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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 Ham. mond 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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by experiment; for Hammond, having given thirty grains of urea to a full grown fasting dog, killed him fifteen minutes later, and found in the stomach a tenacious mucus exhaling a powerful ammoniacal odour. • But while I thus differ from the eminent Frerichs —and I am sure no one can esteem him more than I even in differing from him—as to the precise toxæmic agent presented in uræmia, I admit that there are occasionally acute uræmic cases, in which, towards their finale, either from decomposition of urea in the blood, or from some change in the destruction of tissue coeval with the formation of urea itself, ammonia in absolute excess is presented in the blood, and even in the respiratory products. These cases present many of the symptomatic characters of modified yellow fever. The skin becomes of a bronzed tinge; the breath is ammoniacal; there is vomiting of fluid of melænic colour; and the blood when drawn remains permanently liquid until treated with lime or baryta: the blood in such cases presents an excess of ammonia. I have seen such an example of disease as is here described; but it is not a fair sample of common uræmia, it is uræmic intoxication complicated with hepatic obstruction.

Discarding, then, the hypothesis that in simple uræmia there is necessarily an excess of ammonia in the blood, I pass to the second question. Does the exhibition of ammonia in large doses produce the symptoms of uræmia ? . When ammonia is injected into the blood of animals through the veins in sufficient dose to produce symptoms at all, the effects exhibited, very violent so long as they last, terminate almost immediately either in death or in recovery. The great symptom evinced is active violent convulsion, tetanic convulsion. In its intensity, this spasm is different from uræmic convulsive movement, and equally different from the convulsion that may be excited by urea; in its termination also it is different from the paroxysm caused by urea; there is no recurrence, it has for its finish death or convalescence; but in the convulsion from urea and in the convulsion of uræmia there is first convulsion, then respite, and so on, over and over again for hours perhaps, or even days.

The physical characters of the two poisons, in fact, necessarily lead to these differences of action.

Ammonia, a diffusible volatile body, spreads out its influence rapidly through every tissue, and strikes an instant effect. By virtue of the same physical properties, however, it escapes as rapidly and leaves the system free. Urea, on the other side, though a very soluble and easily decomposable body, can escape from the blood by transudation only. Hence, when urea has accumulated in the blood by suppression of its main outlet, or by direct introduction into the blood-current, it is transuded into a variety of parts—into the serous cavities, into the alimentary canal, or into the structures of vascular organs. The blood in this way clears itself for long periods of a portion of the poison; then the poison, reaccumulating faster than it can be thrown off, produces its toxæmic effects in all their intensity, in violent convulsions.

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The very act of convulsion hastens excretion ; the blood is once more relieved; and the effect ceases, to be renewed whenever the proportion of the poison is sufficient to excite the paroxysm. • We cannot, therefore, on analysing the effects of ammonia or its salts in a large dose, come to any other fair conclusion than that the symptoms produced by the ammonia are not identical with those of common uræmia; there is truly an analogy, but not an identity. On the contrary, between the effects produced by the introduction of a large dose of urea into the system, and the symptoms of common uræmia, there is an absolute identity. But it may be suspected that the presence of carbonate of ammonia in less poisonous doses than those referred to above may be sufficient to produce uræmic symptoms. On this point most fortunately we have good evidence, derived not only from experiment on inferior animals, but from observation on the human subject.

In 1856, Dr. Barker, of Bedford, carried out for me a series of important experiments, bearing on the toxical effects of carbonate of ammonia, when given not in poisonous, but in free and continued doses. In one case, a large and healthy dog having been selected for experiment, Dr. Barker commenced on November 29th, to administer to the animal five grains of carbonate of ammonia daily. The dose was repeated each day until December 3rd; no marked effect following, the dose was given twice in the day. Symptoms were now induced which deserved observation; blood drawn from the ear of the animal

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