Effect of sympathectomy on extracellular potassium ionic activity and blood flow in experimental spinal cord contusion

Abstract

Contusion injury of cat spinal cords causes a rapid loss of evoked potential transmission across the impact site. We have previously shown that this initial loss of action potential conduction is transient and recovers partially within an hour after injury, often diminishing 2–4 h later when white matter blood flow decreases from pre-injury levels of < 12ml/100 g/min to < 6ml/100 g/min. The causes of the initial and delayed loss of evoked potentials are not well understood. Although K + release has been suggested to cause action potential blockade in spinal injury neither the levels nor time course of K + shifts have been shown. We used K +-selective microelectrodes to record extracellular K + activity in contused thoracic spinal white matter, comparing K + changes with loss and recovery of somatosensory-evoked potentials and local blood flow measured by the hydrogen clearance technique. If K + plays a role in the initial evoked potential loss, extracellular K + should rapidly increase to levels sufficient to block action potential conduction and clear with a time course relating to evoked potentials recovery. The paravertebral sympathetic ganglia were ablated in some cats, a procedure which we have shown to prevent post-traumatic ischemia and the delayed loss in evoked potentials. If ischemia causes the delayed loss of evoked potentials by increase in extracellular K +, we should observe this is untreated injured cats but not in sympathectomized cats. In 5 cats subjected to 400 g·cm contusions, extracellular K + in the thoracic lateral columns rose rapidly from normal pre-injury levels (3–4 mM) to a mean of 54 mM, clearing with an exponential half-time of 45 min. In 5 sympathectomized cats, extracellular K + rose to 47 mM, clearing with a half-time of 35 min. In 5 cats that were not injured, extracellular K + and blood flow did not change significantly. In all injured cats, evoked potentials were rapidly lost after contusion but partially recovered at 1–2 h with normalization of extracellular K +. Extracellular K + did not again transcend 15 mM even after blood flow below 6 ml/100 g/min. Blood flow fell below 6 ml/100 g/min only after extracellular K + returned to < 15mM. The magnitude and time course of the extracellular K + changes can thus account for the pattern of evoked potential loss and recovery in spinal contusion. However, the delayed loss of evoked potentials cannot be related to increases in extracellular K +. With exception of a slightly faster K + clearance rate, we found no dramatic differences in the extracellular K + behavior between sympathectomized and untreated cats. The finding that blood flow did not fall until extracellular K + returned below 15 mM suggests that the ionic derangements may prevent vasoconstriction for the first 1–2 h after injury.