RESUMEN
Congenital heart disease with left-to-right shunt easily lead to pulmonary hypertension.Currently agreed about its mechanism:shear stress induced by high pulmonary blood flow stimulus pulmonary endothelium,to start regulation of genetic transcription,to initiate a series of molecular biology and pathophysiology changes,and finally to lead to pulmonary vascular pathologic remolding.Nuclear factor(NF)-?B is a kind of nuclear factor with multiple biological effect and play an important role in pulmonary vascular remolding.NF-?B signal can be actiacted by high blood flow.Its target gene products,for example,vasoactive mediators,cytokines,make pulmonary vessels difficulty to maintain the normal structure and cause pulmonary vascular contraction and remolding,thus,pulmonary arterial pressure increases.
RESUMEN
Hypoxic pulmonary hypertension(HPH) is a common disease featured by acute hypoxic pulmonary vasoconstriction(HPV) and chronic hypoxic pulmonary vascular remolding(HPVR) leading to the sustained increasing of pulmonary artery pressure.There are many mediators involved in the HPH but none can illustrate it successfully.Primary work has found 15-lipoxygenase(15-LO) and its catalyzed production 15-hydroxyeicosatetraenoic acid(15-HETE)(from arachidonic acid) are up-regulated in pulmonary vascular when exprosed to hypoxia.And it has been found 15-LO/15-HETE involved in many processes of both the HPV and HPVR,indicating 15-LO/15-HETE may be an important mediator of HPH.Advances research on 15-LO/15-HETE may illustrate the mechanism of HPH,and will give some message in looking for a potential clinical target of HPH.