[Pathophysiology of development of pulmonary hypertension after acute pulmonary embolism].

Acute pulmonary embolism (PE) is the life-threatening condition with high incidence and mortality where the death is the result of pulmonary hypertension followed by right side heart failure. There are two important mechanisms concerned in the development of pulmonary embolism--induced pulmonary hypertension--mechanic obstruction of pulmonary vessels by the embolus and vasoconstriction. The effect of mechanic obstruction is quite clear, in contrast to the role of vasoconstriction. Activation of endothelial cells, thrombocytes and leucocytes, which release vasoconstricting substances (ET-1, 5-HT etc.) and production of reactive oxygen species (ROS) are the most important factors causing the vasoconstriction after PE. ROS are produced as a result of hypoxia, increased (and decreased) shear stress and are released from activated leukocytes. Vasoconstriction after PE is caused by change of conformation voltage-gated potassium channels, the decrease of vasodilatation effect of NO and activation of matrix metalloproteinases.. Most of the current therapeutic protocols in PE are focused on mechanic obstruction of pulmonary vessels. Thus, the research of the role of vasoconstriction in PE and potentially protective factors in vasocostriction--induced injury represent clinically highly important field.