like the corpuscles of human blood, with their long diameter transverse to the axis of the vessel. The white corpuscles are not unfrequently seen of a pyriform shape, dragging slowly along, or actually sticking to the sides of the vessels; that they do possess some degree of adhesiveness is manifest, but it does not seem to be so considerable or general as Dr. Williams supposes. When the inflammation is subsiding, and the stagnant blood beginning again to resume its course, all that can be observed is, that the agglomerated mass of red corpuscles in a vessel loosens and breaks up, so that the individual corpuscles are again visible, while the impulse of the heart makes itself more and more felt, and at last sweeps away the accumulation altogether, having first detached small portions successively. Fibrinous coagula also form occasionally, as Mr. Wharton Jones describes, and are similarly disintegrated, and carried away by the returning current during resolution of the inflammation. While stagnation continues, a small quantity of hæmatin dissolved in the serum exudes, and imparts to the tissues bordering the vessels some degree of yellow staining.

We intend the foregoing account to serve as a description of what may

An exact copy of a portion of the web in the foot of a young frog, after a drop of strong alcohol had been placed upon it. The view exhibits a deep-seated artery and vein, somewhat out of focus; the intermediate or capillary plexus running over them, and pigment-cells of various sizes scattered over the whole. On the left of the figure, the circulation is still active and natural. About the middle it is more slow, the column of blood is oscillating, and the corpuscles crowded together. On the right, congestion, followed by exudation, has taken place, constituting inflammatory action in the part.

a. A deep-seated vein, partially out of focus. The current of blood is of a deeper color, and not so rapid as that in the artery. It is running in the opposite direction. The lymph-space on each side, filled with slightly yellowish blood-plasma, is very apparent, containing a number of colorless corpuscles, clinging to or slowly moving along the sides of the vessel.

b. A deep-seated artery, out of focus, the rapid current of blood allowing nothing to be perceived but a roddish-yellow broad streak, with lighter spaces at the sides.

Opposite c, laceration of a capillary vessel has produced an extravasation of blood, which resembles a brownish-red spot.

At d, congestion has occurred, and the blood-corpuscles are apparently merged into one semitransparent, reddish mass, entirely filling the vessels. The spaces of the web, between the capillaries, are rendered thicker and less transparent, partly by the action of the alcohol, partly by the exudation. This latter entirely fills up the spaces, or only coats the vessel.-Bennett.

be actually observed of the process of inflammation, as it occurs in the frog's web. Most of the statements we have verified by our own examination, and we believe they are in accordance with those of the best observers. The question now presents itself, what occasions the stasis? and this is, in fact, the great and unsolved problem of inflammation. The carlier speculations as to the vessels being in a state of spasm, or, on the other hand, of atony, need not occupy our attention; nor can we see that any definite ground is gained by the hypothesis of Hunter, that the vessels are in a state of active dilatation, except that he seems thereby to recognize the true nature of active hyperæmia. Three opinions, of later date, may be said to be still sub judice. Two of them we have already referred to, when speaking of active hyperæmia. The third is that maintained by Dr. Williams. He considers "that an essential part of inflammation is the production of numerous white globules in the inflamed vessels; and that the obstruction of these vessels is mainly due to the adhesive properties of these globules." With regard to this doctrine, a reference to the description we have given will show that we agree with Professor Paget and Mr. Wharton Jones, in rejecting it. Nothing can be more evident, we think, than that the white corpuscles play no important part in causing the stagnation of the bloodcurrent. But we differ from Mr. Paget, and agree with Rokitansky and Williams, as to the increased production of white corpuscles in the inflamed vessels. The numbers which present themselves in some of the small veins, cannot, we think, be brought together merely by accumulation, especially when we consider that most of the communicating capillaries are plugged up, and that they cannot therefore be transmitted from them. The neuro-pathological theory of Henle is the one which Rokitansky prefers; but he acknowledges that it gives no satisfactory explanation of stasis of the blood. Henle himself thinks he can. account for it according to his view as follows: "As a physical consequence of dilatation of the vessels, there takes place a retarded flow of blood. This, together with the relaxation and dilatation of the vessels, favors the exudation of serum; the consequence of which is, that the plasma of the blood in the part becomes inspissated by a preponderance of protein matter over the salts. This inspissation of the plasma determines endosmotic changes in the red corpuscle, in consequence of which they are disposed to aggregate." Rokitansky, stating that mere paralysis and dilatation of the vessels cannot give rise to stasis, gives the following as his own opinion of its mode of production: "It proceeds (a) from the sticking together of the blood-corpuscles, the heaping up and wedging together of them in the capillaries, while the plasma in part flows off towards the veins; (b) from the inspissation of the plasma occasioned by the exudation of serum through the dilated and attenuated walls of the vessels, and its saturation with fibrin and albumen; (c) from the heaping up of the colorless corpuscles-i. e. nuclear and cell-formations, together with blood-globules; from their sticking together, and from the delicate, hyaline, fibrinous coagula, which develop themselves among them. This is certainly the most important

