Hall E D
Central Nervous System Diseases Research Unit, Upjohn Company, Kalamazoo, Michigan 49001.
J Emerg Med. 1993;11 Suppl 1:31-6.
Lipid peroxidation is believed to be a major cause of posttraumatic cell damage and death. In patients with head and spinal injuries, this process is believed to contribute significantly to the development of permanent neurological dysfunction. Lipid peroxidation can be inhibited by pharmacological agents such as the antioxidants methylprednisolone and tirilazad mesylate. Animal models of head and spinal cord injuries have been used to investigate the physiological bases of the effects of antioxidants. These studies have found that antioxidants are capable of inhibiting posttraumatic events such as edema, metabolic dysfunction, and ischemia, indicating that lipid peroxidation participates in all of these processes. Early treatment appears to be essential for antioxidant-mediated neuroprotection. The multiple levels at which lipid peroxidation causes damage suggest that pharmacological modulation of this process may be beneficial in the treatment of a wide range of neural injuries.
脂质过氧化被认为是创伤后细胞损伤和死亡的主要原因。在头部和脊髓损伤患者中，这一过程被认为对永久性神经功能障碍的发展有显著影响。脂质过氧化可被抗氧化剂甲泼尼龙和甲磺酰替拉扎特等药物抑制。头部和脊髓损伤的动物模型已被用于研究抗氧化剂作用的生理基础。这些研究发现，抗氧化剂能够抑制创伤后事件，如水肿、代谢功能障碍和局部缺血，表明脂质过氧化参与了所有这些过程。早期治疗似乎对抗氧化剂介导的神经保护至关重要。脂质过氧化造成损伤的多个层面表明，对这一过程进行药物调节可能对治疗多种神经损伤有益。
