Chen LE, Liu K, Qi WN, Joneschild E, Tan X, Seaber AV, Stamler JS, Urbaniak JR.
Role of nitric oxide in vasodilation in upstream muscle during intermittent
pneumatic compression.
J Appl Physiol 2002 Feb;92(2):559-66

The Orthopaedic Microsurgery Laboratory, Department of Surgery, Duke University
Medical Center, Durham, North Carolina 27710, USA. chen0006@mc.duke.edu

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.