Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Clinical Trial
. 2009;32(5):538-44.
doi: 10.1080/10790268.2009.11754555.

Effects of acute nitric oxide synthase inhibition on lower leg vascular function in chronic tetraplegia

Michael F La Fountaine  1 , Miroslav Radulovic, Christopher P Cardozo, Ann M Spungen, Ronald E DeMeersman, William A Bauman
Affiliations
Clinical Trial

Effects of acute nitric oxide synthase inhibition on lower leg vascular function in chronic tetraplegia

Michael F La Fountaine et al. J Spinal Cord Med. 2009.

Abstract

Background/objective: To improve our understanding of the lower-leg vascular responses of nitric oxide synthase inhibition in persons with tetraplegia.

Participants: Six people with chronic tetraplegia and 6 age-matched controls.

Methods: Lower-leg relative vascular resistance and venous volume variation were obtained by venous occlusion plethysmography and blood pressure by auscultation at baseline. Postintravenous infusion of the nitric oxide synthase inhibitor NG-nitro-L-arginine-methyl-ester (1 mg x kg(-1) or placebo on separate days.

Results: At baseline in the group with tetraplegia compared with controls, mean arterial pressure and relative vascular resistance of the leg were significantly lower. After nitric oxide synthase inhibition, mean arterial pressure and lower leg vascular resistance were significantly elevated in both groups. There were no group or intervention differences in venous volume variation.

Conclusion: These preliminary results suggest that nitric oxide synthase inhibition with 1 mg x kg(-1) N(G)-nitro-L-arginine-methyl-ester normalizes seated blood pressure and lower leg vascular resistance to control group baseline levels.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Representation of cuff and strain gauge placement for venous occlusion plethysmography collection (strain gauge enhanced for visualization).
Figure 2
Figure 2
Representation of the venous occlusion plethysmography parameters used for calculations.
Figure 3
Figure 3
Percent change of lower leg vascular resistance (arbitrary units) after nitric oxide synthase inhibition in both groups. †P < 0.01.
See this image and copyright information in PMC

References

    1. Teasell RW, Arnold JM, Krassioukov A, Delaney GA. Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury. Arch Phys Med Rehabil. 2000;81(4):506–516. - PubMed
    1. Guizar-Sahagun G, Castaneda-Hernandez G, Garcia-Lopez P, Franco-Bourland R, Grijalva I, Madrazo I. Pathophysiological mechanisms involved in systemic and metabolic alterations secondary to spinal cord injury. Proc West Pharmacol Soc. 1998;41:237–240. - PubMed
    1. Claus-Walker J, Halstead LS. Metabolic and endocrine changes in spinal cord injury: II (section 1). Consequences of partial decentralization of the autonomic nervous system. Arch Phys Med Rehabil. 1982;63(11):569–575. - PubMed
    1. Munakata M, Kameyama J, Nunokawa T, Ito N, Yoshinaga K. Altered Mayer wave and baroreflex profiles in high spinal cord injury. Am J Hypertens. 2001;14(2):141–148. - PubMed
    1. Mathias CJ, Christensen NJ, Corbett JL, Frankel HL, Goodwin TJ, Peart WS. Plasma catecholamines, plasma renin activity and plasma aldosterone in tetraplegic man, horizontal and tilted. Clin Sci Mol Med. 1975;49(4):291–299. - PubMed

Publication types

MeSH terms

LinkOut - more resources