1 Wharton Jones's Report on Inflammation, April, 1844.

moment in the inflammatory process, since, on the one hand, it very specially throws light upon the phenomenon of stasis, and, on the other hand, comprehends also the plastic processes which take place in the heaped up and stagnant blood. It separates in this way the process of inflammation from a merely simple one of exudation. The elementary formations above mentioned are not merely swept together towards the demesne of the stasis, but they originate as new (productions) in the stagnant blood, for this generally presents remarkable alterations. .

We believe the latter paragraph to contain views of very great importance, especially with regard to the effects of local inflammation upon the system. Nor do we doubt that the changes wrought by exudation, draining away of Liq. Sanguinis, multiplication of white corpuscles, and coagulation of the fibrin, may all exercise considerable influence in prolonging and confirming the stasis, and determining its results. But we do not think they are the primary and causative phenomena. It seems to us a very important fact, which Mr. Wharton Jones states, and which we have observed ourselves, that "stagnation commences in the capillaries, and extends from them to the veins on the one hand,

Production of stasis from Mr. Wharton Jones's Essay, Guy's Hospital Reports, vol. vi. p. 35.

and the arteries on the other." We have seen the blood stagnant in the capillaries, while it was moving on steadily through an adjacent artery and vein. This points to the capillaries as the part where the arrest commences. Again, it is a very important circumstance, that, if a strong stimulus be applied, the stasis takes place almost immediately: it seems as if the blood were suddenly coagulated in the capillaries. When the arrest comes to pass more slowly, so as to admit of being watched, it is described by Mr. Wharton Jones as taking place in the following way: Red corpuscles, more collapsed and darker-looking than natural, first adhere to the walls of the vessels, and then other red corpuscles adhere to them. "The first adhesion of red corpuscles to the wall of a vessel usually takes place at a bifurcation, and in this manner (see Fig. 6): The stream c, striking with force on the wall of the vessel, at the bifurcation A, some of the red corpuscles adhere to the wall of the vessel. Other red corpuscles adhering to them, an agglomerated mass results, which is sometimes seen to be moved along the vessel a short way by the force from behind; but more red corpuscles adhering

