[Pathophysiology of non-cardiogenic pulmonary hypertension].
The pathophysiology of non cardiogenic pulmonary hypertension consists mainly of pulmonary vascular changes and alveolar hypoxia. Pulmonary vascular changes might have different etiologies. First the vessel itself with local thrombosis, embolic obstruction, vasoconstriction and endothelial cell dysfunction with intimal proliferation. Secondly parenchymal changes with secondary vascular affection could contribute to pulmonary hypertension. The mechanism of hypoxic pulmonary vasoconstriction is unknown, a direct interaction of oxygen with the smooth muscle cell is possible. The interaction of activated circulating cells - i.e. platelets or leukocytes - and - possibly predamaged - endothelial cells could be the initiating mechanism for several forms of pulmonary hypertension. This could be especially true for the so called primary forms or for dietary pulmonary hypertension e.g. after ingestion of toxic oil.
D004727:Endothelium / Q000503:physiopathology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology; D008171:Lung Diseases / Q000503:physiopathology; D010100:Oxygen / Q000097:blood; D011651:Pulmonary Artery / Q000503:physiopathology; D011652:Pulmonary Circulation; D011655:Pulmonary Embolism / Q000503:physiopathology; D011669:Pulmonary Wedge Pressure; D014655:Vascular Resistance
D010100:Oxygen
Pathophysiologie der nicht kardialen pulmonalen Hypertension.