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JOHN C. HOAK, MD; WILLIAM E. CONNOR, MD; EMORY D. WARNER, MD

Arch Intern Med. 1966;117(1):25-31.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

ALTHOUGH THE usual sequence in experimental medicine is to go from laboratory experiments to the clinic, at times it is valuable to work in the opposite direction and bring laboratory investigation to bear on problems which have not been solved by direct clinical approach. Despite the widespread clinical use of anticoagulant drugs in the treatment of thromboembolic disease, important questions remain about their antithrombotic efficacy, methods of administration, and relative effectiveness of the different drugs. It is common experience that patients with adequate anticoagulant activity as measured by in vitro tests still develop thrombosis.

At least three general approaches have been used in the production of thrombosis in animals. These involve injury to the endothelial surface of blood vessels, retardation of blood flow, and production of hypercoagulability of the blood. Usually two of the three factors are required to produce experimental thrombosis.

In the present study, jugular vein thrombosis was . . . [Full Text PDF of this Article]

Author Affiliations
IOWA CITY

From the Cardiovascular Research Laboratories of the Department of Internal Medicine (Drs. Hoak and Connor) and the Department of Pathology (Dr. Warner), University of Iowa College of Medicine, Iowa City. Dr. Hoak is an Advanced Research Fellow of the American Heart Association.

Footnotes
Received for publication June 24, 1965; accepted Aug 23.

Read in part before the 16th Annual Meeting of the Council on Arteriosclerosis of the American Heart Association, 1962.1

Reprint requests to Department of Medicine, University Hospitals, Newton Rd, Iowa City, Iowa 52241 (Dr. Hoak).

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