[Spinal cord protection and opioids]

Masui. 2007 Mar;56(3):298-304.
[Article in Japanese]

Abstract

Opioids, when administered in large doses, were reported to produce brain damage primarily in limbic system and association areas in animals. We recently found the result that intrathecal (IT) morphine after a short interval of aortic occlusion in the rodent model induced transient spastic paraparesis via opioid receptor-coupled effects in the spinal cord. Histopathological analysis revealed the possibility that IT morphine could induce degeneration of spinal ventral neurons even after a short lasting of spinal cord ischaemia in rats, and this degeneration was associated with the activation of spinal N-methyl-D-aspartate receptors by elevation of glutamate release in cerebrospinal fluid after IT morphine. Therefore, we would like to emphasize that all anesthesiologists should be aware of the possibility of morphine-induced paraplegia after thoracic aortic surgery and that we should carefully select appropriate analgesic agents from the several available opioids for these patients.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Analgesics, Opioid / administration & dosage*
  • Analgesics, Opioid / adverse effects*
  • Animals
  • Anterior Horn Cells / drug effects
  • Anterior Horn Cells / pathology
  • Dose-Response Relationship, Drug
  • Fentanyl / administration & dosage
  • Fentanyl / adverse effects
  • Glutamic Acid / cerebrospinal fluid
  • Humans
  • Morphine / administration & dosage
  • Morphine / adverse effects
  • Naloxone / administration & dosage
  • Nerve Degeneration / chemically induced
  • Paraparesis, Spastic / chemically induced
  • Rats
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Spinal Cord Ischemia / chemically induced*
  • Spinal Cord Ischemia / prevention & control*
  • Thoracic Surgical Procedures

Substances

  • Analgesics, Opioid
  • Receptors, N-Methyl-D-Aspartate
  • Naloxone
  • Glutamic Acid
  • Morphine
  • Fentanyl