Biomedical Engineering Reference
In-Depth Information
Arg (0 mol/L) +
L-NMMA (100
m
Arg (100 mol/L) +
L-NMMA (100
m
m
mol/L)
m
mol/L)
Fig. 1
Plasma and peritoneal drain l uid (PDF)-stimulated migration of PMNs across HUVECs
cultured with the addition of dif erent Arg and L-NMMA concentrations. Among the groups
stimulated with patients' plasma and PDF, PMN migration was the lowest with 1000 μM Arg
compared with the other Arg levels. In addition, PMN migration was lower with 100 μM than
with 0 μM and 50 μM Arg. h e reduced PMN migration was abrogated when L-NMMA was
administered. Reprinted from Yeh
et al.
(2007), with permission.
NO and Adhesion Molecules
Evidence from previous reports pointed out that the inl uences of Arg on
inl ammatory mediators including adhesion molecules may mainly depend on
regulation of NO. Numerous studies used an NO donor and NOS inhibitors to
investigate the roles of NO in leukocyte adherence to the vascular endothelium
and emigration. A study by Kubes
et al.
(1991) designed an experiment to assess
the direct ef ects of L-NAME and L-NMMA on PMN adherence. Cat mesenteric
venules were used to observe leukocyte adherence to the venular endothelium by
intravital video microscopy. h ey found that both inhibitors of NO production
increased leukocyte adherence, and leukocyte emigration was also enhanced.
Incubation of isolated cat neutrophils with L-NMMA resulted in direct upregulation
of the leukocyte adhesion glycoprotein, CD11/CD18. L-NAME-induced adhesion
was inhibited by L-Arg but not D-Arg. h ese i ndings suggest that endothelium-
derived NO is an important endogenous modulator of leukocyte adherence, and
impairment of NO production results in leukocyte adhesion and emigration. A
study performed by Armstead
et al.
(1997) added L-NAME and an NO donor to
