Biomedical Engineering Reference
In-Depth Information
Figure 4
Pathobiology of pulmonary hypertension in COPD, where cigarette
smoke products or inflammation may initiate the sequence of changes by producing
endothelial dysfunction. eNOS: endothelial nitric oxide synthase; HPV: hypoxic
pulmonary vasoconstriction; V
A
=
Q: ventilation-perfusion; VEGF: vascular endothe-
lial growth factor; SMCs: smooth muscle cells.
of VEGF, enhanced by endothelial dysfunction, might contribute too to SMC
proliferation. All these changes result in intimal hyperplasia with the ensuing
reduction of arterial lumen, which increases pulmonary vascular resistance.
Arteries with endothelial dysfunction are more susceptible to the
action of additional factors. Among those, sustained arterial hypoxemia
and alveolar hypoxia in poorly ventilated lung units play a crucial role, since
they may induce further endothelial impairment and vessel remodeling,
either directly or through VEGF-dependent mechanisms, thus amplifying
the initial effects of cigarette smoke products (Fig. 4). Similar effects might
be produced by cytokine release by inflammatory cells, and by shear stress
induced by increased vascular resistance.
ACKNOWLEDGMENTS
The authors have been supported by research grants from the Fondo de
Investigacion Sanitaria (02
=
0026, 03
=
0549) the Sociedad Espanola de
Neurologia y Cirugia Toracica, and the Comissionat per a Universitats
i Recerca de la Generalitat de Catalunya (2001-SGR00286).
