Being convinced that dietary influences have been
a prolific source of confusion in the past, decided
to use fasting subjects. we had also come to the conclusion that the role played by fixed base in the neutralisation of acid can be more accurately studied, if some acid
other than hydrochloric acid is used. v'e chose sulphuric
acid. In choosing maximum dose we were guided by the normal
daily acid production in fasting cats - our experimental
subjects. This also corresponds to the magnitude of the
excess acid production in phorhizinized dogs and cats. Vie
did not wish to get too far away from the rate at which acid
may be formed in the tissues spontaneously, so that our
results may be expected to have more bearing on the fate
of acid produced under natural conditions than is the case
with some previous work.
ACID PER OS.: Sulphuric acid was given from 30 c.c. to 125 c.c.
per kilogram weight in single doses to starving cats.
About 8O% of the total amount of the acid given was
recovered from urine as sulphate. It was found that
ammonia neutralised about 60%; of the acid given by the
mouth and subsequently recovered from the urine, or 50%
of the total amount given. This figure for ammonia is very much higher,. than (20 or 30%) had been observed in experiments performed on animals that had been fed during the
Varying proportions of the acid were neutralised by
fixed base. Taking the extreme case noted by us, the amount
of fixed base lost is 55 c.c. of 0.1N base in a cat of 2.55kg. weight. This corresponds to a loss equivalent to 6.7
volume per cent carbon- dioxide, - a small fraction of the
normal range of variation in the bicarbonate content of
plasma. If acid feeding deprives the body of fixed base at
all, it draws only on a supply which is not particularly
needed and which is, therefore, not tenaciously retained.
No appreciable change in phosphate excretion was
noted in any of the experiments.
PARENTERAL ADMINISTRATION OF ACID.
Approximately the same dose of sulphuric acid was
given as per Os. To approximate the rate of absorption
when acid is given by mouth, the acid was given at from
about 0.015 c.c. per kilogram per minute to about 0.09 c.c.. per
kilogram per minute. It was noted that little or no increase in ammonia took place, and that a sufficient
rise in residual fixed base excretion occurred to account
for all the acid injected. But in every experiment profound secondary changes occurred, chief among which. were haemolysis interfering with the action of the kidney and
hyperpnoea. The latter alone would explain the apparent
absence of ammonia production; over -ventilation evidently
setting free more than enough fixed base to neutralise the
acid, so that ammonia production was rendered unnecessary.
' "'e were forced to the conclusion that this method of parent - eral introduction of acid defeated the object we had in
view, i.e. to see whether acid entering the systemic circulation directly is neutralised by ammonia at all. Such
neutralisation had been denied by Keeton. We therefore
tried parenteral administration under less severe conditions, i.e. Subcutaneously, and it served the purpose
100 per cent. of the acid when administered by this
route was recovered from the urine. Increased ammonia production neutralised about 40% of the acid. This average is
based on two experiments only, while the average for alimentary route administration is based on a very much larger
number of experiments, and we are not sure the causes of
the peculiar results of intravenous injections are wholly
No increase in phosphate excretion in urine was
noticed in response also to the parenteral administration