CHAPTER XIV

DEATH AND DISSOLUTION OF THE ORGANISM

1. It is an old saying that we cannot understand life unless we understand death. The dead body, if its temperature is not too low and if it contains enough water, undergoes rapid disintegra­tion. It was natural to argue that life is that which resists this tendency to disintegra­tion. The older observers thought that the forces of nature determined the decay, while the vital force resisted it. This idea found its tersest expression in the defini­tion of Bichat, that “life is the sum total of the forces which resist death.” Science is not the field of defini­tions, but of predic­tion and control. The problem is: first, how does it happen that as soon as respira­tion has ceased only for a few minutes the human body is dead, that is to say, will commence to undergo disintegra­tion, and second, what protects the body against this decay while the respira­tion goes on, although temperature and moisture are such as to favour decay?

The earlier biologists had already raised the question why it was that the stomach and intestine did not digest themselves. The hydrochloric acid and the pepsin in the stomach and the trypsin in the intestine digest proteins taken in in the form of food; why do they not digest the proteins of the cells of the stomach and the intestine? They will promptly digest the stomach as soon as the individual is dead, but not during life. A self-diges­tion may also be caused if the arteries of the stomach are ligatured. Claude Bernard and others suggested that the layer of mucus protected the cells of the stomach and of the intestine from the digestive enzymes; or that the epithelial layer had a protective effect. Pavy suggested that the alkali of the blood had a protective action. All these theories became untenable when Fermi showed that all kinds of living organisms, protozoans, worms, arthropods, are not digested in solu­tions of trypsin as long as they are alive, while they are promptly digested in the same solu­tion when dead.[294] This is in harmony with the fact that many parasites live in the intestine without being digested as long as they are alive. Fermi concluded that the living cell cannot be attacked by the digestive ferments, while with death a change occurs by which they can be attacked. But what is this change? Fermi seems to be inclined to think that the “living molecule” of protein is not hydrolysable (perhaps because the enzyme cannot attach itself to it?), while a change in the constitu­tion or configura­tion of the proteins takes place after respira­tion has ceased. The fact that the living cell resists the digestive action of trypsin and pepsin has found two other modes of explana­tion, first, that the cells are surrounded by a membrane or envelope through which the enzyme cannot diffuse, and second, that the living cells possess antiferments. But the so-called antiferments are also said to exist after the death of the cell, whereas after death the cell is promptly digested. Frédéricq, as well as Klug, has shown that worms which are not attacked by trypsin are digested by this enzyme when they are cut into small pieces; although the pieces of course contain the antienzyme. The other sugges­tion that a membrane impermeable for trypsin protects the cells would explain why living protozoa are not digested by trypsin, but it leaves another fact unexplained, namely, the autodiges­tion of all the cells after death by enzymes contained in the cells themselves.

2. The disintegration of the body after death is not caused exclusively or even chiefly by the digestive enzymes of the intestinal tract or the micro-organisms entering the dead body from the outside, but by the enzymes contained in the cells themselves. This phenomenon of autolysis[295] was first characterized by Hoppe-Seyler.[296]

All organs suffering death within the organism, in the absence of oxygen, undergo softening and dissolu­tion in a manner resembling that of putrefac­tion. In the course of that process, albuminous matter gives rise to leucin and tyrosin, fat to free acids and soaps. This macera­tion, identical with the pathological concep­tion of softening, is accomplished without giving rise to ill odour and is a process similar to the one resulting from the action of water, acids, and digestive enzymes.

In work of this kind, rigid asepsis is required to exclude the possibility of bacterial infec­tion and this was first done by Salkowski, who showed that in aseptically kept tissues like liver and muscle the amount of substances that can be extracted with hot water increases considerably. By the work of others, especially Martin Jacoby and Levene, it was established that the power of self-diges­tion is shared by all organs. Analysis of the products of the autodiges­tion of tissues shows that, e. g., the amino acids, which constitute the proteins, are produced. Dakin, Jones, and Levene demonstrated the hydrolytic products of the nucleins, in the case of the self-diges­tion of tissues.[297]

Again the ques­tion arises: Why do the tissues not undergo autolysis during lifetime and what protects them, and the answer is that self-diges­tion is a consequence of the lack of oxida­tions. The presence of antiferments must continue after death and cannot be the cause which prevents the self-diges­tion during life, since nothing indicates the destruc­tion of the hypothetical antidigestive enzymes through lack of oxygen. The recent work of Bradley and Morse[298] and of Bradley[299] has thrown some light on the problem. These authors found that proteins of the liver which are indigestible can be made digestible by the liver enzymes if an acid salt or a trace of acid is added to the mixture. A m/200 HCl solu­tion gives marked accelera­tion of the autodiges­tion of the liver. This would explain why autodiges­tion takes place after oxida­tions cease. In many if not all the cells, acids are constantly formed during lifetime, e. g., lactic acid, which through oxida­tion are turned to CO2, and this diffuses into the blood so that the H ion concentra­tion in the cells does not rise materially. If, however, the oxida­tions cease, as is the case after death, the forma­tion of lactic acid continues, but the acid is not oxidized to CO2 and thus removed, and as a consequence the H ion concentra­tion increases in the cells and the self-diges­tion of proteins, which the digestive enzymes contained in the cells themselves could not attack formerly, becomes possible. Acid increases the digestibility of a protein, probably by salt forma­tion. Theoretically we should not be surprised that while in the liver an increase in the CH favours autolysis in other tissues the same result is produced by the reverse effect. We might say that the preserva­tion of a certain CH probably at or near the point of neutrality during life prevents self-diges­tion, while the gross altera­tion of the CH in either direc­tion after death (or after the cessa­tion of oxida­tions in the tissues) induces autolysis. Bradley indeed suggests that many of the phenomena of autolysis during lifetime, such as atrophy, necrosis, involu­tion, might be due to an increase in the CH in the tissues.