PROTEOSE INTOXICATIONS AND INJURY OF BODY PROTEIN

Abstract

Sterile abscess, pleuritis, and pancreatitis give a clinical reaction in the experimental animal very like the same acute inflammatory processes due to bacterial activity, provided the bacterial agents are limited to the initial location. The curve of urinary nitrogen excretion in the fasting dog shows the same precipitous and sustained rise in sterile and bacterial inflammatory reactions. This indicates that the same type of protein injury and autolysis in the body is produced by the sterile inflammatory reaction as by the bacterial reaction. It is assumed that the primary effect of the chemical agent or of the bacterial growth in the tissues is local cell injury or necrosis. This injured cell protoplasm undergoes prompt autolysis with escape of toxic protein split products. These toxic protein split products may be, in part at least, of the proteose group and are absorbed into the circulation, producing the familiar general reaction. The injury of body protein is obvious from the great increase in elimination of nitrogen in the urine and appears to be the same in sterile and in bacterial inflammation. The injurious agent in the sterile inflammation must be derived from the host protein, and we may assume with safety that much of the injurious material emanating from a septic inflammation must come from the host protein rather than from the bacteria. Acute sterile pancreatitis is one of the purest examples of an acute non-specific reaction where the intensity of the host's intoxication may reach a maximum in 12 to 24 hours. We believe that fundamentally this reaction is very similar to that observed after the production of a sterile abscess or pleurisy. Non-specific intoxication must account for the sterile reactions described above. Septic inflammations show the same acute reaction and injury of body protein. The deduction is obvious—that a great part, at least, of the reaction in septic inflammation is truly non-specific and results from the primary injury of the host's protein and cell autolysis.