Structural and functional definition of the pulmonary vein system in a chronic hypoxia-induced pulmonary hypertension rat model

摘要

Pulmonary hypertension (PH) is characterized by increased pulmonary vascular pressure and resistance in pulmonary circulation, which progressively leads to right ventricle hypertrophy, right heart failure, and eventual death. To date, the pathophysiological changes in the pulmonary arteries (PAs) during PH development have been widely studied; however, less attention has been paid to the pulmonary vein (PV) system. Similar to the PA, the vasomotor activity of the PV is also critical in regulating both the distention and recruitment of blood flow from alveolar wall capillaries, facilitating the ven-tilation-perfusion matching in the lung. Studies from numerous species all suggested that PV can react to multiple vasocon-strictive stimuli, including hypoxia (10, 22, 26), endothelin (1, 20, 25), platelet-activating factor (25), and thromboxane (11, 19). In response to the hypoxic exposure, vasoconstriction and structural alteration occur in both PA and PV, significantly contributing to the total pulmonary vascular resistance (18, 19, 33). Considering the functional importance of both PA and PV in regulating pulmonary circulation, more attention is required to further dissect the pathophysiological changes of the PV system, which has the potential to uncover novel molecular mechanisms underlying PH.