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Received March 1, 2005
Revised March 16, 2005
Accepted after revision March 29, 2005
1 Radboud University Nijmegen Medical Centre
* To whom correspondence should be addressed. E-mail: p.smits{at}pharmtox.umcn.nl.
Deconditioning is a risk factor for cardiovascular disease. Exercise reduces this risk, possibly by improving the vascular endothelial nitric oxide (NO) pathway. The effect of deconditioning on the NO-pathway is largely unknown. This study was designed to assess baseline NO-availability in the leg vascular bed after extreme, long-term deconditioning (spinal cord-injured individuals, SCI) as well as after moderate, short-term deconditioning (4 weeks of unilateral lower limb suspension, ULLS). For this purpose, seven SCI were compared with 7 matched controls. Additionally, 7 healthy subjects were studied Pre- and Post-ULLS. Leg blood flow was measured by venous occlusion plethysmography at baseline and during infusion of 5 incremental dosages of NG-monomethyl-L-arginine (L-NMMA) into the femoral artery. Sodium nitroprusside (SNP) was infused to test vascular responsiveness to NO. Baseline leg vascular resistance tended to be higher in SCI compared with controls (37 ± 4 versus 31 ± 2 AU, P=0.06). Deconditioning did neither alter the vasoconstrictor response to L-NMMA (increase in resistance in SCI versus controls: 102 ± 33% versus 69 ± 9%; Pre- versus Post-ULLS: 95 ± 18% versus 119 ± 15%), nor the vascular responsiveness to NO. In conclusion, two human in-vivo models of deconditioning show a preserved baseline NO-availability in the leg skeletal muscle vascular bed.
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