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KMID : 0359819930220010109
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Journal of Korean Neurosurgical Society
1993 Volume.22 No. 1 p.109 ~ p.122
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The Effect of Nimodipine on Spinal Cord Blood Flow and Neuronal Function in Acute Spinal Cord Injured Cat
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Abstract
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Spinal cord injury causes immediate neuronal dysfunction and remained paralysis in life without clinical improvement. The spinal cord injury is caused by initial mechanical damage and secondary neuronal damage. The exact mechanisms of secondary
neuronal
damage are still unknown and their treatment is obscure even though many studies about them. The vascular change after injury is supported widely as a mechanism of secondary neuronal damage which causes decreased microcirculation and cord
ischemia.
There is considerable evidence that Ca++ ions play a key role in the pathogenesis of posttraumatic ischemia and Ca++ ion influx promotes cellular dysfuction and cell death. So calcium antagonist is considered that it can improve spinal cord blood
fiow
and restore impaired neuronal function.
In this report, the effects of calcium channel blocker, nimodipine on spinal cord blood flow and spinal somatosensory evoked potential were measured and it was compared with vehicle group in 400 g-cm cord injured cat. And the effects of
nimodipine
were
compared between nimodipine and adrenaline treated group of which mean systolic blood pressure was maintained above 100mmHg and nimodipine only treated group. Spinal cord blood flow was measured at T6 (mjury level) T4, T12 by the hydrogen
clearance
technique and spirral somatosensory evoked potential was recorded at T4, T12 after injury at T6 level.
@ES The results of this study are summarized as follows :
@EN 1) The spinal cord blood flow was decreased abruptly just after spinal cord injury and it decreased progressively.
2) In nimodipine treated group, there was a improvement of spinal cord blood flow inspite of decreased mean systemic arterial pressure. It might be thought that the vasodilatory effect of nimodipine was more potent in spinal vasculature than in
systemic peripheral vessels.
3) The increased spinal cord blood flow was more prominant and prolonged in nimodipine and adrenaline treated group than nimodipine only treated group. It was thought that increased heart beat and carciac contractility by adrenaline counteracted
systemic hypotension which resulted from vasodilatory effect of nimodipine. It suggests that maintenance of mean systemic arterial pressure is important during nimodipine teraphy 8n spinal cord injury.
4) The improvements of spinal somatosensory evoked potential were more evident in nimodipine and adrenaline treated group. In might be caused by spinal cord blood flow improvement.
From the above result it is speculated that the calcium channel blocker nimodipine can improve spinal blood flow and impaird neuronal function in spinal cord injury.
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KEYWORD
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