at an angle with the current of the blood, the concretion may simply float loosely in the direction of the stream, and may be merely composed of a few layers of deposited matter, or it may be affixed firmly to the projection by mechanical or even organic adhesion.

In the cases I have here been specially describing, the formation of the concretion seemed due in great part to an excess of fibrin in the blood. They were all inflammatory cases, in which what has been called hyperinosis by Franz Simon was present. In twenty-three cases of death from acute inflammation of the respiratory organs, and which ended fatally in the first stages by rapid sinking, I found in every case a fibrinous concretion, answering to one or other of the above named varieties; and, in the blood which remained in the form of red clot, the proportion of fibrin was far above the normal amount. These observations are confirmed by Grisolle; who, however, assigns for the concretion a different cause, viz., pulmonary obstruction.

Since the time of Pasta, a dispute has been going on in the medical world, as to the existence or non-existence of these fibrinous masses previous to death. I have explained that there are two definite forms of concretion; one formed from blood at rest-after death; the other from blood in motion-before death. I think, for my own part, that the arguments are conclusive which explain the probability of these last named depositions; for, could a concretion seize firm hold upon the walls of the heart, or become modeled into a hollow tube, or be grooved by blood currents, when all motion has ceased? Still, as the settlement of this dispute has not been definitely made as yet, I have thought it well to push the matter to a more perfect demonstration, by

inquiring whether a concretion could not be artificially produced in an animal, and be laid bare in its heart while the animal had not fully ceased to live, and while its heart was still pulsating.

Assuming, therefore, as a basis of experimental research, that in inflammatory cases the deposition takes place from an absolute increase in the amount of fibrin in the blood, and having repeated with satisfactory and affirmative results some of the interesting experiments of Dr. Gairdner,* in which he showed that by inhalation of oxygen gas the fibrin could be increased in quantity, I carried out a series of experiments with animals on the inhalation of oxygen, in which the inhaling process was continued for a period long enough to produce a decided class of symptoms, which were considered to afford evidence of fibrinous deposition. Then I rapidly destroyed the sensation of the animal, and at once laid open the heart.

Before passing to the details of experiment, it is necessary to premise, that many of the statements ordinarily made, to the effect that oxygen is a narcotic poison, are fundamentally incorrect. This error has arisen from the mode in which the experiments which led to it have been performed. I found, in the very first step of my labours, that, if an animal were placed in a jar of oxygen, with lime water beneath to remove the carbonic acid, in a short time the animal became subjected to symptoms of asphyxia and insensibility, notwithstanding the fact that a taper placed in the jar would burn more brightly than in common air. But I found, further, that when these symptoms presented

* Essay on Gout, 2nd Edition.

themselves, they could be at once removed by the admission of more oxygen. Hence the inference was clear, that the animals were either suffering from carbonic acid gas, or from the exhaustion of the gas, incident to its being turned rapidly into carbonic acid, and being removed by the lime, while no new supply was forthcoming. I therefore modified the experiment, and, instead of placing an animal in a closed chamber filled with oxygen, subjected it to a constant stream of the gas; or, in other words, kept it in a room ventilated with oxygen.

In an

I had made a chamber with glass sides, capable of holding 3,350 cubic inches of gas. The chamber was air-tight, except at the top and the bottom. opening at the top a tube was inserted for the introduction of the gas. From an opening at the bottom, beneath a perforated zinc stage, another tube ran downwards, for the escape of the current. This tube dipped

to the extent of an inch into some lime-water held in a beaker beneath. When this arrangement was completed, a large Pepys' gas-holder, capable of receiving 2,000 cubic inches of gas, was charged with oxygen made by the decomposition of chlorate of potash.

EXPERIMENT I. All being prepared, I introduced into the chamber, at 9 P.M., a full grown healthy cat. The escape tube from the gas-holder was connected with the tube at the top of the chamber, and a free current of oxygen was constantly driven through. The apparatus played well, and bubbles of gas were kept always escaping through the lime-water, no care being taken to save the gas. If at any time the limewater became changed in colour, the ventilation was increased; and thus the animal was soon in an atmo

sphere of pure oxygen, always newly supplied. By means of an additional gas-holder, I was further enabled to keep up the current steadily, since one was always ready when the other was exhausted of its gas; while, by means of a funnel-tube, running perpendicularly from the top of the chamber to a saucer inside, food was supplied. The drawing beneath represents the chamber and its appliances, while the experiment was progressing.

gas.

After the animal had been breathing the oxygen for an hour and a half, the number of respirations was markedly increased, and the act of inspiration was accompanied by a dry harsh sound. The creature was excited and thirsty, often licking the sides of the chamber. At the end of seven hours, she became restless, and slightly convulsed. The supply of oxygen was now

cut off, and she was allowed to breathe the ordinary atmosphere quite freely. For three hours later, she continued in a restless, sinking state, and died.

About two hours after death the body was opened, and carefully examined.

The brain and spinal cord were perfectly natural throughout. The lungs were intensely red, but showed no indication of structural change. The blood in the veins was firmly coagulated. In the portal vein there was a thread of fibrin. The right auricle was literally choked with a tough fibrinous mass, which was firmly adherent to the wall of the auricula. It was covered on its superior surface by a thin layer (about a line in thickness) of red blood, which was easily removable. A prolongation of this fibrinous con

cretion passed into the ventricle, and curved upwards to the pulmonary artery. In the left auricle also there was a concretion, but of less size. The

Fig. 3.

right side of heart. Natural size.

of the same

tricuspid and mitral valves were fringed Fibrinous concretion in the with fibrin; and, at the root of the pulmonary artery, there was a small cord kind, which adhered by its lower extremity to the cardiac wall. No trace of organic disease existed; but the muscles of the body and the vascular organs were unusually red. The bronchial membrane was dry throughout, but in no way red or congested.

Here there was a case of hyperinosis artificially produced, and fibrin was deposited in the heart.

[It was unfortunate that this experiment was not sufficiently conclusive; for, thinking that the death would not be so rapid, the animal being left in the open air, I, tired with watching all night, went for about