Inability of the organism to resolve the noxious intervention through the mechanism involved in the diphasic phenomenon leads to abnormal prolongation of one phase or another. If it is unable to destroy the noxious factor in the first phase or to mobilize the repair process in the second and thus correct the damage induced by the first phase, the organism remains in a prolonged first phase of hemo shock. If the second phase is quantitatively or especially qualitatively inadequate, the organism remains in a prolonged second phase, continuing to try to resolve the offbalance by a quantitatively greater mobilization of the otherwise qualitatively inadequate weapons which are at its disposal. It is the predominant intervention of the lipids which characterizes these extended phases. We wish to note again that the fatty acids intervene in the prolonged first phase while anti fatty acid agents, especially sterols, are active in the second.

The adrenals play a particularly important role in the immediate and prolonged defense process. In the first phase, the increased amount of fatty acids with four or more double bonds found in blood and in the organism in general appears to come from the adrenals, which are usually extremely rich in these substances. In an exaggeratedly intensive prolonged first phase, we found small reddish adrenals practically devoid of fatty acids. This occurrence, together with the concurrent increase in fatty acids in the blood, relates these changes in fatty acid content of the blood largely to a liberation of the adrenal fatty acids into the circulation. Another important factor for the prolonged first phase appears in the intervention of lymphocytes able to induce a lysis of compounds of very high fatty acids such as present even in waxes. (Note 4) A lymphopenia corresponds to the prolonged first phase. In the elevation of the amount of anti fatty acid agents in blood, characteristic of the prolonged second phase of the diphasic phenomenon, the adrenals seem to intervene again providing a portion of the increased circulating sterols. The exaggerated manufacture of sterols can be attributed to the reticuloendothelial system in general. Granulocytosis and lymphocytosis occur in this prolonged second phase. The intervention of sterols, which are relatively simple steroids, can explain the clinical manifestations such as fever, which characterize the prolonged second phase, since fever can be induced by the administration of large amounts of sterols.

We can separate, from the point of view of its manifestations, the immediate diphasic hemo shock phenomenon with a short evolution, from the more prolonged forms. While the former, if not too exaggerated, would correspond to a physiological phenomenon, the latter is always abnormal. In the former, the principal intervention is that of hydrolytic enzymes; in the latter, lipids play the most predominant role. Pathogenically, each phase of the diphasic phenomenon, if unable by itself to resolve the immediate problem, will be followed by a corresponding lipidic predominance. The result may be either one of the two phases, with fatty acids or sterols predominant. We call this entire response "the antiheterogeneous reaction" of the defense, separating its diphasic manifestations into immediate hydrolytic and prolonged lipidic stages.