Role of nitric oxide in vasodilation in upstream muscle during intermittent pneumatic compression.

Published

Journal Article

This study investigated the dosage effects of nitric oxide synthase (NOS) inhibitor N(G)-monomethyl-L-arginine (L-NMMA) on intermittent pneumatic compression (IPC)-induced vasodilation in uncompressed upstream muscle and the effects of IPC on endothelial NOS (eNOS) expression in upstream muscle. After L-NMMA infusion, mean arterial pressure increased by 5% from baseline (99.5 +/- 18.7 mmHg; P < 0.05). Heart rate and respiratory rate were not significantly affected. One-hour IPC application on legs induced a 10% dilation from baseline in 10- to 20-microm arterioles and a 10-20% dilation in 21- to 40 microm arterioles and 41- to 70-microm arteries in uncompressed cremaster muscle. IPC-induced vasodilation was dose dependently reduced, abolished, or even reversed by concurrently infused L-NMMA. Moreover, expression of eNOS mRNA in uncompressed cremaster muscle was upregulated to 2 and 2.5 times normal at the end of 1- and 5-h IPC on legs, respectively, and the expression of eNOS protein was upregulated to 1.8 times normal. These increases returned to baseline level after cessation of IPC. The results suggest that eNOS plays an important role in regulating the microcirculation in upstream muscle during IPC.

Full Text

Duke Authors

Cited Authors

  • Chen, L-E; Liu, K; Qi, W-N; Joneschild, E; Tan, X; Seaber, AV; Stamler, JS; Urbaniak, JR

Published Date

  • February 2002

Published In

Volume / Issue

  • 92 / 2

Start / End Page

  • 559 - 566

PubMed ID

  • 11796664

Pubmed Central ID

  • 11796664

Electronic International Standard Serial Number (EISSN)

  • 1522-1601

International Standard Serial Number (ISSN)

  • 8750-7587

Digital Object Identifier (DOI)

  • 10.1152/japplphysiol.00365.2001

Language

  • eng