Spinal cord ischemia may develop into
paraplegia in some cases during operation of the thoracoabdominal aorta. This is attributable to the vulnerability of spinal motor neurons to
ischemia. In this study,
iloprost was used as an agent to decrease the severity of
ischemia and
reperfusion injury to the spinal cord motor neurons. Twenty-one rabbits were randomized into three groups of seven animals each: group A (
iloprost not administered), group B (25 ng/kg per minute
iloprost), and group S (
sham-operated). The
spinal cord ischemia model was created by a 15-min occlusion of the aorta just caudal to the renal artery with a balloon
catheter. Administration of
iloprost began 10 min before occlusion of the aorta, and continued thereafter for 60 min. The pre- and postocclusion arterial pressure and heart rate recordings, results of blood gas analyses, and hematocrit and
glucose levels were recorded. The spinal cords were removed after 8-h monitoring of neurologic function. Viable and nonviable motor neurons in the anterior horn of the spinal cord were counted under light microscopy. Any significant alteration in hemodynamics, blood
gases, and other physiologic parameters could not be detected within the groups.
Iloprost had a moderately hypotensive effect. Neurologic function in terms of Johnson scoring was significantly better in the
iloprost group (P<0.05). The number of viable cells was higher, whereas the number of nonviable cells was lower in
iloprost group, when compared with the control group (P<0.05). Higher numbers of viable motor neurons were consistent with the neurological findings. As a result of this study we concluded that
iloprost infused during clamping of the aorta mitigates the
spinal cord injury due to
ischemia and reperfusion, and has a significant protective effect.