Biomedical Engineering Reference
In-Depth Information
Mean sP-selectin
Mean sICAM-1
0 1 2 3
Number of coronary vessels with significant stenoses
0 1 2 3
Number of coronary vessels with significant stenoses
Mean sVCAM-1
Mean hsCRP
0 1 2 3
Number of coronary vessels with significant stenoses
0 1 2 3
Number of coronary vessels with significant stenoses
Fig. 1
Serum cellular adhesion molecules and highly sensitive C-reactive protein and the
extent of coronary atherosclerosis among 291 patients referred for coronary angiography (mean
with 95% CI). h e extent of coronary atherosclerosis is quantii ed on the basis of the number of
af ected coronary vessels into 0, 1, 2, or 3-vessel disease. A signii cant stenosis is present if there
is a reduction in the luminal diameter of more than 50%. h e i gure shows increasing levels of
soluble cellular adhesion molecules with increasing number of af ected vessels. (Authors' own
data; details of study can be found in Eschen et al. 2005).
which may explain the negative association between n-3 PUFA and expression of
CAMs.
Marine n-3 PUFA may also exert anti-inl ammatory actions by modulation of
production of pro-inl ammatory and anti-inl ammatory cytokines. At er dietary
intake, EPA and DHA are incorporated into the membranes of inl ammatory
cells and serve as substrates for the production of eicosanoids and cytokines that
modulates the inl ammatory response (Calder 2006). An increased intake of i sh
and a reduction in the intake of n-6 PUFA will result in a higher level of EPA and
DHA and less arachidonic acid (AA) in leucocyte cell membranes (Schmidt
et al
.
1991). h e inl ammatory eicosanoids derived from EPA are much less potent than
eicosanoids derived from AA. h us, while AA is metabolized via the lipoxygenase
pathway in leucocytes to leucotriene B4 with very powerful pro-inl ammatory
ef ects, EPA is metabolized to leucotriene B5 with an inl ammatory activity of only
10% of leucotriene B4 (Schmidt
et al
. 1991). EPA and DHA may also decrease
the production of inl ammatory cytokines like tumour necrosis factor alpha,
interleukin-1 and interleukin-6 (Calder 2006).
