Publication details

Plicní hypertenze - patofyziologické mechanizmy

Title in English Pulmonary hypertension - disease mechanisms
Authors

HELÁN Martin KONIECZNA Anna KLABUSAY Martin ŠRÁMEK Vladimír

Year of publication 2014
Type Article in Periodical
Magazine / Source Vnitřní lékařství
MU Faculty or unit

Faculty of Medicine

Citation
Web http://www.vnitrnilekarstvi.eu/vnitrni-lekarstvi-clanek/plicni-hypertenze-patofyziologicke-mechanizmy-50194
Field Cardiovascular diseases incl. cardiosurgery
Keywords endothelium; intracellular calcium signaling; nitric oxide; pulmonary artery; pulmonary hypertension; remodeling; smooth muscle cell
Description Pulmonary hypertension (PH) is known for its variable etiology. PH pathophysiology is very complex and our therapeutic options are limited. Most of known underlying disease mechanisms play a role across all etiological groups of PH, and they are followed by the same morphological and functional changes of pulmonary vasculature. Mostly, we are not able to determine whether one particular mechanism works as a cause or consequence in the chain of events. An imbalance between vasoconstriction and vasodilation becomes the major functional change of pulmonary vasculature in PH. The main morphological changes (termed together as "remodeling") include cell hyperplasia of pulmonary artery leading to its thickening and narrowing, and impaired regulation of extracellular matrix production leading to reduction in its elasticity. As a result of all these changes, the peripheral vascular resistance in pulmonary vascular bed rises, thus increasing afterload of the right ventricle and finally progressing to its failure. This review aims to summarize and explain the nature of the functional and histological changes in pulmonary arteries which occur in pulmonary hypertension, separately define the role of endothelium and pulmonary artery myocytes, and discuss the most important known pathophysiological mechanisms that lead to these changes.

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