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Effects of vascular endothelial growth factor on ischemic spinal cord injury caused by aortic cross-clamping in rabbits.
Journal of Surgical Research 2009 January
BACKGROUND: Spinal cord injury remains a devastating complication of thoracic and thoracoabdominal aortic operations. We aim to investigate neuro-protective role of vascular endothelial growth factor (VEGF) administered to rabbits after occlusion against ischemia-reperfusion (I/R) injury.
MATERIALS AND METHODS: Occlusion of the abdominal aorta was applied to adult rabbits, followed by removal of aortic clamp and reperfusion. The abdominal aortas of New Zealand White albino rabbits were occluded for 30 min. Experimental groups were as follows: control group (sham operation group, n = 7), I/R group (n = 9) undergoing occlusion but receiving no pharmacologic intervention, and VEGF-treated group (n = 7) receiving 0.8 microg/kg VEGF intravenously after occlusion. Neurological status was assessed at 6, 24, and 48 h after the operation. All animals were killed at 48 h after the operation. Spinal cords were harvested for histopathologic and biochemical analyses.
RESULTS: According to Tarlov's scale, neurological status of the rabbits at postoperative h 48 was better in the VEGF-treated group compared to the I/R group (P < 0.05). Decreased tissue and serum malondialdehyde levels and increased tissue and serum glutathione levels were observed in VEGF-treated group (P < 0.05). In the same group tissue and serum nitrate levels were decreased (P < 0.05). Histopathologic analyses demonstrated typical morphological changes characteristic of necrosis in the I/R group. VEGF attenuated ischemia-induced necrosis.
CONCLUSIONS: This is the first study that shows the effects of VEGF administered after occlusion on induced oxidative damage to injured spinal cords. VEGF administration may significantly reduce the incidence of spinal cord injury following temporary aortic occlusion.
MATERIALS AND METHODS: Occlusion of the abdominal aorta was applied to adult rabbits, followed by removal of aortic clamp and reperfusion. The abdominal aortas of New Zealand White albino rabbits were occluded for 30 min. Experimental groups were as follows: control group (sham operation group, n = 7), I/R group (n = 9) undergoing occlusion but receiving no pharmacologic intervention, and VEGF-treated group (n = 7) receiving 0.8 microg/kg VEGF intravenously after occlusion. Neurological status was assessed at 6, 24, and 48 h after the operation. All animals were killed at 48 h after the operation. Spinal cords were harvested for histopathologic and biochemical analyses.
RESULTS: According to Tarlov's scale, neurological status of the rabbits at postoperative h 48 was better in the VEGF-treated group compared to the I/R group (P < 0.05). Decreased tissue and serum malondialdehyde levels and increased tissue and serum glutathione levels were observed in VEGF-treated group (P < 0.05). In the same group tissue and serum nitrate levels were decreased (P < 0.05). Histopathologic analyses demonstrated typical morphological changes characteristic of necrosis in the I/R group. VEGF attenuated ischemia-induced necrosis.
CONCLUSIONS: This is the first study that shows the effects of VEGF administered after occlusion on induced oxidative damage to injured spinal cords. VEGF administration may significantly reduce the incidence of spinal cord injury following temporary aortic occlusion.
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