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Human hypoxic pulmonary vasoconstriction is unaltered by 8 h of preceding isocapnic hyperoxia

机译:先前的等碳酸血症高氧8小时后人体缺氧性肺血管收缩未改变

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摘要

Exposure to sustained hypoxia of 8 h duration increases the sensitivity of the pulmonary vasculature to acute hypoxia, but it is not known whether exposure to sustained hyperoxia affects human pulmonary vascular control. We hypothesized that exposure to 8 h of hyperoxia would diminish the hypoxic pulmonary vasoconstriction (HPV) that occurs in response to a brief exposure to hypoxia. Eleven healthy volunteers were studied in a crossover protocol with randomization of order. Each volunteer was exposed to acute isocapnic hypoxia (end‐tidal PO2 = 50 mmHg for 10 min) before and after 8 h of hyperoxia (end‐tidal PO2 = 420 mmHg) or euoxia (end‐tidal PO2 = 100 mmHg). After at least 3 days, each volunteer returned and was exposed to the other condition. Systolic pulmonary artery pressure (an index of HPV) and cardiac output were measured, using Doppler echocardiography. Eight hours of hyperoxia had no effect on HPV or the response of cardiac output to acute hypoxia.
机译:持续8h的持续性缺氧会增加肺血管对急性缺氧的敏感性,但尚不清楚持续性高氧暴露是否会影响人的肺血管控制。我们假设暴露于8 h高氧会减少因短暂暴露于低氧而引起的低氧性肺血管收缩(HPV)。以交叉随机顺序研究了11名健康志愿者。每位志愿者在高氧(潮气末PO2 = 420 mmHg)或缺氧(潮气末PO2 = 100 mmHg)的8小时之前和之后暴露于急性等碳酸低氧(潮气末PO2 = 50 mmHg,持续10分钟)。至少3天后,每位志愿者返回并暴露于其他情况。使用多普勒超声心动图测量收缩期肺动脉压(HPV指数)和心输出量。八个小时的高氧对HPV或对急性缺氧的心输出量反应无影响。

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