首页> 外文期刊>The Journal of Physiology >Hypoxia, not pulmonary vascular pressure, induces blood flow through intrapulmonary arteriovenous anastomoses
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Hypoxia, not pulmonary vascular pressure, induces blood flow through intrapulmonary arteriovenous anastomoses

机译:缺氧而非肺血管压力会通过肺内动静脉吻合术诱导血流

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摘要

Key points Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased by acute hypoxia during rest by unknown mechanisms. Oral administration of acetazolamide blunts the pulmonary vascular pressure response to acute hypoxia, thus permitting the observation of IPAVA blood flow with minimal pulmonary pressure change. Hypoxic pulmonary vasoconstriction was attenuated in humans following acetazolamide administration and partially restored with bicarbonate infusion, indicating that the effects of acetazolamide on hypoxic pulmonary vasoconstriction may involve an interaction between arterial pH and PCO2. We observed that IPAVA blood flow during hypoxia was similar before and after acetazolamide administration, even after acid-base status correction, indicating that pulmonary pressure, pH and PCO2 are unlikely regulators of IPAVA blood flow.
机译:要点休息时急性缺氧会通过未知机制增加通过肺内动静脉吻合术(IPAVA)的血流量。口服乙酰唑胺会使对急性缺氧的肺血管压力反应变钝,因此可以观察到IPAVA血流,而肺压力变化最小。服用乙酰唑胺后,人的低氧性肺血管收缩作用减弱,并通过碳酸氢盐输注部分恢复。这表明乙酰唑醇对低氧性肺血管收缩的作用可能涉及动脉pH与PCO2之间的相互作用。我们观察到,即使在酸碱状态校正后,缺氧期间IPAVA血流在乙酰唑胺给药前后也相似,这表明肺压,pH和PCO2不太可能是IPAVA血流调节剂。

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