Comparison of Naloxone and Thyrotropin-Releasing Hormone in the Treatment of Experimental Spinal Injury: Endogenous Opioids and Experimental Spinal Injury

摘要

Traumatic injuries to the central nervous system (including spinal cord and brain) cause neurologic impairment not only by directly interrupting neuronal pathways but by initiating a series of pathophysiologic changes which lead to progressive ischemic damage. The secondary ischemic changes resulting from experimental spinal trauma are potentially reversible and result, in part, from a reduction of spinal cord blood flow related to the release of endogenous opioids. The opiate receptor antagonist naloxone improves both spinal cord blood flow and neurological outcome following experimental traumatic spinal cord injury in the cat. Thyrotropin-releasing hormone (TRH), which acts in part as a physiologic antagonist of endogenous opioid systems, also significantly improves blood flow and neurological recovery after experimental spinal injury. The effects of TRH and naloxone against corticosteroids and saline-treated controls have been compared. Both naloxone and TRH proved significantly superior to either saline or high-dose corticosteroids in improving long-term, functional neurological recovery in the cat. THR proved significantly better than naloxone in this regard. The therapeutic effects of THR were clearly dose-related. Because of the increased expenses for cats, particularly the pathogen-free variety, an alternative traumatic injury model in the rat has been developed.