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ceived 1760 grains of blood from the neck of a sheep. Coagulation occurred, as nearly as could be determined, in fifty-five seconds. The clot was rather dark, but became red on exposure to the air; it was not very firm, and serum exuded from it freely. On the upper surface of the blood there was a thin separation of fibrine. The blood-corpuscles were much modified in character, being oval-shaped, rounded, and some even almost rectangular. They were reduced in number.

Into a second cup, containing four drachms of simple distilled water, 1760 grains of blood were received from the same animal. The blood coagulated at the same moment as in the previous specimen. The clot, dark at first, became red on exposure to the air, and gave out serum freely. On its upper surface there was also a thin separation of fibrine. The corpuscles were modified precisely as in the preceding observation. The normal period of coagulation of the blood of this animal was forty seconds. The clot naturally formed was of bright red colour and very firm and uniform, showing no fibrinous separation. The corpuscles were natural.

On the same day four grains of urea, with eight fluid-drachms of distilled water, in which the urea was dissolved, were placed in a cup having a capacity of 2000 grains. Into this cup I received from the neck of another sheep 1520 grains of blood. Coagulation occurred in fifty-six seconds. The clot, at first dark, became red on exposure to the air, yielded at once a large exudation of serum, and was loosely

held together. On its upper surface there was a well-marked soft fibrinous coat. The clot soon became very small, and again of deep dark colour. The corpuscles presented the peculiarities of form and scantiness noticed in the last experiments, but in a more marked degree.

Into another cup containing 480 grains of simple distilled water, were received from the neck of the same animal 1520 grains of blood. Coagulation occurred at the same time to a second, as in the preceding observation. The coagulum presented the same characteristic changes, and the corpuscles did not vary in any single particular.

The blood in this animal coagulated naturally in forty seconds. The clot was red from the first, and firm. The corpuscles were normal.

The temperature of the day on which these experiments were made was high, 70° in the shade.

Comparing these experiments one with the other, and comparing them also with another series of experiments on the addition of water to blood, to which I have already drawn the attention of the profession, the conclusion to which I am brought is, that urea in the blood, in such proportions as we consider extreme, as during uræmia in the human subject, does not, per se, produce any extra fluidity of blood; and that when it is largely diluted and added to blood, the results presented are due, exclusively, to the physical effects produced by the water.

Comparing further these experimental truths with the pathological conditions of the blood in uræmia,

we find that there is an identity of representation to an extent that is singularly remarkable.

In uræmia, uncomplicated with acute inflammatory action, the blood shows a tendency to soft gelatinous fibrinous separation; the clot produced is soft and dark, and yields abundance of water; the corpuscles are not broken, but rendered irregular and scanty. The hæmatine consequently is not effused; and, although there may be congestion of soft parts and effusions of serum, there is no true hæmorrhagic exudation.

The effects presented are due to the suppression of urinary water, and not to the urea; which, though active in its way as a poison, is not a blood-solvent.

The comparisons here instituted obtain as a general rule; and when that rule is broken, it is through a modification, either in the course of the diseased manifestation itself, or in changes occurring immediately before or after death. In other words, when in uræmia the blood is found permanently fluid and surcharged with ammonia, the fluidity, dependent on the alkaline constituent, is produced either by some unusual circumstance giving origin to an excess of alkali, or by chemical changes occurring in the urea itself, at or after death, by which its conversion into carbonate of ammonia is brought about.

We have thus, step by step, followed out the cause of uræmic coma. We have determined absolutely that the disease depends on suppression of secretion of the urine; we have analysed this secretion, and examined the various constituents; we have excluded

all producing causes except urea; we have turned to synthesis, and have definitely shown that urea is capable of acting as a narcotic poison, and of producing symptoms identical with those of uræmia absolute. Lastly, by the analytical, as well as by the synthetical process, we have proved that the said symptoms, and the pathology coincident with them, are dependent on urea acting primarily as a poison, and not on its resolution into another poison, viz. carbonate of ammonia.

THE CAUSE OF DEATH IN URÆMIA.

The cause of death in uræmia is primarily to be traced to the accumulation of urea in the system. Against fatal accumulation the body seems to hold a long power of resistance, except in cases such as acute scarlet fever, where the obstruction of the kidney is sudden and complete; for the urea, in chronic cases of kidney-disease, appears to find a moderately free exit by other emunctories than the renal organs, especially by the skin.

For a time, therefore, in cases where there is renal obstruction, the urea may be eliminated with sufficient freedom to save the system from immediate and serious mischief; there may be premonitory symptoms, such as occasional drowsiness, but these symptoms become relieved by a sharp purgation or a free perspiration, upon which the impending danger is removed.

But when once the balance is destroyed, when once there is an excess of urea in the blood, although

at first it be slight, one singular and important fact succeeds; the kidneys, embarrassed by the excessive demand made upon their secreting power, become rapidly congested, and, as a result, rapidly resistant to excretion. Thus, when urea is injected into the body of a healthy animal, and death occurs even within an hour, the kidneys are found so charged with blood, that their structure is distended, and when an incision is made into the structure, fluid dark blood copiously exudes from the divided surface.

This observation, first made by Hammond, I have fully confirmed by repeated experiment. It explains clearly the suddenness of acute uræmic attacks, and their persistency often to the death; for as the resistance to the excretion of urea, by its main channel, increases in proportion to the degree of accumulation, so is the fatal influence of the poison brought out with a steadily increasing force.

The train of evils thus set up, urea accumulating, and the kidneys failing in action, congestion of blood commences in them as from two centres, and extends to the whole venous system, with more or less of intensity. The obstruction put on the venous current passes to the arterial; for, the heart being made to act against an universal blockade, the weakest portion of the capillary system will either give way, or permit a portion of its fluid contents to exude through its coats. The latter alternative is the one most common, and effusions of serum are therefore exceedingly frequent in uræmia; indeed, I doubt whether

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