The Role Played by Leucocytes and Platelets in Anaphylactic and Peptone Shock

Abstract

If one goes back to the earlier theories of anaphylaxis, the number of separate points of view, or schools, defending entirely independent ideas on the mechanism of this important phenomenon becomes quite impressive. We might distinguish among the different conceptions-the immunological, the hematological, and the physiological or pharmacological-according to the main principles involved and the personal interests and scientific outlook of their proponents. Today, it is rather trivial to say that the liberation of histamine plays a major role in the production of the symptoms and that other metabolites, such as adenosine, acetylcholine, a "slowly reacting substance" (S.R.S.), etc., might also contribute to initiate or aggravate shock. There is also no question that heparin, as such, is released from the liver and that it could explain incoagulability of the blood, and that the opposite effect (Le., the decrease in clotting time as it has been observed in anaphylactic and peptone shock during the so-called negative phase) might depend upon activation or release of thromboplastic agents, among which one might include activation of a proteolytic enzyme of the trypsin type.It is obvious, however, that this description does not include many other phenomena that occur in anaphylactic and peptone shock with at least an equal degree of frequency. I pass over the immunological point of view, since there is a general agreement that the whole anaphylactic reaction takes place as a consequence of a combination of the antigen with the antibody, this being a sort of trigger mechanism for the whole physiological process to develop. The fact that similar phenomena and symptoms can be obtained by injecting peptone led to the conclusion that the symptoms following combination of the antigen with the antibody are common to other forms of aggression to the cell and by no means represent the direct, toxic effect of the so-called antigen-antibody complex. Therefore, reconciliation of the physiological or pharmacological point of view with the immunological one is much easier than might appear by reading papers from either side.First of all, I wish to mention the old French conception of the "colloidoclastic shock," which implies a disturbance of the colloidal equilibrium of the blood, with consequent fall in leucocytes and platelets, as the main reason for the symptoms observed during anaphylactic and peptone shock. I never understood what point was involved in the idea of the disturbance of the colloidal equilibrium of the blood. There is no question, however, that something remained from this old conception. This refers to the fall in leucocytes and platelets as a characteristic feature of anaphylactic and peptone shock. More detailed studies have subsequently shown that a fall in platelets is one of the most constant indications of a state of sensitization when the antigen i s injected, at least in certain species of animals. In 1924, Webb' 1045 But, now, let us consider the hematological point of view.

Some Pharmacodynamic Properties of Cellulose Sulphate, a Kininogen‐depleting Agent in the Rat

“…Glycogen and certain other polysaccharides have been shown to cause leucopenia and thrombocytopenia in the rabbit (Rocha e Silva, 1950). Such effects could also be obtained when cellulose sulphate 25 mg/kg was given to this species (Rothschild, 1968); however, neither leucopenia nor loss of circulatory platelets were observed in rats treated with cellulose sulphate at concentrations causing maximal kininogen breakdown.…”

The release of histamine and formation of a slow‐reacting substance (SRS‐A) during anaphylactic shock

“…Rocha e Silva (1950) found that the perfused liver of the sensitized dog released only traces of histamine, when challenged by the antigen, unless the perfusion fluid consisted of whole blood without an anticoagulant.…”

Concentration of histamine in different parts of the brain and hypophysis of rabbit: effect of treatment with histidine, certain other amino acids and histamine

“…The possible effect of residual blood on histamine values was also tested in the following way. Each of two rabbits received an intravenous injection of glycogen in a dose which produced a rapid lowering of blood histamine concentration (Rocha e Silva, 1950;. At the time of killing the animals, 10 min after glycogen injection, the blood histamine had fallen to 14% of that before glycogen.…”