The

to the mass, the vessel is at last wholly blocked up by it at D. stream c, being no longer permitted to pass in part by D, passes off by E; but in leaving E, the stream strikes on the wall of the vessel at the bifurcation B, where red corpuscles adhere, and form a nucleus for an agglomeration, which blocks up both the vessels F and G-E and c also becoming blocked up, and so on the process goes. Stagnation is seen first to take place in those capillaries which are least in the direct course from the artery to the vein. . In those capillaries which lead most directly from the artery to the vein, and in which, consequently, vis à tergo operates most advantageously, the blood is latest in stagnating." The main point, that stasis is produced by the red corpuscles adhering to the walls of the vessels and to each other, is confirmed by others, and by our own observation. On one occasion, we distinctly noticed a single red corpuscle adhering, by one end, to the wall of a vessel, in which circulation was returning, while several other red corpuscles, in motion one after another, swept slowly past, brushing against it, as it waved in the current. That in the healthy state the red corpuscles pass on so smoothly and uninterruptedly within their even relatively narrow channels, that they shun, as is well known, the walls, and allow a thin layer of the fluid in which they float to intervene, while the colorless corpuscles show no such tendency, but affect a preference for the so-called still layer, and move slowly onwards in it; that there is decidedly a tendency of the red globules to aggregate together in blood drawn from the body, while this seems to be held in abeyance, while the blood is within the vessels; that the smallest capillaries, according to Wharton Jones, are traversed chiefly by plasma, and by a few colorless corpuscles, one after the other, with only a single red corpuscle now and then; that the red and colorless corpuscles show no tendency to stick together, appear to us very significant facts, which require some such hypothesis as that offered in Wharton Jones's report, April, 1844, viz: "That there exists some sort of attraction between the colorless corpuscles and the walls of the vessels, but an absence of attraction, if not a repulsion, between the red corpuscles and their walls, as also between the red and colorless corpuscles.' Mr. Wharton Jones formerly conceived that it was the nervous influence which prevented the red corpuscles from aggregating together within the vessels, as they do out of the body, and that stasis depended on the suspension of this influence. It was an ingenious and probable opinion, but is disproved by the experiments which he himself has performed, and which are related in the Astley Cooper Prize Essay. In these he shows, that, after the nerve accompanying an artery had been divided, the flow of blood, though interrupted for a short time, soon returned, and became quite free; and also that, after section of the ischiatic nerve, the arteries of the web of the same side are found somewhat more dilated, and the flow of blood in them freer and more rapid than in the web of the uninjured side, while stagnation was induced more readily in the web of the limb whose nerves were entire, than in that of the limb whose nerves had been divided. He now adopts the opinion of Henle, though somewhat modified, that stagnation depends on inspissation of the plasma, on its containing an increased quantity of fibrin and albumen,

and rests much on the fact that such a condition of the Liq. Sanguinis, whether natural or imitated artificially, is found to increase the tendency of the red corpuscles to aggregate together. Our limits forbid discussion; and we therefore simply pass on to state our own opinion, so far as we may venture to offer one on this quæstio vexata. We saw reason to believe that the tissues, in yirtue of their nutrition power, exercised an influence on the movement of the blood; that in active hyperæmia their attractive force was increased; and we would now add, that it is through the failure of this nutrition power that we believe stagnation takes place. The exact nature of the influence exercised by the tissues over the blood, which traverses the capillary channels, is unknown. All that we can discern is, that it is such as promotes its free passage through them; and therefore, when it is in abeyance or greatly altered, it is to be expected that the circulation will be interrupted also. More than this we cannot gather from the observed phenomena; and we would only offer the remark, in conclusion, that in coincidence with the establishment of complete stasis, cessation of the natural function of the part occurs, and other processes commence-the exudative, in which the plasma, that in a healthy state would have ministered to and maintained healthy action, is consumed in wasteful or even destructive changes. Whether the stasis depend solely on a persistence and exaggeration of the attraction of the tissues for the blood which exists in active hyperæmia, or upon this and an abolition of the natural non-aggregative tendency, or even repulsive tendency of the red corpuscles for each other and for the walls of the vessels, must remain uncertain; but the coincidence above noticed must be allowed to give considerable support to the main point, on which we would insist, viz: that the nutrition power of the tissues is chiefly concerned in the production of the flow of active hyperæmia, and the stasis of inflammation.

We must take some notice of the different varieties of inflammation, which depend, partly on differences inherent in the subject, partly on different exciting causes. What is called Sthenic inflammation is that which occurs in a healthy person, either spontaneously, or from exposure to cold, or the application of some irritant which does not contaminate and depress the general system. The symptoms, if the inflammation is extensive, run high, the febrile excitement is considerable, and free depletion is required and borne well. The exudations contain much plastic matter, and pus, if formed, is of the kind termed laudable. Asthenic inflammation occurs in persons originally weakly, or rendered so by the action of the exciting cause, as in the inflammations of influenza; the pulse, though frequent, has no strength, the fever is of a lower type, and the effused matters manifest little plasticity. The terms acute, sub-acute, and chronic, have reference mainly to the periods of duration of the inflammation, or to the rapidity or slowless of its course. Acute inflammation is often, but not necessarily, sthenic; chronic and sub-acute are often not asthenic. Many changes are commonly said to proceed from chronic inflammation which probably belong more to the class of degenerations: it is, however, difficult to draw any marked line between the two. The chief value of the terms lies in their