Lj role of sodium in the pathophysiology of secondary spinal cord injury

Michael G. Fehlings, Sandeep Agrawal

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Study Design.Experimental study using an in vitro model of compressive injury to isolated adult rat dorsal column axons Objectives. To examine the role of extracellular Na+ (Na+) in mediating secondary injury to spinal cord axons after compressive trauma. The mechanisms of intracellular sodium entry were examined using ion substitution techniques and pharmacologic blockers.Summary of Background Data. There is evidence that intracellular Na+ entry potentiates hypoxicischemic cell death by causing cytotoxic cell swelling, intracellular acidosis, and gating of Ca++ entry through reverse activation of the Na+-Ca++ exchanger. In the present study, we have examined the role of Na+e in the pathophysiology of spinal cord injury.Methods. Dorsal column segments isolated from the thoracic cord of adult rats (n = 40) were pinned in a recording chamber and superfused with oxygenated Ringer's solution. Extracellular field potentials were recorded from glass microelectrodes (150 mmol KCI5-10 mol). Injury was accomplished in vitro by compression with a modified aneurysm clip (closing force,2 g) for 15 seconds. The effect of zero Na+e (equimolar substitution with NMDG+), the Na+-H+ exchange blocker amiloride, the Na+ channel blocker procaine, and the Na+-Ca++ exchanger blocker benzamil on CAP recovery after compressive injury were assessed.Results. Pretreatment with zero Na+, amiloride and procaine conferred significant neuroprotection (P <0.05). In contrast, the NCE blocker benzamil was ineffective in attenuation secondary injury.Conclusions. Reduction of extracellular Na+, inhibition of the Na+-H+ exchanger or blockade of voltage gated Na+ channels is neuroprotective after spinal cord injury. The mechanism of Na+-associated cytotocity does not involve reverse gating of the Na+-Ca++ exchanger.

Original languageEnglish (US)
Pages (from-to)2187-2191
Number of pages5
JournalSpine
Volume20
Issue number20
StatePublished - Oct 1995

Fingerprint

Spinal Cord Injuries
Sodium
Wounds and Injuries
Procaine
Amiloride
Axons
Sodium-Hydrogen Antiporter
Microelectrodes
Acidosis
Surgical Instruments
Aneurysm
Glass
Spinal Cord
Cell Death
Ions
benzamil
In Vitro Techniques

Keywords

  • Axons
  • Ischemia
  • Neuroprotection
  • Sodium-calcium exchanger

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine
  • Clinical Neurology

Cite this

Lj role of sodium in the pathophysiology of secondary spinal cord injury. / Fehlings, Michael G.; Agrawal, Sandeep.

In: Spine, Vol. 20, No. 20, 10.1995, p. 2187-2191.

Research output: Contribution to journalArticle

Fehlings, Michael G. ; Agrawal, Sandeep. / Lj role of sodium in the pathophysiology of secondary spinal cord injury. In: Spine. 1995 ; Vol. 20, No. 20. pp. 2187-2191.
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