Changes that Occur in Mation

cells, vessels, tissues, tissue, blood, injury, irritation, process, repair and processes

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The final stage of the inflammatory process, as regards the blood-vessels, is that the blood experiences ever-increasing difficulty in passing onwards, until at length the flow ceases alto gether in the inflamed part, the vessels remain ing choked with blood. This is the stage called stasis, that is, stoppage.

Changes in the Tissues, outside the blood vessels, also occur in inflammation.

These tissues are found crowded with white cells, a large number of which consists of those that have emigrated, as the phrase is, from the vessels, many of them being doubtless descend ants of the emigrant cells, which have the power of multiplication by division, and some being, perhaps, produced by the tissues, which share in the inflammation. The cells that have escaped from the vessels are remarkably active, exhibit the anneboid movement described on p. 293, by means of which they push their way through the tissues and wander some distance from the vessels out of which they have come. On this account they have been called "wander cells." • Three things must be borne in mind regard ing the tissues themselves : firstly, the injury or irritation has damaged them, diminished their vitality, perhaps actually quite destroyed the vitality of some portion ; secondly, they are invaded by the numerous white cells escaping from the vessels, as described, and they are being saturated and compressed by the fluid exuding from the vessels. In these two re spects the tissues may be regarded as mere passive victims of processes in which they play no part. It must not be forgotten, also, that the injury or irritation may be continuing. But, thirdly, unless the injury or irritation has been so intense as either immediately, or quickly, to destroy or kill the tissue altogether, the tissues themselves " react" to the matory process. One of the chief evidences of ' this is that the cells of the tissue itself become active and proceed to multiply, so that speedily large numbers of round cells are produced within the area where the inflammatory pro cess is going on. It has been pointed out that every special tissue whatever—muscle tissue, nerve tissue, and so on—contains a supporting and packing connective tissue (see p. 56), and that this connective tissue, besides containing round cells, is always and everywhere more or less rich in special connective-tissue corpuscles. It is particularly these cells which become active and proliferate or multiply. Thus the area which is the scene of the inflammatory process becomes crowded with white cells, a large num ber of which have emigrated from the blood or are the offspring of emigrant cells, but a large proportion of which also have been produced, from the fixed cells of the tissues, by the reaction of the tissues themselves.

What explanation can be offered of these two sets of changes? There is no doubt that the explanation is twofold.

In part the changes are due to the fact that the area is damaged or irritated. The widening of the blood-vessels and the fuller supply of blood is to some extent caused by a species of temporary paralysis of the vessels' walls by the injury or irritation. They lose their tone, lose

their grip, so to speak, of the blood stream, and the blood, therefore, from neighbouring unin jured vessels surges into them. Some alteration of the walls also occurs, so that the cells roll along them less easily, and tend to stick to them, and it is doubtless owing to this change—this lowered vitality--of the vessel walls that the cells are able to work their way through them, and that they permit the oozing through them of a much larger quantity of fluid than they would do if their vitality had been unimpaired. That some of the changes occurring outside the vessels, in the tissues, are also merely the result of damage is evident from the fact that many of the cells that escape from the vessels into the tissues there liquefy and break down, as do also many of the cells of the tissues themselves. But this is not the whole explanation. For if a fine, very slight wound be made, with a perfectly clean sharp instrument, in a tissue so thin as to be capable of observation under a microscope, similar changes are observed in the widening of blood-vessels, increased flow of blood, emi gration of white cells, and rapid production of new cells by the injured tissue, where there is no evidence of liquefaction or breaking down, and where the only result is rapid repair of the breach that has been made, the changes in the vessels and in the tissues ceasing as soon as the repair is completed.

In part, therefore, the changes that have been described are due to an effort to repair the injury and to arrest the irritation.

We may, therefore, say that the changes that have been described, taking them altogether, are the evidences and consequences of two sets of processes going on side by side, one set being the effects of the injury and irritation to which the part has been subjected, and another set being time efforts of the part to repair the dam age, and these two processes are going on simul taneously side by side--a destructive process and a reparative process. They are so mixed up together that it is impossible sharply to dis tinguish what change belongs exclusively to one process and what to the other. But, whether the result is the more or less complete destruc tion of the part, or the more or less perfect restoration of the part, will depend on which of the processes gains the mastery. To some extent the same change may be destructive or reparative according to the extent to which it goes. Thus the widening of the vessels and the increased flow of blood may be at once the result of the damage and the means of repair. If it does not go to excess, the increased blood supply, primarily due to the injury, may yet bring the material for repair, and the cells which escape from the vessels may, and indeed do, act as repairers of the breach that has been made. But if the vessels became so engorged that the circulation becomes completely arrested for a lengthened period, and the cells escap ing are so numerous that the tissue becomes, so to speak, smothered with them, then the very excess of reparative material may only secure the death of the already imperilled tissue.

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