The regulation of the general circulation rate in man
The regulation of the general circulation rate in man
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人体总循环速率的调节
DOI：
10.1113/jphysiol.1922.sp001993
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发表时间：
1922
期刊：
影响因子：
--
通讯作者：
J. Haldane
中科院分区：
文献类型：
--
作者：
C. G. Douglas;J. Haldane
屏住呼吸四秒钟后，大约一半的气体通过一根管子呼出，以便通过 Haldane-Priestley 方法获得肺泡空气样本。六秒后，从剩余的呼吸中采集了第二个肺泡样本。在成功的实验中，两个样品中的CO 2 百分比实际上是相同的，因为肺泡空气中的CO 2 压力与含氧静脉血中的CO 2 压力平衡。并且由于当使用刚刚描述的方法时，静脉血在肺部被充氧，因此经计算，在休息期间，充氧的静脉血的CO 2 压力超过动脉血的CO 2 压力应比未充氧的静脉血的CO 2 压力高约50至60%。因此，我们发现含氧静脉血的CO2压力为8毫米。由于氧合前静脉血的CO2压力比动脉血的CO2压力高，计算出的CO2压力仅为5mm左右。更高，从论文的图 3 中可以很容易地看出。为了在氧合之前直接测量静脉血的真实CO 2 压力，显然需要吸入气体混合物，使得静脉血的氧压力和CO 2 压力与肺泡中的气体混合物的氧压力和CO 2 压力平衡。然后可以使用根据氧气压力计算的循环速率来检查根据CO 2 压力计算的结果。我们提到，根据CO 2 压力计算的循环速率（出乎意料的快）是通过根据观察到的氧气压力计算来确认的。氧压实验揭示了一个谬误的根源，当我们试图在用力呼吸后立即确定静脉氧压时，这一谬误变得特别明显。正如我们中的一位在 1915 年指出的 (3)，通过 Haldane-Priestley 方法获得的“肺泡空气”代表了 Miller (4) 描述的“气囊”系统肺泡的内容物。除了构成肺泡大部分的气囊肺泡外，还有呼吸性细支气管、肺泡管和心房的肺泡。这些充当通向气囊肺泡的空气通道，并在吸气期间随气囊肺泡扩张。当深呼吸与气囊空气成分显着不同的混合物时，该混合物充满气道肺泡并与气囊肺泡中的空气混合。但是留在气囊或深部肺泡中的混合物的成分必须与气道肺泡中的混合物不同。因此，除了血液和空气之间气体交换的影响之外，深部肺泡的第一部分
After holding the breath four seconds, about half of it was expired through a tube arranged so that a sample of alveolar air was obtained by the Haldane-Priestley method. A second alveolar sample was then taken from the rest of the breath six seconds later. In a successful experiment the C02-percentage in thetwo samples was practically the same, as the C02-pressure in the alveolar air was in equilibrium with that in the oxygenated venous blood.As we had shown, oxygenation of reduced or partially reduced defibrinated blood raises its C02-pressure; and since the venous blood is oxygenated in the lungs when the method just described is used, the excess in C02-pressure of the oxygenated venous blood over that of the arterial blood ought by calculation to be about50 to 60 pc greater during rest than that of the unoxygenated venous blood. When, therefore, we found that the C02-pressure of the oxygenated venous blood was 8 mm. higher than that of the arterial blood, the calculatedCO2-pressure of the venous blood before oxygenation was only about 5 mm. higher, as can easily be seen from Fig. 3 of the paper. To measure directly the true C02-pressure of thevenous blood before oxygenation it was evidently necessary to inhale a gas-mixture such that both the oxygenpressure and C02-pressure of the venous blood were in equilibrium with those of the gas-mixture in the alveoli. The circulation rate, as calculated from the oxygen-pressure, could then be used to check the result calculated from the C02-pressure. We mentioned that the circulation rate (an unexpectedly rapid one) calculated from the C02-pressure was confirmed by calculation from the observed oxygen-pressure. The oxygen-pressure experiments revealed a source of fallacy which became specially evidentwhen we attempted to determine the venous oxygen-pressure just after forced breathing. As was pointed out by one of us in 1915 (3), the" alveolar air" as obtained by the Haldane-Priestley method represents the contents of the alveoli of the" air-sac" system described by Miller (4). Besides the air-sac alveoli which make up by far the greater part of the lung alveoli there are the alveoli of the respiratory bronchioles, alveolar ducts, and atria. These'act as air-passages to the air-sac alveoli, and expand with the air-sac alveoli during inspiration. When a deep breath is taken of a mixture differing considerably in composition from the air-sac air, this mixture fills the air-passage alveoli and mixes with the air in the air-sac alveoli. But the mixture left in the air-sac or deep alveoli must differ in composition from that in the air-passage alveoli. Hence, apart from the effects of gaseous interchange between blood and air, the first portion of deep alveolar