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Deciphering the molecular mechanisms of pulmonary hypoxia and its health sequelae: proceedings of the first international DECIPHER symposium on pulmonary hypoxia, Iquique, Chile, 16–17 October 2019

机译:解读肺缺氧及其健康后遗症的分子机制:第一次国际破解研讨会肺缺氧,Iquique,智利,2019年10月16日至17日

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Hypoxia is a major threat for the integrity of every cell as well as for the organism as a whole. It is therefore not surprising that regulatory mechanisms have evolved to compensate reduced oxygen supply for more or less limited periods of time. One such mechanism by which the human body compensates phases of reduced ventilation of parts of the lung is hypoxic pulmonary vasoconstriction (HPV). First described in the 1940s by the Swedish Physiologist, Ulf van Euler, and his co-worker from Pharmacology, Go¨ran Liljestrand,1 this effect, which can be found as the Euler-Liljestrand mechanism in any Physiology textbook, has been a topic of research into the exact molecular mechanisms behind it. HPV contributes to many pulmonary diseases, especially in advanced stages, and may be a cause of pulmonary hypertension, right ventricular hypertrophy, and heart failure. Chronic hypoxia as it may occur at high altitude serves as a model for such lung diseases, which allows to better dissect the pathophysiological consequences of HPV from other pathophysiological events occurring in lung diseases, such as inflammation and fibrosis.
机译:缺氧是对每个细胞的完整性以及整体生物体的主要威胁。因此,由于更多或多或少有限的时间,调节机制已经进化以补偿减少的氧气供应,因此并不令人惊讶。一种这样的机制,人体可以补偿肺部部位的局部通风的阶段的阶段是缺氧肺血管收缩(HPV)。首先在20世纪40年代描述了瑞典生理学家,ULF Van Euler,以及他来自药理学的同事,Go¨ranLiljestrand,1这个效果,可以在任何生理学教科书中发现作为欧拉 - Liljestrand机制,一直是一个话题作者:王莹,王莹,王莹,王莹,王莹,王莹,王莹,王莹,王莹,王莹,王莹HPV有助于许多肺部疾病,特别是在高级阶段,并且可能是肺动脉高压,右心室肥厚和心力衰竭的原因。慢性缺氧,因为它可能发生在高海拔处用作这种肺病的模型,这允许更好地将HPV的病理生理学结果从肺部疾病(如炎症和纤维化等其他病理生理学事件中)进行疏松。

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