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Possible protective effect of endogenous opioids in traumatic brain injury
55
Citations
50
References
1990
Year
Opioid EpidemicTraumatic Brain InjuryPain MedicineExperimental PharmacologyBrain InjuryNeurologyAnesthetic PharmacologyHealth SciencesNeurological DeficitsPostoperative Pain ManagementNeuropharmacologyPharmacologyAnaesthetic AgentNeurophysiologyAddictionOpioid OverdoseFluid-percussion Brain InjuryConcussionAnesthesiaMedicineTrauma PainOpioid Use DisorderAnesthesiology
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.
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