Abstract
In a previous paper (Necheles, Ling and Fernando) we stated, that the trypsin inhibiting factor of the serum is not an antibody and that the survival of living tissue exposed to the action of trypsin 1 does not depend upon immunization against the ferment, but on some unknown factor.
In the course of this previous work we were struck by the fact that delayed clotting of the blood was frequently associated with a high “antitryptic” titer. We therefore tested in a series of experiments the possible relationship between clotting time and “antitryptic” titer.∗ The clotting time and “antitryptic” titer of the blood of 2 normal dogs (No. 870, 9.7 kg., and No. 871, 9 kg.) was determined. The blood was withdrawn daily (in the morning) by heart puncture from the left ventricle (a paraffined syringe and needle was used†). The dogs were fed in the afternoon; the food consisted mainly of carbohydrates. In the course of a week, the clotting time varied from 7′ 30” to 13′ and the “antitryptic” titer from 0.2-0.4 in dog 870, and from 7′15” to 11′ 30” and 0.2-0.4 in dog 871, but no relationship could be found between these 2 values. There was no difference between the “antitryptic” titer of blood which had clotted in plain and that in paraffined glass tubes, although there were differences of 30 to 100% in clotting time. Blood in paraffined glass tubes to which tissue fibrinogen was added clotted about 10 times quicker than the control but had the same “antitryptic” titer.
In order to see whether increasing metabolism would influence clotting time and titer, both dogs were treated with subcutaneous injections of thyroxin, till pulse rate and body temperature indicated full action of this drug. In dog 870 there were insignificant variations of the titer between 0.3 and 0.5 and no change of clotting time. In dog 871 the titer went up from 0.3 to 20.0†† without change in clotting time. This experiment confirms our former statement about the inconsistency of changes of the “antitryptic” titer. 2
Get full access to this article
View all access options for this article.