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Endorphin-parasympathetic interactions in spinal shock

A I Faden, T P Jacobs, J W Holaday

    Journal of the Autonomic Nervous System
    |October 1, 1980
    PubMed

    Insights

    Naloxone, an opiate antagonist, reverses hypotension after spinal cord injury by interacting with central parasympathetic pathways. This challenges traditional views and suggests therapeutic potential for spinal cord injury management.

    Area of Science:

    • Neuroscience
    • Cardiovascular Physiology
    • Pharmacology

    Background:

    • Spinal cord transection causes hypotension, traditionally attributed to sympathetic pathway interruption.
    • Opiate receptors in the central nervous system are implicated in this hypotension.

    Purpose of the Study:

    • To investigate the role of the parasympathetic system in naloxone's effect on post-spinal transection hypotension.
    • To explore the interaction between endorphin systems and central parasympathetic centers in spinal shock.

    Main Methods:

    • Studies conducted on rats and cats following spinal cord transection.
    • Administration of naloxone, vagotomy, atropine, and peripherally acting methyl-atropine.

    Main Results:

    • Vagotomy or atropine prevented naloxone from reversing spinal transection-induced hypotension.
    • Peripherally acting methyl-atropine blocked the cardiovascular effects of centrally administered naloxone.
    • Findings suggest a cholinergic vagal efferent pathway mediates cardiovascular depression in spinal shock.

    Conclusions:

    • Endorphin systems interact with central parasympathetic centers, leading to cardiovascular depression via vagal pathways in spinal shock.
    • Naloxone's efficacy challenges the sole reliance on interrupted sympathetic pathways to explain spinal hypotension.
    • Naloxone shows potential therapeutic benefits for managing spinal cord injury-related cardiovascular dysfunction.

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