This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Matsumoto, M. Articles by Sakabe, T. Search for Related Content PubMed PubMed Citation Articles by Matsumoto, M. Articles by Sakabe, T.

---

NEUROSURGICAL ANESTHESIA

The Effects of N^G-Nitro-L-Arginine-Methyl Ester on Neurologic and Histopathologic Outcome After Transient Spinal Cord Ischemia in Rabbits

Department of Anesthesiology-Resuscitology, Yamaguchi University School of Medicine, Yamaguchi, Japan

Address correspondence and reprint requests to Mishiya Matsumoto, MD, Department of Anesthesiology-Resuscitology, Yamaguchi University School of Medicine, 1-1-1 Minamikogushi, Ube, Yamaguchi, 755-8505, Japan.

Little is known about the role of nitric oxide in the pathophysiology of spinal cord ischemia. We evaluated the effects of nitric oxide synthase (NOS) inhibition by N^G-nitro-L-arginine-methyl ester (L-NAME) in rabbits whose abdominal aorta was occluded for 20 min (Experiment 1) or 25 min (Experiment 2). In Experiment 1, the L-NAME group (n = 6) received 3 mg/kg IV L-NAME, followed by an IV infusion of 3 mg · kg^-1 · h^-1 until 6 h after reperfusion. Ischemia was induced 20 min after the start of L-NAME. The phenylephrine group (n = 6) received phenylephrine to maintain comparable blood pressure. The control group (n = 6) received saline. In Experiment 2, L-NAME (3 mg/kg IV L-NAME, followed by an IV infusion of 3 mg · kg^-1 · h^-1 until 6 h after reperfusion) and phenylephrine groups (n = 6 each) were studied. Ischemia was induced 100 min after the start of L-NAME. Forty-eight hours after reperfusion, hindlimb motor function and histopathology of the spinal cord were examined. In Experiment 1, L-NAME and phenylephrine both improved neurologic outcome, with higher intraischemic blood pressures than saline. In Experiment 2, L-NAME worsened the neurologic and histopathologic outcome compared with phenylephrine. Attenuation of damage by L-NAME in Experiment 1 may be attributable to an intraischemic blood pressure increase. The worse outcome with L-NAME in Experiment 2 suggests that NOS inhibition exacerbates ischemic spinal cord damage.

Implications: Nonselective inhibition of nitric oxide synthase activity has aggravating effects on the neurologic and histopathologic outcome after transient spinal cord ischemia.

This article has been cited by other articles:

				M. Sirlak, S. Eryilmaz, M. Bahadir Inan, Y. S. Sirin, O. Besalti, L. Yazicioglu, E. Ozcinar, E. Erdemli, R. Tasoz, A. H. Elhan, et al. Effects of carbamazepine on spinal cord ischemia. J. Thorac. Cardiovasc. Surg., October 1, 2008; 136(4): 1038 - 1043.e4. [Abstract] [Full Text] [PDF]

				D. Nagamizo, S. Tsuruta, M. Matsumoto, H. Matayoshi, A. Yamashita, and T. Sakabe Tight Glycemic Control by Insulin, Started in the Preischemic, but Not Postischemic, Period, Protects Against Ischemic Spinal Cord Injury in Rabbits Anesth. Analg., November 1, 2007; 105(5): 1397 - 1403. [Abstract] [Full Text] [PDF]

				S. Tsuruta, M. Matsumoto, S. Fukuda, A. Yamashita, Y. J. Cui, H. Wakamatsu, and T. Sakabe The effects of cyclosporin a and insulin on ischemic spinal cord injury in rabbits. Anesth. Analg., June 1, 2006; 102(6): 1722 - 1727. [Abstract] [Full Text] [PDF]

				H. Saeki, M. Matsumoto, S. Kaneko, S. Tsuruta, Y. Jun Cui, K. Ohtake, K. Ishida, and T. Sakabe Is Intrathecal Magnesium Sulfate Safe and Protective Against Ischemic Spinal Cord Injury in Rabbits? Anesth. Analg., December 1, 2004; 99(6): 1805 - 1812. [Abstract] [Full Text] [PDF]

				S. Matsumoto, M. Matsumoto, A. Yamashita, K. Ohtake, K. Ishida, Y. Morimoto, and T. Sakabe The Temporal Profile of the Reaction of Microglia, Astrocytes, and Macrophages in the Delayed Onset Paraplegia After Transient Spinal Cord Ischemia in Rabbits Anesth. Analg., June 1, 2003; 96(6): 1777 - 1784. [Abstract] [Full Text] [PDF]

				T. Kiyoshima, S. Fukuda, M. Matsumoto, Y. Iida, S. Oka, K. Nakakimura, and T. Sakabe Lack of Evidence for Apoptosis as a Cause of Delayed Onset Paraplegia After Spinal Cord Ischemia in Rabbits Anesth. Analg., March 1, 2003; 96(3): 839 - 846. [Abstract] [Full Text] [PDF]

				A Sola, J Rosello-Catafau, E Gelpi, and G Hotter Fructose-1,6-biphosphate in rat intestinal preconditioning: involvement of nitric oxide Gut, February 1, 2001; 48(2): 168 - 175. [Abstract] [Full Text] [PDF]