Hereditary haemophilia : deficiency in the coagulability of the blood the only immediate cause of the condition / by Thomas Addis.

  • Addis, Thomas, 1881-1949.
Date:
1910
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Licence: In copyright

Credit: Hereditary haemophilia : deficiency in the coagulability of the blood the only immediate cause of the condition / by Thomas Addis. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    before comparing this with the results obtained by similar observations on blood from haemophilic wounds, it will be of advantage briefly to consider the present position as regards the physiology of coagulation and the explanation which is advanced of this progressive acceleration of the rate of coagulation. There have been in the past many theories of the coagulation of mammalian blood which are now discredited or greatly modified, but certain facts remain, though the interpretation of their meaning and significance has changed. These essential facts can be put very shortly. Coagulation is the formation of fibrin. There are four factors necessary—fibrinogen, prothrombin, thrombokinase, and calcium. By the interaction of the last three thrombin is produced, and thrombin acting on fibrinogen precipitates fibrin. Fibrinogen is a globulin in solution in the plasma. The action of thrombin upon it is generally believed to consist in a cleavage of the molecule into two parts—serum-globulin, which is soluble, and fibrin, which is insoluble. Prothrombin 2 is a substance of unknown chemical constitution, present in circulating blood. In itself it has no action on fibrinogen, but in the presence of thrombokinase and calcium, after a certain interval of time, a change is found to have taken place in its physical and chemical properties and the new body, thrombin, is formed, whose action on fibrinogen has been noted. Thrombokinase3 is also of unknown chemical constitution. It is not found in the plasma of the circulating blood, but is present in the tissues, particularly those rich in nucleo-proteins, and in the formed elements of the blood. Without it no thrombin can be formed. The greater the quantity of thrombokinase added to the blood from the tissues or formed elements, the more rapid is the change of prothrombin into thrombin. Calcium salts are also essential for the formation of thrombin. Thrombin, the result of the action of thrombokinase and calcium on prothrombin, is often called fibrin ferment, but this is an unfortunate term, since it does not possess all the properties of a ferment. Thus it acts quantitatively, that is to say, a measured quantity will coagulate a certain definite amount of fibrinogen and no more. In the act of coagulating the fibrinogen it becomes attached to the fibrin, and most of it is precipitated with it. That part which remains free after all the fibrinogen has been coagulated disappears after a short time. This is generally ascribed to the action of a substance in the plasma which is termed anti-thrombin. Although thrombokinase and calcium are necessary for the building up of thrombin, they are not required for its action once it has been formed. All fibrinogen-containing fluids, whether they contain thrombokinase and calcium or not, are coagulated when thrombin is added to them. Time is required for the formation of thrombin, but the action of thrombin once formed is practically instantaneous. Work on coagulation has centred round the theory which Schmidt advanced towards the end of last century, after a lifetime of work devoted to this subject. 2 Prothrombin was the term originally used by Alexander Schmidt, but it has been called thrombogen by Morawitz and plasmozym by Fuld. 3 Corresponds to the zymoplastic substance of Schmidt, the cytoplasm of Fuld, the tissue- coagulin of Loeb, and the thrombozym of Nolf.