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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 symp

toms 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.

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 uremic 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

coagulated slowly and imperfectly; the corpuscles were scattered, and entirely modified, some collapsed, and all more or less irregular in shape-oval or manysided. The animal was also unwell, was thirsty, and inactive; yet he took his food, as he had done throughout, with avidity. On the evening of the 9th he vomited. His breath from the first administration was markedly ammoniacal. It was observed, too, that the animal, although he had eaten heartily in the course of the inquiry, was losing flesh.

In the course of the 10th and 11th days of December, the animal received four five-grain doses of the carbonate. On December 12th, two doses of eight grains each were given. On the morning of December 13th, before any dose was administered, the breath was examined, and found markedly ammoniacal. The blood-corpuscles were much more generally modified; there were none perfect. Some were oval, some many-sided, some star-like. The dark central point was absent in all.

On December 14th, an eight-grain dose was administered in the morning; on December 15th and 16th, the same; on December 17th and 18th, ten grains were given each forenoon. On this latter date, a little blood was extracted, and was watched for twenty minutes, during which time it did not coagulate.

On December 19th, 20th, and 21st, ten-grain doses were given each day. On December 21st, the breath was strongly ammoniacal, as before.

Dr. Barker now gave the animal a respite for seven

days. On December 28th, he recommenced by giving a scruple dose of the carbonate in the morning, and a second dose of the same quantity in the evening. These doses produced vomiting and a staggering gait; but the effects passed off in a few minutes.

On December 29th, one scruple dose was given in the morning. On December 30th, a little blood was drawn, which did not coagulate for nearly an hour. After this observation, another scruple dose was administered. On December 31st, a scruple dose was given in the morning and in the evening.

On

On January 1, 1857, a scruple dose was given; but none on the 2nd. The breath continued markedly ammoniacal on January 1st, 2nd, and 3rd. the 3rd, a scruple dose was given; two scruple doses on January 4th, and three scruple doses on the 5th. At this point, the animal became decidedly ill; his appetite fell off, and he was prostrated and drowsy. On January 6th and 7th, two scruple doses were given each day; on January 8th, three similar doses; on the 9th, two; and on the 10th, three. During this time, the symptoms above described became more evident; the breath was more strongly ammoniacal; the blood coagulated slowly and feebly, and the red corpuscles underwent remarkable modifications. They assumed various shapes-stellate, many-sided, and oval. Some were entirely disintegrated. All were free from central opacity. They sometimes aggregated loosely in circular groups, lying out flattened, not surface to surface like coins. They continued long in motion, and had but little

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