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as are above given from the experiment by Dr. Hammond. Indeed, the effects which resulted from his experiment may be considered due to the congestion of kidney produced, as much as to the direct influence of the urea injected; for the fact is that urea, after being injected into the veins, is carried out of the body by the kidneys with such rapidity that its toxæmic properties are not elicited, unless some obstruction be induced in the secerning organ. Impressed with a knowledge of these facts, I have recently instituted a different series of experiments, by injecting the urea in watery solution, not into the blood, but simply under the skin or into the peritoneal cavities of animals. The following is an epitome of the results obtained.

Injected in solution into the dorsal cuticular sac of frogs weighing from 600 to 650 grains, urea is a poison, fatal or not according to the dose. Thirty grains of urea dissolved in a drachm of water produce profound coma and prostration in twenty minutes, with death within the hour. There is great collapse of the tissues, but there are no convulsions, death being too rapid for this effect. Previously to death there is no indication of ammoniacal evolution from the animal, but afterwards the putrefactive changes are very rapid.

When doses of fifteen grains are injected in like manner into similar animals, the symptoms do not appear within a period of half an hour after the injection, and life is prolonged nearly to the second hour. In other respects the symptoms are the same.

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From doses of five to ten grains, injected into frogs of the weight already mentioned, severe symptoms are elicited, but with recovery in the end. Symptoms of prostration and coma appear in from two to three hours, and remain little abated for four hours or four hours and a half; there is usually convulsive movement in these cases towards the end of the third hour, such movement seeming to augur recovery. The bodies of the animals thus treated assume externally a dark aspect; and, while recovery is taking place, the whole skin is covered with a frothy excretion.

In young warm blooded animals, as young rabbits, the injection of sixty grains of urea dissolved in a hundred and twenty grains of water is followed within an hour by tremors and coma; the tremors soon lapse into active convulsions, with rolling on the side, and constant twitching of the ears. In three hours the coma is most profound, and the convulsions more feeble. Death occurs about the fourth hour after the injection; while recovery, if that take place, commences about the same period. The pupils are fixed and dilated, and the breathing is very irregular.

I would suggest to any practitioner who, conversant with acute uræmia as it is seen in the human subject-say in the child suddenly struck down by suppression of the renal secretion during an attack of scarlet fever-has not seen uræmia as synthetically presented, to perform the experiment I have named on a young rabbit; he will be astounded at the analogy of the symptoms induced with those which he has seen in the human sufferer from uræmic toxæmia.

After death from injection of urea into the body of an animal, the muscles are found slightly darker than natural; the blood very dark and loosely coagulated; the surface of the serous cavities suffused, and not unfrequently lined with serous exudation. The kidneys are intensely congested and dark; the alimentary canal is sometimes suffused over its mucous surface.

With these synthetical facts so unmistakably presented to us, we need not, I think, go further for a cause of uræmia than to the urea. For although creatinine, one of the substances which we have noticed as a possible cause of the uræmic symptoms, is in truth an ammonia, and may therefore ultimately be found to have a physiological effect analogous to that of urea itself, we have a sufficient cause of the phenomena, independently of a consideration of that organic compound. The same remark applies to creatine.

Accepting, therefore, the urea as the primary toxic agent in uræmia, we are led to ask further, whether the effects demonstrated are due to urea itself, i. e. to urea acting unchanged as the poison; or, whether it undergoes decomposition, and the veritably acting poison is a product of that decomposition? Whether, in fact, Frerichs is right or wrong in suggesting that the poison is such a product, in the form of carbonate of ammonia?

The inquiry opens two questions. 1. In the blood, during uræmia, is an excess of ammonia an universal

and necessary fact? 2. Does the exhibition of ammonia, in poisonous doses, produce the symptoms of uræmia?

To the first of these questions Dr. Hammond has given a reply decidedly negative. Confirming by a large number of experiments the observation first made by myself, that ammonia is normally present in blood, he questions altogether the deduction of Frerichs, that the presence of the alkali in uræmic blood is to be set down as the cause of the symptoms. I am bound in the main to agree with Hammond; inasmuch as the evidence afforded by Frerichs is not, in this instance, of a character to substantiate on a satisfactory basis a pathological theory.

It is obvious that Frerichs looked on ammonia as an abnormal constituent of blood, and this constitutes his primary error; but there are other suggestions on which the hypothesis is based which do not hold their ground; for instance, in order to explain the resolution of urea into carbonate of ammonia, he is led to suggest the presence of a ferment, of the existence of which there is really no proof.

Again, as Hammond very acutely argues, the methods by which Frerichs endeavoured to establish the presence of ammonia in blood in uræmic cases were illogical. Not content to search simply for the volatile alkali by merely collecting and examining the vapours given off by blood recently drawn, or exposed to blood heat, Frerichs distilled blood and collected an ammoniacal fluid; while in other experiments he added to the blood caustic potassa, and produced the

evolution of an ammoniacal odour. I follow Hammond in asserting, from direct experiment, that by either of these proceedings a blood containing urea would be made to evolve ammonia, granting even that no ammonia were present in such blood previously.

In like manner, Frerichs seems to me to have erred in taking the fact of evolution of ammonia by the breath as evidence of the correctness of his hypothesis, that in uræmia urea is converted into carbonate of ammonia. For, again, the truth on this point is that the evolution of ammonia by the breath is a normal act. So far is this the case, and in such contrast does the fact stand in relation to uræmia, that during the acute symptoms of the disease the presence of ammonia, before well marked in the breath, is often lost altogether; the acute symptoms themselves being the immediate result of the suppressed respiratory excretion.

Once more, while the fact is undeniable that during uræmic coma ammoniacal excretions are often formed in the alimentary canal, I cannot in any way assure myself that the presence of such ammonia implies an excess of the alkali in the blood. I can advance with Hammond much more safely towards explaining this phenomenon on the supposition that urea, which is a very soluble body, is itself excreted first into the canal, and that the ammoniacal compound is formed there, i. e., in the canal, by the action of the contained matters of the canal on the urea. The supposition here put forward is indeed now almost confirmed

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