The factors of coagulation in the experimental aplastic anemia of Benzol poisoning : with special reference to the origin of prothrombin / by S.H. Hurwitz, M.D., and C.K. Drinker, M.D.

  • Hurwitz, S. H.
Date:
[1915?]
Catalogue details

Licence: In copyright

Credit: The factors of coagulation in the experimental aplastic anemia of Benzol poisoning : with special reference to the origin of prothrombin / by S.H. Hurwitz, M.D., and C.K. Drinker, M.D. Source: Wellcome Collection.

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    irfectly normal in hemophilia in which the coagulation time may i markedly prolonged in consequence of a deficiency in the amount f the contained prothrombin (7). Furthermore, in a recent pub- cation, Howell (11) has shown that prothrombin is present in solu- on in the circulating lymph, although blood platelets do not con¬ fute a normal element of this fluid. The delayed clotting of miph depends rather upon a deficiency in the contained thrombo- lastin, and consequently upon a relative excess of antithrombin, uch evidence suggests the possibility that some tissue in addition to le bone marrow is concerned with prothrombin formation. This iew is supported also by the knowledge, to which reference has Iready been made, that the elaboration of fibrinogen depends upon le combined activity of at least two organs,—liver and intestine, 'he maintenance of the prothrombin equilibrium of the blood is bviously so important for the organism that the assumption that ther tissues or organs participate in this process harmonizes better nth our present conception of the factors of safety in physiological rocesses emphasized by Meltzer. Our experiments afford no support for or against the view of sfolf and others that liver cell activity is essential for prothrombin iroduction, nor do they make it clear what tissues besides the narrow play a part in its elaboration. CONCLUSIONS. 1. Subcutaneous injections of benzol in rabbits produce marked lestructive changes in the hematopoietic organs, especially in the nyeloid tissue. 2. Benzol poisoning registers a change not only in the formed dements of the blood, but also in the factors of coagulation. 3. The circulating prothrombin is considerably reduced in amount md in most instances animals in which such a diminution occurs show aplasia of the bone marrow. 4. The association of extreme aplasia of the marrow without a fatal diminution in the circulating prothrombin suggests one of two possibilities: either other tissues and organs in addition to the bone marrow are concerned with prothrombin formation; or a minimum amount of myeloid tissue suffices to maintain the quantity of pro¬ thrombin above a dangerous level.