Original Article
Spinal Cord (2008) 46, 113–117; doi:10.1038/sj.sc.3102066; published online 10 April 2007
The correlation between nitric oxide and vascular endothelial growth factor in spinal cord injury
S Savas1, C Savas2, I Altuntas3 and A Adiloglu4
- 1Department of Physical Medicine and Rehabilitation, Süleyman Demirel University Medical School, Isparta, Turkey
- 2Department of Pediatric Surgery, Süleyman Demirel University Medical School, Isparta, Turkey
- 3Department of Biochemistry, Süleyman Demirel University Medical School, Isparta, Turkey
- 4Department of Microbiology, Süleyman Demirel University Medical School, Isparta, Turkey
Correspondence: Dr S Savas, Department of Physical Medicine and Rehabilitation, Süleyman Demirel University Medical School, Cunur Kampus, Posta Kutusu 76, Isparta 32000, Turkey. E-mail: serpilsavas@yahoo.com
Received 29 September 2006; Revised 27 February 2007; Accepted 8 March 2007; Published online 10 April 2007.
Abstract
Study design:
Prospective, randomized, placebo-controlled, experimental study.
Objectives:
The issue of whether nitric oxide (NO) production is beneficial or deleterious on ischemic injuries of the central nervous system still remains doubtful. Vascular endothelial growth factor (VEGF) is known to induce the release of NO from endothelial cells. However, the effect of NO on VEGF synthesis is not clear. We aimed to determine the effects of L-arginine and NG-nitro-L-arginine methyl ester (L-NAME) on VEGF synthesis and free radicals in a rat model of spinal cord ischemia-reperfusion (IR) injury.
Setting:
Surgical Research Laboratory of a Medical School.
Material and methods:
Twenty-eight Wistar rats were divided into four groups as follows (n=7): Sham, IR injury, L-arginine, and L-NAME. Infrarenal abdominal aorta was occluded to induce spinal cord ischemia. L-Arginine (100 mg/kg) and L-NAME (10 mg/kg) were given before aortic occlusion. Biochemical assays of malondialdehyde (MDA), NO and VEGF were carried out in spinal cord specimens.
Results:
L-Arginine treatment significantly increased MDA and NO, but decreased VEGF levels in spinal cord. However, nonselective inhibition of NOS with L-NAME significantly decreased MDA and NO, but increased VEGF levels. Besides, the positive linear correlation between MDA and NO, and negative linear correlations between MDA, NO and VEGF levels have also been demonstrated.
Conclusion:
Nonselective inhibition of NO synthase activity with L-NAME attenuated free radical formation and increased VEGF level when compared with NO precursor L-arginine in a rat model of spinal cord ischemia. We suggest that inhibition of NO synthase, as well as induction of VEGF, may be a therapeutic option in spinal cord IR injury.
Keywords:
spinal cord injury, nitric oxide, vascular endothelial growth factor
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