Abstract
Vosburg and Richards 1 first noted that blood coagulated more rapidly in animals after administering adrenalin, and Cannon and his coworkers reasoned from their experiments with adrenalin and from other evidence that the liver furnished some factor to increase the clotting process of the blood. In a study to determine just what this factor was, Grabfield 2 concluded that adrenalin decreases the coagulation time by increasing the amount of prothrombin in the circulating blood.
Grabfield could find no change in the anti-thrombin or in the fibrin content of the blood following the administration of adrenalin, but he says: “The fibrin determinations were made by the heat coagulation method of Whipple and Hurwitz, an unsatisfactory and unreliable method for this work because, chiefly, the amounts of blood required for accurate results are too large to obtain from cats without introducing the factor of hemorrhage.”
In reviewing the problem it seemed that fibrin instead of prothrombin may have been an active factor in initiating the decreased coagulation time and that Grabfield's work should be repeated, using larger animals. Cannon was able to show that the increase in blood sugar concentration after adrenalin could not alone decrease the coagulation time, and since it has been shown by Whipple and Foster 3 that fibrin is probably stored in the liver, it was decided to study particularly this substance.
Dogs were injected subcutaneously with 1:1,000 adrenalin chloride. Of the 6 animals used, 4 were healthy and 2 had chronic secondary anemia from hemorrhage. Coagulation time was determined by a modified method of Howell 4 using test tubes 12 mm. in diameter. Blood sugar determinations were made by the method of Folin 5 and fibrin by the method of Schultz, Nicholes, Schaefer. 6
Get full access to this article
View all access options for this article.