The Effect of the Vegetative Nerve Poisons and Some Other Drugs upon the Uric Acid Concentration of the Blood

Abstract

In looking over the results of these experiments we find that the uric acid and the urea-nitrogen concentrations of the blood seem to undergo separate and independent changes by the actions of these drugs and to have no connection with each other whatever. By pilocarpine the ureanitrogen content is distinctly increased, and the uric acid slightly decreased, while by atropine the results are entirely opposite. By adrenaline first the ureanitrogen content decreases hand in hand with the uric acid value, but when later the latter increases gradually the former can not be called always increasing. By caffeine they both increase, the uric acid, always showing a significant increase even in an instance, in which the ureanitrogen content has decreased. By guanidine the uric acid greatly increases in spite of the decrease of the ureanitrogen content, while by insuline they both decrease. The increase of the ureanitrogen content due to pilocarpine is necessarily followed by the increase of the uric acid. Minkowski2) has reported that in a goose the injection of ammonia or urea augments the uric acid elimination and the removal of the liver is followed by a reduced output of uric acid and urea and by an increased elimination of ammonia. If a large amount of aminoacid is injected into a liverless goose, the ammonia excretion only is found increased, while the urea, which has been injected, is eliminated unchanged. According to the experiments of Scaffidi34) and Avellone35) when the liver is extirpated from a goose or a duck, the uric acid elimination is only temporarily decreased, and after two or three days it comes to excrete a normal amount of uric acid. Avellone, on injecting urea into a normal duck, observed the outputs of urea, uric acid and ammonia all increased. He found also that when urea was injected into a duck with its liver vessels tied, after the restoration of the uric acid excretion to its normal value, the uric acid elimination was seen increased. From these facts Minkowski's2) assertion, that the liver is the only organ for the uric acid synthesis, must be denied, but it can never lose its supreme position as an organ, in the goose, of synthetizing the uric acid. It is at the same time a very important organ perhaps for urea synthesis. Seen from the experiments above mentioned, the changes of the urea-synthetizing function of a goose by such drugs as pilocarpine, atropine, adrenaline, caffeine, guanidine and insuline, may be said to be nearly in accord with those in a rabbit. The uric acid synthetic functions probably undergo changes contrary to those of the ureanitrogen due to pilocarpine, atropine and guanidine and sometimes adrenaline and caffeine. Thus, it is ascertained that the uric acid and the ureanitrogen contents of the blood are influenced independent of each other. In view of this fact, the assertion that uric acid is directly formed out of the urea in the liver of bird seems to be most doubtful. When we analyse pharmacologically the nervous regulation in the process of the uric acid synthesis, the evidence that the blood uric acid content is slightly decreased by a parasympathetic stimulant such as pilocarpine, and slightly increased by atropine, suggests that the stimulation of the parasympathetic nervous system inhibitingly regulates the uric acid synthesis. The facts that it is markedly increased by adrenaline after a lapse of a certain time and that it is considerably augmented by caffeine, even when the ureanitrogen content shows a manifest decrease, point out that there is an accelerating action of sympathetic excitations upon the uric acid synthesis. That it is significantly increased by guanidine and decreased by insuline can not be explained from the side of the vegetative nervous system. The effect of these drugs upon the ureanitrogen content of a goose is similar to that of a rabbit.