The neuroprotective effect of trimetazidine (TMZ) was tested prospectively
in a rabbit spinal cord ischemia model. Ischemia was induced by clamping th
e aorta just distal to the left renal artery and proximal aortic bifurcatio
n for 20 min. Twenty-five male New Zealand white rabbits were randomized as
follows: TMZ group (n = 10) receiving 3 mg/kg trimetazidine intravenously
before the occlusion of the aorta; control group undergoing occlusion but r
eceiving no pharmacologic intervention (n = 10); sham-operation group (n =
5) subjected to operative dissections without aortic occlusion. Physiologic
al parameters and somatosensory evoked potentials (SEP) were monitored in a
nimals before the ischemia, during the ischemia and in the 1st, 15th and 60
th min of reperfusion. Neurologic status was assessed 24 and 48 h after the
operation. The spinal cord, abdominal aorta, and its branches were process
ed for histopathologic examinations 48 h after the operation. At the end of
the ischemic period, the average N1-P1 amplitude was reduced to 22% of the
baseline in all ischemic animals. This was followed by a gradual return to
90 +/- 2% of the initial amplitude in the TMZ group and 81 +/- 2% in the c
ontrol group (P < 0.05) after 60 min of reperfusion. The average motor func
tion score was significantly higher in the TMZ group than the control group
(3.7 +/- 0.5 vs 3.1 +/- 0.6 at 24 and 3.5 +/- 0.7 vs 2.9 +/- 0.6 at 48 h;
P < 0.05). Histologic observations were clearly correlated with the neurolo
gic findings. The results suggest that trimetazidine reduces spinal cord in
jury during thoracoabdominal aortic operations and may have therapeutic uti
lity during high risk operations.