Fibrinous pleurisy produced by a sterile inflammatory irritant offers opportunity for study of the part taken by enzymes of leucocytes in the resolution of a fibrinous exudate. When turpentine is injected into the subcutaneous tissue of the dog, an abscess results, but when an equal quantity of turpentine is injected into the pleural cavity, there is abundant exudation of coagulable fluid and the serous surfaces are covered by a layer of fibrin. Accumulation of fluid which can be followed during life by percussion of the animal's chest reaches a maximum at the end of three days, and then gradually subsides, so that at the end of six days, in most instances, the cavity contains no fluid. Fibrin, though diminished in amount at the time when fluid has been absorbed, is still present, and gradually disappears; at the end of two or three weeks the cavity has returned to the normal, save for a few organized adhesions.

Turpentine injected into the right pleural cavity may cause serofibrinous pleurisy on the left side; this inflammation may reach a maximum intensity at a time when pleurisy on the right side is subsiding.

During the early stage of inflammation fibrinous exudate, freed from the serum by washing in salt solution, undergoes digestion when suspended in an alkaline (0.2 per cent. sodium carbonate) or in an acid medium (0.2 per cent. acetic acid). At the end of five days, at a time when fluid is disappearing from the pleural cavity, digestion fails to occur in an alkaline medium, but occurs with much activity in the presence of acid.

During the first stage of the inflammatory reaction, when fluid is abundant and the fibrin which is present digests in alkali, thus indicating the presence of leucoprotease, polynuclear leucocytes are very numerous in the meshes of the fibrin. In the second stage, the exuded fibrin contains only one enzyme digesting in the presence of acid. At this time polynuclear leucocytes have disappeared and only mononuclear cells are embedded in the fibrin.

Products of proteolytic digestion, namely, peptone and albumose, absent in the exuded fluid during the first day or two days of inflammation, are present after three days and are found in less quantity at a later period.

The exuded fluid does not at any stage of the inflammatory reaction lose it spower to inhibit both enzymes contained in the leucocytes.

The exudate remains alkaline throughout the period of inflammation, but its alkalinity is less than that of the blood and diminishes slightly with the progress of inflammation.

Since the acids, which in vitro favor the action of the enzyme, present alone during the second stage of the inflammatory reaction, do not occur in the body, the possibility has suggested itself that carbon-dioxide brings this enzyme into action. If carbon-dioxide is passed through normal salt solution in which strips of such fibrin are suspended, digestion is greatly hastened. The normal inhibition exerted by blood serum upon the enzyme is overcome by carbon-dioxide and in the presence of a small quantity of blood serum, carbon-dioxide causes greater enzymotic activity than in the presence of salt solution alone.

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