Literature DB >> 19867391

FIBRINOGEN OF THE BLOOD AS INFLUENCED BY THE LIVER NECROSIS OF CHLOROFORM POISONING.

G H Whipple1, S H Hurwitz.   

Abstract

1. Chloroform anesthesia for two hours or more will cause more or less central liver necrosis in dogs, depending on the length of the anesthesia and the susceptibility of the animal. 2. If the fibrinogen of the blood of such an animal be estimated at intervals, it is found that this proteid shows a drop corresponding to the amount of liver necrosis. 3. By administering chloroform, the fibrinogen may be almost eliminated from the circulating blood, and the poisoned animal may bleed for hours from small skin pricks or cuts. 4. The liver can recover from a grave injury due to chloroform and return practically to a normal condition in about ten days. 5. The fibrinogen reappears in the blood as the liver effects its repair. It seems that the quantity of fibrinogen present is a good indicator of the liver efficiency and a fairly accurate index of the amount of liver injury. 6. Shortly after the recovery of the liver from an injury due to chloroform, one may find an excess of fibrinogen in the blood. 7. In severe cases of chloroform poisoning, the calcium of the blood was normal or slightly increased, and the thrombin was normal. 8. These experiments give no evidence that the formation of thrombin or prothrombin is dependent upon liver activity. 9. The hemorrhages of chloroform poisoning are due not to lack of blood clotting but to inefficient coagulation. The clot has not the body and toughness supplied by the fibrinogen, and is, therefore, unable to check even capillary hemorrhage. 10. Fibrinogen is either formed in the liver or is wholly dependent upon liver activity for its production.

Entities:  

Year:  1911        PMID: 19867391      PMCID: PMC2124853          DOI: 10.1084/jem.13.1.136

Source DB:  PubMed          Journal:  J Exp Med        ISSN: 0022-1007            Impact factor:   14.307


  12 in total

Review 1.  Functional impact of oxidative posttranslational modifications on fibrinogen and fibrin clots.

Authors:  Marissa Martinez; John W Weisel; Harry Ischiropoulos
Journal:  Free Radic Biol Med       Date:  2013-07-11       Impact factor: 7.376

Review 2.  Plasma fibrinogen levels in normal and sick cows.

Authors:  B J McSherry; F D Horney; J J DeGroot
Journal:  Can J Comp Med       Date:  1970-07

Review 3.  Role of Fibrin(ogen) in Progression of Liver Disease: Guilt by Association?

Authors:  Anna K Kopec; James P Luyendyk
Journal:  Semin Thromb Hemost       Date:  2016-05-04       Impact factor: 4.180

4.  CELLULAR REACTIONS TO A DYE-PROTEIN WITH A CONCEPT OF THE MECHANISM OF ANTIBODY FORMATION.

Authors:  F R Sabin
Journal:  J Exp Med       Date:  1939-06-30       Impact factor: 14.307

5.  Studies on serum proteolytic enzyme inhibition; effect of tissue destruction, cortisone acetate, and splenectomy on the serum trypsin inhibitor.

Authors:  F C MOLL
Journal:  J Exp Med       Date:  1956-03-01       Impact factor: 14.307

6.  THE FACTORS OF COAGULATION IN THE EXPERIMENTAL APLASTIC ANEMIA OF BENZOL POISONING, WITH SPECIAL REFERENCE TO THE ORIGIN OF PROTHROMBIN.

Authors:  S H Hurwitz; C K Drinker
Journal:  J Exp Med       Date:  1915-05-01       Impact factor: 14.307

7.  PLASMA ESTERASE ACTIVITY IN PATIENTS WITH LIVER DISEASE AND THE NEPHROTIC SYNDROME.

Authors:  H G Kunkel; S M Ward
Journal:  J Exp Med       Date:  1947-09-30       Impact factor: 14.307

8.  THE RESISTANCE OF PUPS TO LATE CHLOROFORM POISONING IN ITS RELATION TO LIVER GLYCOGEN.

Authors:  E A Graham
Journal:  J Exp Med       Date:  1915-02-01       Impact factor: 14.307

9.  LATE POISONING WITH CHLOROFORM AND OTHER ALKYL HALIDES IN RELATIONSHIP TO THE HALOGEN ACIDS FORMED BY THEIR CHEMICAL DISSOCIATION.

Authors:  E A Graham
Journal:  J Exp Med       Date:  1915-07-01       Impact factor: 14.307

10.  THE LIVER AS THE SOURCE OF FIBRINOGEN.

Authors:  D R Drury; P D McMaster
Journal:  J Exp Med       Date:  1929-10-31       Impact factor: 14.307

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