The Effect of Nimodipine on Spinal Cord Blood Flow and Neuronal Function in Acute Spinal Cord Injured Cat.
- Author:
Yong Eun CHO
1
;
Young Soo KIM
Author Information
1. Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Spinal cord injury;
Cord blood flow;
Ischemia;
Nimodipine
- MeSH:
Animals;
Arterial Pressure;
Blood Pressure;
Calcium;
Calcium Channels;
Cats*;
Cell Death;
Epinephrine;
Evoked Potentials, Somatosensory;
Heart;
Hydrogen;
Hypotension;
Ions;
Ischemia;
Microcirculation;
Neurons*;
Nimodipine*;
Paralysis;
Spinal Cord Injuries;
Spinal Cord*
- From:Journal of Korean Neurosurgical Society
1993;22(1):109-122
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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 flow 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(injury level). T4, T12 by the hydrogen clearance technique and spinal somatosensory evoked potential was recorded at T4, T12 after injury at T6 level. The results of this study are summarized as follows: 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 prominent and prolonged in nimodipine and adrenaline treated group than nimodipine only treated group. It was thought that increased heart beat and cardiac 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 theraphy in spinal cord injury. 4) The improvements of spinal somatosensory evoked potential were more evident in nimodipine and adrenaline treated group. It 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.
