On discussing the data above stated, it is obvious that the augmentation in the respiratory volume during CO
2 inhalation is based on the accumulation of CO
2 in the blood and tissues, because as is well known, the respiratory centre is very sensitive to the increased H-concentration in the blood. That the oxygen consumption is lowered by CO
2 inhalation is presumably due to diminished oxidation of tissues caused by acidosis through CO
2 inhalation. The fact, confirmed by Lehmann,
18) Chvostec,
19) Raeder,
20) Loewy and Münzer,
21) and Ito
22) that in rabbits when the animals undergo an intravenous injection of hydrochlorid acid, the oxygen consumption diminishes, is accounted for by the acidosis. It is placed beyond doubt by the experiments of Ito, one of us (Hayasaka)
23) and Dürr
24) that an acidosis, deteriorating the oxidation in tissues, decreases the oxygen consumption.
As already pointed out it is thought to be a strange phenomenon that CO
2 output is appreciably decreased, in spite of profuse intake of CO
2. But in Eppinger's
25) experiments a dog (14 kilos body weight) showed after the inhalation of air containing 12% CO
2 for 90 minutes an accumulation of 7.68 liters CO
2, of which only 6% was exhausted in 1 hour after the cessation of CO
2 inhalation, and an another dog (12.6 kilos body weight) during the inhalation of air containing 14.3% CO
2 lasting 90 minutes, an accumulation of 9.01 liters CO
2, of which only 19% was discharged in 1 hour thereafter. In brief, the majority of inspired CO
2 has been retained in the tissues, that is, the latter have a considerable power of combination with CO
2. This is in accordance with the fact observed by Stinzing,
26) that CO
2 was evolved in an amount of about 180% from a muscle by boiling it. Thus, although the process, in which CO
2 is combined with the tissues, is accounted for with difficulty, it has been illustrated by Eppinger
25) that even the quantity of CO
2 which is only physically dissolved in the human tissues, would amount to 25-30 liters, if the profuse water content of the tissues and its absorbent coefficient of CO
2 at body temperature are taken into consideration.
Thus, when we reflect on these presumptions, it is quite right that the carbon dioxide which is accumulated in the tissues after CO
2 inhalation should be considerable in amount. In reviewing our data, the difference obtained by reducing CO
2 output per minute from the sum of the amount of inspired CO
2 and the physiologically produced CO
2 amount per minute, i. e. the accumulated CO
2 amount in the body per minute is culculated as 333-913c. c., as is shown in Table III.
As above stated, through CO
2 inhalation the oxygen consumption is decreased, but CO
2 output is more intensively diminished, whereby it is quite natural that the respiratory quotient is lowered. The fact that the pulse rate is increased owing to CO
2 inhalation can be regarded chiefly as a sign following the accelerated respiratory function, but may partly be provoked by the stimulation of the sympathetic nervous system due to the increased secretion of adrenaline, which results through acidosis aroused by the CO
2 accumulation in the body, as Macleod
27) has maintained.
The evidence that the minute volume is augmented by CO
2 inhalation falls in with the condition that the cardiac function ought to be accelerated in order to supply plenty of oxygen to make good the decreased oxidation of the tissues, which is presumed from the lowering of the oxygen consumption.
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