Hayes R L, Lyeth B G, Jenkins L W, Zimmerman R, McIntosh T K, Clifton G L, Young H F
Richard Roland Reynolds Neurosurgical Research Laboratories, Department of Surgery, Medical College of Virginia/Virginia Commonwealth University, Richmond.
J Neurosurg. 1990 Feb;72(2):252-61. doi: 10.3171/jns.1990.72.2.0252.
Naloxone (0.1, 1.0, or 20.0 mg/kg), morphine (1.0 or 10.0 mg/kg), or saline was administered systemically intraperitoneally to rats 15 minutes prior to moderate fluid-percussion brain injury. The effects of the drugs were measured on systemic physiological, neurological, and body-weight responses to injury. The animals were trained prior to injury and were assessed for 10 days after injury on body-weight responses and neurological endpoints. Low doses of naloxone (0.1 or 1.0 mg/kg) significantly exacerbated neurological deficits associated with injury. Morphine (10.0 mg/kg) significantly reduced neurological deficits associated with injury. The drugs had no effect on neurological measures or body weight in sham-injured animals. Drug treatments did not significantly alter systemic physiological responses to injury. Data from these experiments suggest the involvement of endogenous opioids in at least some components of neurological deficits following traumatic brain injury and suggest the possibility that at least some classes of endogenous opioids may protect against long-term neurological deficits produced by fluid-percussion injury to the rat.
在对大鼠进行中度液体冲击性脑损伤前15分钟，经腹腔向其全身注射纳洛酮（0.1、1.0或20.0毫克/千克）、吗啡（1.0或10.0毫克/千克）或生理盐水。测量这些药物对损伤的全身生理、神经和体重反应的影响。在损伤前对动物进行训练，并在损伤后10天评估其体重反应和神经学指标。低剂量纳洛酮（0.1或1.0毫克/千克）显著加剧了与损伤相关的神经功能缺损。吗啡（10.0毫克/千克）显著减轻了与损伤相关的神经功能缺损。这些药物对假损伤动物的神经学指标或体重没有影响。药物治疗并未显著改变对损伤的全身生理反应。这些实验数据表明，内源性阿片类物质至少参与了创伤性脑损伤后神经功能缺损的某些成分，并表明至少某些种类的内源性阿片类物质可能对液体冲击性损伤大鼠产生的长期神经功能缺损具有保护作用。
