Biomedical Engineering Reference
In-Depth Information
Table 1
Systemic Effects of COPD
Systemic inflammation
Oxidant stress
Increased plasma levels of cytokines and acute phase proteins
Activated inflammatory cells (neutrophils
=
lymphocytes)
Weight loss and skeletal muscle dysfunction
Loss of muscle mass
Abnormal structure
=
function
Exercise limitation
Cardiovascular effects
Endothelium dysfunction
Abnormal left ventricular function
Nervous system effects
Abnormal brain metabolism
Depression
Abnormal ANS function
Osteoporosis
Anemia
II.
SYSTEMIC INFLAMMATION
An excessive
=
inadequate inflammatory response to a variety of noxious
inhaled gases or particles (mostly cigarette smoking) is considered a key
pathogenic mechanism of COPD (4). This inflammatory response is char-
acterized by the presence in the lung parenchyma of increased concentra-
tions of inflammatory cells (including neutrophils, macrophages, and T-
lymphocytes with a CD8
þ
predominance) and proinflammatory cytokines
(such as leukotriene B4 (LTB
4
), interleukin-8 (IL-8), and tumor necrosis
factor alpha (TNF
a
)), as well as by the presence of oxidative stress (6).
A similar pattern can also be detected in the systemic circulation of these
patients.
A.
Systemic Oxidative Stress
Rahman et al. (7) were the first to show evidence of systemic oxidative stress
in patients with COPD. These authors showed that both the Trolox-equiva-
lent antioxidant capacity and the levels of products of lipid peroxidation
were significantly increased in the plasma of patients with COPD, particu-
larly during the episodes of exacerbation of the disease (7). Subsequently,
Pratic´ et al. (8) have reported increased urinary levels of isoprostane
F2
a
-lll in COPD. Isoprostane F2
a
-lll is a stable prostaglandin isomer
formed by reactive oxygen species (ROS)-dependent peroxidation of arachi-
donic acid (9). Again, this was particularly pronounced during exacerba-
tions of the disease (8).
