸生成增加，PCr/Pi比值无法恢复，脑水肿也无减轻。另一方面，给予THAM可减少脑乳酸生成和脑水肿，并促进脑能量功能障碍的恢复。研究发现，THAM通过最小化能量紊乱来减轻过度通气的有害影响，并且还能减轻脑水肿。作者得出结论，THAM可能有效减轻脑组织酸中毒，作为重度颅脑损伤后的代谢稳定药物可能有益。
