Abstract：
The pathophysiology of pulmonary hypertension (PH) is not fully understood. Here, we tested the hypothesis that hypoxic perfusion of the vasa vasorum of the pulmonary arterial (PA) wall causes PH. Young adult pig lungs were explanted and placed into a modified ex vivo lung perfusion unit (organ care system, OCS) allowing the separate adjustment of parameters for mechanical ventilation, as well as PA perfusion and bronchial arterial (BA) perfusion. The PA vasa vasorum are branches of the BA. The lungs were used either as the control group (n = 3) or the intervention group (n = 8). The protocol for the intervention group was as follows: normoxic ventilation and perfusion (steady state), hypoxic BA perfusion, steady state, and hypoxic BA perfusion. During hypoxic BA perfusion, ventilation and PA perfusion maintained normal. Control lungs were kept under steady-state conditions for 105 min. During the experiments, PA pressure (PAP) and blood gas analysis were frequently monitored. Hypoxic perfusion of the BA resulted in an increase in systolic and mean PAP, a reaction that was reversible upon normoxic BA perfusion. The PAP increase was reproducible during the second hypoxic BA perfusion. Under control conditions, the PAP stayed constant until about 80 min of the experiment. In conclusion, the results of the current study prove that hypoxic perfusion of the vasa vasorum of the PA directly increases PAP in an ex situ lung perfusion setup, suggesting that PA vasa vasorum function and wall ischemia may contribute to the development of PH.NEW & NOTEWORTHY Hypoxic perfusion of the vasa vasorum of the pulmonary artery directly increased pulmonary arterial pressure in an ex vivo lung perfusion setup. This suggests that the function of pulmonary arterial vasa vasorum and wall ischemia may contribute to the development of pulmonary hypertension.
摘要：
肺动脉高压（PH）的病理生理学尚未完全了解。这里,我们检验了肺动脉（PA）壁血管的低氧灌注引起PH的假设。将年轻的成年猪肺外植并放入改良的离体肺灌注单元（器官护理系统，OCS)允许单独调整机械通风的参数，以及PA灌注和支气管动脉（BA）灌注。PAvasavasorum是BA的分支。肺被用作对照组(n=3)或干预组(n=8)。干预组的方案如下：常氧通气和灌注（稳态）-低氧BA灌注-稳态-低氧BA灌注。在低氧BA灌注期间，通气和PA灌注维持正常。将对照肺保持在稳态条件下105分钟。在实验过程中,经常监测PA压力（PAP）和血气分析。BA的低氧灌注导致收缩压和平均PAP增加，常氧BA灌注后可逆的反应。在第二次低氧BA灌注中，PAP的增加是可再现的。在对照条件下,PAP保持恒定直到实验的约80分钟。总之,本研究的结果证明，在非原位肺灌注设置中，PA血管血管的低氧灌注直接增加PAP，这表明PA血管血管功能和壁缺血可能有助于PH的发展。
