Biomedical Engineering Reference
In-Depth Information
the absence coronary artery disease, it is presently unclear whether left ven-
tricular function is normal in stable patients with COPD (111). These
patients show an abnormally low peak oxygen uptake and, correspondingly,
a low peak cardiac output, which is equivalent to that of a healthy subject at
that level of exercise (111). This observation suggests that either the regula-
tion of cardiac output during exercise in lung disease may remain so tight
that, despite the capacity for a higher cardiac output, it matches the level
of exercise achieved (111) or, alternatively, that despite the absence of over
heart failure left ventricular function may be compromised in COPD, and a
higher cardiac output could not be achieved. Although this possibility is
speculative, it may merit future studies because similar mechanisms to those
described for the skeletal muscle may be operative for the myocardium
(112-115).
Endothelium function is abnormal in the pulmonary vessels of patients
with COPD (116). Some studies have shown that it is also abnormal in
other systemic vascular territories, such as the renal circulation (117,118).
Whether or not this abnormality may also occur in other systemic vascular
territories is not known at present.
B. Nervous System Effects
Using nuclear magnetic resonance—spectroscopy—it has shown that the
bioenergetic metabolism of the brain is altered in COPD patients (119).
Whether this represents a physiological adaptation to chronic hypoxia, as
it occurs at altitude (120), or it may be considered another systemic effect
of COPD mediated by other unknown mechanisms is unclear.
Depression is highly prevalent in COPD (121-123). Although this
may represent a physiological response to a chronic debilitating disease,
it is equally plausible that it may have some biological basis. In this con-
text, it is particularly interesting to note that TNF
a
and other cytokines
and molecules such as NO have been implicated in the pathogenesis of
depression in several experimental models (124-126) and that, as discussed
above, patients with COPD present evidence of systemic inflammation. A
better delineation of these questions may open new therapeutic possibilities
in COPD.
Finally, the autonomic nervous system (ANS) may also be altered in
patients with COPD, as suggested by Takabatake et al. (127) who showed
indirect evidence of abnormal ANS control in patients with COPD, particu-
larly those with low body weight. Interestingly, these alterations seem
related to a deregulation of the normal circadian rhythm of leptin (127).
Leptin has important effects on neuroendocrine function, apetite regulation,
body weight control, and thermogenesis in humans (127) and, importantly,
its plasma levels are reduced in COPD (99-101).
