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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    the results represent the quantity of fibrinogen in ioo cubic centi¬ meters of actual plasma. Wide fluctuations in the blood fibrinogen of normal rabbits were observed. The average was 0.560 of a gram per 100 cubic centimeters of plasma, but variations between a min¬ imum of 0.123 of a gram, and a maximum of 0.925 of a gram were noted. This is in harmony with Whipple’s figures for normal healthy dogs (average 0.466 of a gram; minimum 0.198 of a gram; maximum 0.867 of a gram) (13). In almost all instances repeated injections of benzol (four to forty-two cubic centimeters) caused a rise in the blood fibrinogen. The average of the final readings made from two to thirty days after the initial determination was found to be 0.617 of a gram per 100 cubic centimeters of plasma, but in some individual observations enormous rises were observed (experiments I, K, L, N, Q, T, and U). In about three experiments (O, P, and R) little variation from the normal occurred, and in only one instance (experiment G) was there a striking reduction in the blood fibrinogen. A possible explanation for this drop has | been found in the marked loss of weight and extreme cachexia pro¬ duced in this animal by the benzol inoculations. Similar reduc¬ tions in the quantity of fibrinogen have been reported by Whipple in human cases of cachexia. The low values in such cases are difficult to explain. The rise in blood fibrinogen observed in the majority of animals following benzol injections has been observed also in other condi¬ tions associated with intoxication.12 It is possible that benzol may stimulate the fibrinogen-forming organs to over-functional activity and that the fibrinogen may rise above normal at these times. Such an increase is not out of keeping with the gross anatomical and the histological appearance of the liver in benzol poisoning. Aside from a slight degree of parenchymatous change, no other pathological lesion was demonstrable in the liver parenchyma. THE RELATION 01? THE BONE MARROW TO THE ORIGIN OF PROTHROMBIN, ANTITHROMBIN, AND FIBRINOGEN. The experiments and observations already detailed throw some additional light upon this more complex problem of coagulation. In-