the second 25 c.c. of water were added. When estimated the two fluids should show a difference equal to the quantity of salt added." Results very closely corresponding to this were obtained.

These results do not agree with results obtained by Salkowski (Pflüger's Archiv,' vol. 5, 1872, p. 210) and Maly (Pflüger's 'Archiv,' vol. 6, p. 201). Salkowski proposed a volumetric method for the determination of uric acid, very similar to that proposed by Dr. Haycraft; in this he added excess of silver nitrate and estimated the excess of silver present. He gave up this method, however, as on examining the silver precipitate obtained from urine, after complete precipitation of the phosphates by magnesia mixture, he found that it contained magnesium as well as silver, and that the proportion of magnesium to silver varied considerably in precipitates from different urines, though constant for the same urine. Haycraft considers that the presence and variation in amount of magnesium in these precipitates may be due to varying quantities of magnesium ammonium phosphate in them. This is, however, impossible, as the phosphates were precipitated by Salkowski previously, and the urine allowed to stand for twenty-four hours before filtration to ensure their complete separation. Salkowski's results were confirmed by Maly, who found that if in the presence of salts of calcium, magnesium, potassium, and ammonium, a solution of a urate be precipitated by silver nitrate, the precipitate contains these metals as urates as well as silver urate.

As a test of the accuracy of Haycraft's method, I examined samples of various urines both by his method and by Salkowski's method, which is universally acknowledged to be the most reliable, and the accuracy of which has been proved by experimental evidence. This method consists in taking 250 c.c. of urine, adding 50 c.c. of magnesia mixture to precipitate phosphates, and then adding to 240 c.c. of the filtrate (which are equivalent to 200 c.c. of the urine) silver nitrate to precipitate the uric acid. This precipitate of silver urate is decomposed by sulphuretted hydrogen after being suspended in water. The liquid is then acidified, filtered hot, and evaporated to small bulk, and the uric acid allowed to crystallise out. These crystals are then dried and weighed. The following results were obtained :

The results obtained by Haycraft's method were always considerably higher than those obtained by Salkowski's. The reason of this is that Dr. Hay craft has assumed that the silver precipitate from urine consists of an urate containing only 1 atom of silver in the molecule, whereas the proportion of silver in this precipitate is always larger, and varies in amount in different urines. If we assume that the precipitate contains 2 atoms of silver in a molecule of urate and divide the results obtained by Haycraft's method by two, we see that in two cases they are about equal to, in the rest less than those obtained by Salkowski's method. The proportion of the results obtained by one method to those obtained by the other varies. This agrees with the results of Salkowski's researches, from which one would expect that the results obtained by Haycraft's method would not bear a constant relation to the results obtained by Salkowski's, and that the halves of the results by the former method would be lower than, in most cases, those obtained by the latter.

V. "On the Effects of Increased Arterial Pressure on the Mammalian Heart." By JOHN A. McWILLIAM, M.D., Professor of the Institutes of Medicine in the University of Aberdeen. Communicated by Professor M. FOSTER, Sec. R.S. Received May 30, 1888.

The following is a short preliminary statement of some of the main facts elicited in the course of a recent investigation. The experiments were conducted on chloroformed cats. The thorax was laid open, artificial respiration being maintained, and the action of the auricles and ventricles was recorded by means of the graphic method. The contraction of the heart in ordinary circumstances having been observed and registered, the arterial pressure was raised by constricting or clamping the last part of the thoracic aorta-usually for a period of 4-8 seconds. Clamping for longer periods was often accompanied by convulsive movements of the animal.

The results may be briefly summarised as follows:

:

They fall into one or other of two categories according as to whether the medullary cardio-inhibitory mechanism is (I) functionally active in controlling the heart's action, or is (II) incapable of affecting the cardiac beat. The latter condition is one that may result from various causes, such as (a) section of the vagus nerves or paralysis of their function through the influence of drugs, &c.; (b) depression or paralysis of the medullary cardio-inhibitory centre, brought about by drugs or by other causes.

I. In the first-mentioned condition, when the cardio-inhibitory mechanism is in a position to control the heart's action, a marked rise of the arterial pressure (such as results from compression of the descending aorta) causes, as Marey has shown, a slowing of the cardiac rhythm.

I find that the rise of blood-pressure also causes marked changes in the contraction force of the cardiac muscle. For a short time (a few seconds, 1, 2, 3, &c.), after clamping of the descending aorta there occurs an augmentation in the strength of the beat-especially of the ventricular beat; meanwhile the rhythm has become slower than before (fig. 1).

Then there occurs a more or less sudden change. The auricular contractions undergo a striking diminution in force. They remain enfeebled until the compression of the aorta has been discontinued and the blood pressure has fallen; then they gradually recover, though the process of recovery may not always begin at once (figs. 1 and 2).

The changes in the vertricular action consequent upon closure of

the descending aorta do not run parallel with those occurring in the auricles. The ventricles, while they beat more slowly than before, usually beat much more strongly even when the auricular contraction has become markedly weakened (fig. 1). Depression of the ventricular force may occur, but it comes considerably later than the auricular depression, and is very much slighter in degree (fig. 3). The slow strong ventricular systoles are able to empty the cavity of the left ventricle when systoles of less strength fail to do so-as indicated by the fact that the recording lever often fails to descend to the ordinary level in the interval between the contractions (fig. 1). When the descending aorta has been released and the pressure has fallen, a period of marked cardiac acceleration often succeeds; during this acceleration, the individual ventricular beats are much diminished in force (fig. 3).

The above-mentioned cardiac changes attendant on a sudden rise of arterial pressure are brought about through the medullary cardioinhibitory centre and the vagus nerves. They are of such a nature that while the ventricles are contracting slowly and powerfully in such a way as to be able to discharge their contents in spite of the increased arterial pressure, there occurs a striking change in the action of the auricles involving a great reduction in the amount of blood pumped into the ventricles and the degree in which the latter are distended just before their systole. Hence the quantity of blood thrown out by the left ventricle into the systemic arteries is much diminished, and the rise in the blood-pressure is in some measure counteracted and controlled.

II. In conditions where the medullary cardio-inhibitory mechanism has ceased to exert any controlling influence upon the heart (e.g., after section of both vagi), the effects following a sudden rise of arterial pressure are entirely different from those above described.

Marey showed that there was no very constant relation between the rate of the heart's action and the height of the blood-pressure after section of the vagi; some degree of acceleration was commonly observed.

Examining the cardiac changes in the way already mentioned, I find that after section of the vagi or paralysis of the medullary cardio-inhibitory mechanism, a sudden rise of arterial pressure causes no very striking or constant change in the heart's rhythm; frequently there is slight acceleration. There is a complete absence of the characteristic changes in the contraction force above described (under I). As regards the strength and character of the cardiac action, there are two conditions to be noted.

(1.) The heart may at each systole be able to discharge its contents in normal or approximately normal fashion. In such circumstances the principal change to be observed in a vigorous heart is a marked