Abstract
The effect of defibrinated blood and of blood serum in producing contraction of arterial smooth muscle, either in a perfused organ or in a surviving artery suspended in a chamber, has long been observed. It was the cause for many erroneous reports of the finding of epinephrin in the circulating blood until the work of O'Connor1 showed clearly that the vasoconstrictor property is not due to epinephrin, but is developed in connection with the process of coagulation and is not possessed by blood kept fluid by anticoagulants. O'Connor's conclusions were confirmed and extended by Stewart,2 Schultz,3 Stewart and Harvey,4 and Janeway and Park.5 While this demonstration is of importance clinically, chiefly because it discredits all previous work on the supposed detection of epinephrin in shed blood, and invalidates all conclusions therefrom as to the cause of arterial hypertension, nevertheless the problem of the origin and nature of the vasoconstrictor property

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