Initiation of blood coagulation by glass and related surfaces

In spite of the rapid advances in our knowledge of the physiology of blood coagulation, the reason why blood remains fluid in the body and yet clots rapidly in vitro remains obscure. It is taken for granted that the initial stimulus is the exposure to a 'foreign surface', but what this 'foreigness' is and how it acts are still matters of controversy. The subject has been reviewed amongst others by Pickering (1928), Barker & Margulies (1949), Macfarlane (1948, 1956), and Biggs & Macfarlane (1953). In contrast to the earlier emphasis on the blood platelets, recent evidence favours the view that the initial contact reaction takes place in the plasma. Lozner, Taylor & MacDonald (1942) showed that glass contact shortens the clotting time of platelet-poor plasma and concluded that this reaction is associated with the plasma euglobulin fraction. Tocantins (1945) and his coworkers (Tocantins, Carroll & Holburn, 1951) made an extensive study of the effect of different surfaces on the clotting of plasma and decided that the basis of thereactionwas the adsorption of a lipid inhibitor of clotting ('anticephalin'). Conley and collaborators (Conley, Hartmann & Morse, 1949; Hartmann, Conley & Lalley, 1949; Ratnoff & Conley, 1951; Hartmann & Conley, 1952; Dick, Jackson & Conley, 1954) studied the effect of glass contact on human and canine platelet-free plasma and its euglobulin fraction. These workers considered antihaemophilic globulin (AHG) to be the component sensitive to contact and showed that surface is a quantitative factor in prothrombin utilization. Quick, Hussey & Epstein (1953) made similar observations regarding prothrombin consumption, but attributed their findings to the autocatalytic effect of surface-adsorbed thrombin. Fiala (1951) and Fiala & Roth (1953) isolated a thermolabile coagulation inhibitor from horse plasma and presented indirect evidence that contact activation is due to the adsorption of

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