抄録
The results of my investigation may be summarized as follows.
1. The acid administration provokes hyperchloremia in the whole blood, already within about 10 minutes.
2. The chlorine content of corpuscles begins to increase already within about 15 minutes after the acid administration, and the corpusclar hyperchloremia is so regular that it may be regarded as a reliable indication of acidosis.
3. In animals to which acid has been administered, the chlorine content of plasma decreases after an initial increment. If too much acid is given, the animal dies too quickly before the plasma chlorine begins to decrease.
It is for this reason that we find sometimes hyper- and some-times hypochloremia of plasma in the blood of animals that have died from acid administration.
4. When a small subletal dose of acid is employed, the chlorine content of plasma never falls below the normal level. It increases gradually and reaches the highest value within about 3 hours after acid administration, and then gradually falls until the normal value is again attained within about 5-6 hours.
5. As is described in the previous paper, acute suffocation results constantly in the increment of chlorine content of whole blood and corpuscles. The plasma chlorine also increases in amount up to the death, and then diminishes postmortally and finally reaches a subnormal value. Such is also the case with prolonged asphyxia except that the chlorine content of plasma becomes subnormal, already before the death of the animals.
Now we see that these changes in the chlorine contentt of whole blood, erythrocytes and plasma observed in the case of asphyxia, are seen also in animals to which acid has been administered. If the animal survives asphyxia or acidosis relatively long the hypo-chloremia of plasma always becomes manifest, while hyper-chloremia of plasma are met in cases where the animals have died too quickly from asphyxia or acidosis in the stadium of initial increase of chlorine content. We think that our present work throws some light on the rôle of asphyxial acidosis in the chlorine interchange during asphyxiation.
