When an irritant is applied to a transparent vascular tissue, such as the tongue or web of the frog, it produces effects which vary slightly, according to its nature. If croton oil be applied, there is first a contraction of the arteries, extending to their whole length, followed by dilatation. If ammonia be used, there is dilatation without previous contraction. The dilatation affects chiefly arteries and veins, but also, though to a less extent, capillaries. The dilatation of the arteries leads to an Active hyperemia, the current is accelerated in the arteries, capillaries, and veins, and these vessels are overfilled; there is a great excess in the quantity of blood passing through the vessels. The acceleration of the current does not persist, however, in the most affected parts; on the contrary, the blood-corpuscles begin to lag, especially in the capillaries and veins, although there is still acceleration in the arteries, and in the capillaries and veins of the less inflamed parts. This stagnation in the capillaries and veins may assume a high degree, especially in the part most acted on by the irritant. Although the current is slow in these vessels they remain overfilled, a Passive hyperemia supervenes on the active hypersemia; at the same time the white corpuscles accumulate along the internal wall of the veins in the manner already described, and they also adhere at intervals in the capillaries. The circulation may come almost to a standstill in the capillaries of the parts most affected, while at various distances out from this there will be manifest a less and less amount of retardation till a zone is reached where the retardation disappears, and by and by gives place to acceleration.

Fig. 56. - A leucocyte from human blood showing amoeboid movement. (Klein).

We have now to consider what may be the explanation of these various phenomena which the vessels manifest. The observations of Lister present us with a view of this subject which has been largely confirmed by other observers. Saviotti's researches are for the most part confirmatory of Lister's views.

Contraction of the arteries is not, in any proper sense, a part of the inflammatory phenomena. It is simply the result of stimulation of the nerves by the irritant, and while in the case of many irritants it does not occur at all, it is always transitory. Contraction of arteries may be produced either by reflex or direct irritation of nerves. It is produced reflexly by irritation of sensory nerves. Thus the arteries in the web of the frog's foot are seen to contract when the skin is tapped or twitched with the forceps. This contraction does not occur if the nerve stems be first divided. On the other hand the irritant may cause contraction directly, by stimulating the vaso-consfcrictor nerves (as cold does), and so produce a temporary contraction of the arteries.

Dilatation of the arteries, leading to active hypersemia (also called determination of blood), is induced by paralysis of the arteries, just as in other cases of active hyperemia.

It is important here to recall the fact that irritants act injuriously on the tissues, and, in a certain sense, paralyze them. Lister in his important researches on inflammation brought this fact into prominence. The skin of the frog is supplied with pigment cells. These cells, as already illustrated, are contractile bodies. In the state of rest they are extended into numerous branches, which make a fine pigmented reticulum under the skin; in the active state they are drawn together so as to make a dark clump. They are under the command of the nervous system, and by their means the animal is capable of changing its colour, presenting a dark hue when the cells are relaxed, and a lighter colour according to the degree of concentration. Some irritants have the immediate effect of relaxing the pigment cells, and this itself is so far an evidence of paralysis, as the dispersed condition is the state of rest of the cells; but whether the pigment is dispersed or not, the animal loses control of its pigment in the affected area, which does not change its colour with the rest of the skin, and may be found dark while the animal is pale, etc.

In a similar manner the dilatation of the arteries is effected by a paralytic influence of the irritant. It is not easy to determine whether this paralytic influence is exercised through the peripheral ganglia, whose existence we have already seen reason to infer, or directly on the wall of the vessel, but as these ganglia are in or near the vessel-wall, we may infer that both are influenced. The view has been held that the dilatation is reflex, but this is excluded by the observations of Cohnheim. He found that if the sciatic nerve has been divided in a frog's leg the arteries dilate, but the application of an irritant produces a further dilatation. He found also that, after destruction of the brain and spinal cord, irritation of the tongue still produces dilatation of the arteries. The acceleration of the blood-current in the arteries, capillaries, and veins, will be understood from what has gone before to be a direct result of the dilatation of the arteries; we have, in fact, an active hyperemia.

The Retardation is to be referred to an increased adhesiveness of the blood-corpuscles. This is a matter of direct observation. The corpuscles in the inflamed area can be seen to move sluggishly along the wall as if attracted by it, and the Pavementing of the veins with white corpuscles is clearly due to increased adhesiveness between the two, or to an attractiveness exercised on the leucocytes. It has been pointed out by Lister that when the blood is removed from the vessels and comes in contact with dead matter, the blood-corpuscles acquire an adhesiveness which they do not possess inside the normal vessels. The red corpuscles stick together by their flat surfaces and form the well-known rouleaux, The adhesiveness of the white corpuscles is not so obvious when a drop of blood is examined outside the body, but there is reason to believe that it is even greater than that of the red. Now the irritant damages the walls of the vessels, with the result that the corpuscles behave as if in the presence of dead matter - they become adhesive.

This is excellently shown in an experiment of Lister's. He ligatured the leg of a frog, producing thereby stagnation of the blood in the vessels, but on examining the web it could be seen that the corpuscles were able to move freely among one another - there was obviously no adhesiveness. But now, when a piece of mustard was applied to the web, this free movement ceased in the area affected; the corpuscles became aherent among themselves and to the walls of the vessels. The result of this was an accumulation of the corpuscles in the irritated area; any corpuscles which happened to glide into the area remained adherent there, and so, by degrees, the vessels became overfilled - a state of hyperemia superinduced on stagnation. If any corpuscle happened to escape from the affected area, it ceased to be adhesive, and moved freely about.

We may therefore infer that the retardation of the current and the pavementing of the veins with white corpuscles are the result of the injury to the vessel wall, and it may be added that, in connection with inflammations, all degrees of stagnation up to absolute stoppage or Stasis may be produced, and are often manifested together in the same case.

We may now sum up the conditions presented by the blood-vessels in the early periods of inflammation as follows. The arteries dilate by a relaxation, of a paralytic character, of their muscular coats, due to a paralysis of the peripheral ganglia. In some cases this dilatation is preceded by an evanescent contraction. The immediate result of the dilatation of the arteries is active hyperemia, or determination of blood, involving overfilling of the arteries, capillaries, and veins, with acceleration of the current. This is followed by retardation of the current, the vessels remaining dilated and hypersemic, and this retarda tion may go on to almost complete stasis in the capillaries. The retardation is due to adhesiveness of the corpuscles, and to the same cause is to be traced the pavementing of the veins with white corpuscles.

It is sometimes possible in acute inflammation of the skin, as in the case of a boil, to observe conditions directly traceable to the state of the vessels here indicated. Thus at the peripheral parts of such a focus of inflammation the skin presents a fiery-red appearance due to determination of blood; the red colour may be pressed away with the finger, but it immediately returns. Inside this zone there is an area in which the redness is not so vivid, and when the red colour is pressed away it returns sluggishly; the corpuscles are here already adherent, and the current retarded. Then in the-more central parts a dusky red appearance is presented, and on pressure it may be impossible or very difficult to remove the redness; here a condition of stagnation exists.