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Related Experiment Videos

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
    Summary
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    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:

    Related Experiment Videos

  • 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.