Because of its potential for augmentation of blood flow and protection of n
eurons after neurological insult, nimodipine has been investigated as a tre
atment of spinal cord injury (SCI), The results have been inconsistent, pos
sibly because of poor delivery of nimodipine to the injured spinal cord. Th
e following study was designed to determine the delivery of nimodipine to t
he injured spinal cord. It was also hoped that information about the tempor
al and spatial pattern of binding of nimodipine after SCI might further elu
cidate the relationship between calcium channel activation and injury. Four
teen female Wistar rats were divided into three groups: control (n = 3), 30
min post-SCI (n = 6); and 4 h post-SCI (n = 5), The injury was produced by
acute clip compression for 1 min at T1, [H-3]Nimodipine was administered 5
min after laminectomy in the control group, and at the above-specified tim
es after injury in the SCI groups. The drug was then allowed to equilibrate
for 30 min before the animals were killed. The spatial patterns and concen
trations of [H-3]nimodipine in various segments of the spinal cord were aut
oradiographically determined. The highest concentrations of [H-3]nimodipine
were at the injury site after SCI, Also, the mean [H-3]nimodipine concentr
ations in all sites in each animal were higher in the injury groups than in
the control group (p < 0.05), This study indicates that delivery of this a
gent to the injured cord is possible, and provides evidence of widespread C
a2+ channel activation in the first 4 h after injury.