PULMONARY VASODILATOR AND VASOCONSTRICTOR ACTIONS OF CARBON DIOXIDE
PULMONARY VASODILATOR AND VASOCONSTRICTOR ACTIONS OF CARBON DIOXIDE
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DOI：
10.1113/jphysiol.1971.sp009405
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发表时间：
1971-01-01
影响因子：
5.5
通讯作者：
SHAW, JW
中科院分区：
文献类型：
--
作者：
BARER, GR;SHAW, JW
1.本文用三种方法研究了CO_2对肺血管的作用：用同种血以恒定流速灌注的离体大鼠和猫肺，以及在体以恒定流速灌注的猫肺叶。在这三种变化中，肺动脉压（PPa）的变化反映了肺血管阻力的变化.在离体大鼠肺中，当血管张力高时，CO2引起血管舒张。肺首先用N2通气，引起PPa升高。无论初始血CO2水平是低还是正常，以及尽管血液pH值下降（通常会增强N2.3的收缩作用），CO2都会引起缺氧时的血管舒张。在大鼠肺通气与CO2从控制状态通常引起弱的血管收缩。用酸降低血液pH值也引起弱的血管收缩，而碱引起血管舒张。CO2对肺血管系统的总体影响取决于可能由碳酸引起的血管收缩作用与由该分子的某些其他性质引起的血管舒张作用之间的平衡。离体大鼠肺的扩张作用较强.相比之下，在两种猫肺制剂中，未获得CO2血管扩张作用的直接证据。当血管张力因缺氧而升高时，用CO2通气，药物或酸引起进一步的血管收缩。从对照状态CO2引起强烈的血管收缩.从其他工作中得到的间接证据表明，二氧化碳在猫体内具有肺血管扩张作用，但通常被碳酸的强血管收缩作用所掩盖。在生活中，当CO2引起的pH变化通过肾脏代偿最小化时，扩张机制可能很重要。
1. Three preparations were used to study the actions of CO2on the pulmonary vasculature: isolated rat and cat lungs perfused at a constant flow rate with homologous blood and a lobe of cat lung perfused at a constant flow ratein vivo. In all three changes in pulmonary artery pressure (PPa) reflected changes in pulmonary vascular resistance.2. In the isolated rat lung CO2caused vasodilatation when vascular tone was high. The lung was first ventilated with N2causing a rise inPPa. CO2caused vasodilatation during hypoxia whether the initial blood CO2level was low or normal and in spite of a fall in blood pH which usually augments the constrictor action of N2.3. In the rat lung ventilation with CO2from the control state usually caused weak vasoconstriction. Reducing blood pH with acids also caused weak vasoconstriction while alkali caused vasodilatation.4. The over‐all effect of CO2on the pulmonary vasculature depends on a balance between a vasoconstrictor action probably caused by carbonic acid and vasodilatation caused by some other property of the molecule. The dilator action is powerful in the isolated rat lung.5. By contrast, in both cat lung preparations, no direct evidence for a vasodilator action of CO2was obtained. Ventilation with CO2when vascular tone was raised by hypoxia, drugs or acids caused further vasoconstriction. From the control state CO2caused strong vasoconstriction.6. Indirect evidence from other work suggests that a pulmonary vasodilator action of CO2exists in the cat but is usually masked by the strong vasoconstrictor action of carbonic acid. In life the dilator mechanism may be important when pH changes caused by CO2are minimized by renal compensation.