Intravascular Agglutination of the Formed Elements of Blood

Abstract

With ample references to blood coagulation, platelet function, and thrombus formation, the author restricts his discussion to the "part played by the formed elements in (a) the phenomenon known as "blood sludge," (b) the process of spontaneous hemostasis at the small blood vessel level, and (c) the phenomena of white thrombo-embolism." (a) He concludes that "no acceptable direct observations have been reported which prove that true blood sludge exists, or that agglutinated red corpuscles block the capillaries, although conceivably they might if they were held together by a sufficiently tenacious material. The crucial test of microprobing in vivo at high magnifications has not been made by those who report blood sludge resulting from exptl. trauma and burns, or found it in a variety of pathological conditions. The concept of blood sludge as originally defined by Knisely has been extended without adequate supporting evidence, even to the point where normal physiol. processes are held to cause the formation of sludge." The little work on "cold agglutination" or the temporary power acquired by chilled serum either in vitro or in vivo to agglutinate erythrocytes is also briefly reviewed. (b) To produce hemostasis, the platelets plug the openings of cut vessels and supply materials for clotting escaped blood; the vessels (except capillaries) constrict due to mechanical and nervous stimulation and perhaps to liberation of a pressor substance from platelets; and the size of the vessel, size of the injury, and balance between vascular and tissue pressures play a part. (c) "In arthropods and in amphibia, as well as in the higher vertebrates, an agglutination of the white formed elements occurs independently of fibrin deposition, antecedes it, and is not necessarily followed by it." The 2 processes are governed by different mechanisms. White platelet thrombi may exist in living mammalian blood vessels quite independently of the coagulation process. Their occurrence seems conditioned by increased platelet adhesiveness, which in turn is associated with substances released by cellular breakdown anywhere in the body, with bacterial infection, with injn. of heparin, with injn. of various colloidal materials, and perhaps with cancer. A red thrombus may form at times secondarily on the surface of the platelet thrombus, even when the initial platelet thrombus has not caused complete stasis. "Of the factors generally conceded to be involved in thrombo-embolism, namely increased coagulability of the blood, relative venous stasis, vascular wall injury and increased platelet adhesiveness, the last appears to be the most important, although it is certain that endothelial alteration of some sort must occur before a thrombus can become fixed. The other 2 factors, namely, increased coagulability and decreased rate of blood flow, are certainly secondary in initiating thrombus formation, but may be primary in determining its size, nature, and location." Injn. of heparin into a living animal leads to formation of both platelet and leukocytic thrombi. Injn. of Dicumarol likewise leads to the formation of leukocytic thrombi, but prevents that of platelet thrombi. Under conditions in which platelets have been rendered unavailable by injn. of antithrombocytic serum or Dicumarol, pure leukocytic thrombi may occur in the living animal.