Positive results have been obtained in but a single set of experiments, namely those in which turpentine was employed.

In so far as the results of this preliminary study go, one is led to the conclusion that thrombosis is most readily induced when active inflammatory lesions exist in the blood vessels, associated, probably in most instances, with secondary degenerative changes. Purely mechanical lesions are much less apt to be productive of conditions favorable to thrombosis as a sequence of phlebitis.

Marked artificial increase or decrease in the coagulation time of the blood by the use of calcium lactate or citric acid, does not render animals abnormally prone to thrombosis incited by changes other than inflammatory.

When true phlebitis exists, thrombosis is apt to be more extensive and less readily resolved, when the coagulation point of the blood has been shortened by the use of calcium lactate, and it is less extensive and more quickly absorbed when the coagulation time has been increased by the administration of citric acid.

Experiments as yet incomplete appear to suggest that the increasing in rapidity or slowing of the general circulatory stream has but little bearing on the production of thrombosis in phlebitis, much less, indeed, than clinical and anatomical observations have generally led us to think. We have also been led to suspect that the presence or absence of anastomoses of abundant degree is largely concerned as a factor in determining the location and extent of thrombosis in phlebitis.

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