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1 From the Biology Department, Boston College, Chestnut Hill, Massachusetts
The extent of vascular responses to local cold injury is proportional to the length of time the tissue is exposed to the cold source. Following a standard exposure period of 30 seconds all blood flow ceases in the frozen area. Marked arteriolar constrictions occur in the borderline tissue but never in the exposed area. In the postthaw period there is a gradual increase in the rate of blood flow, accompanied by the emergence of many emboli from the injured area. These emboli, apparently of platelet origin, occasionally form thrombi which occlude vessels in the borderline tissue. Within 5 minutes the rate of flow again begins to decline, leading eventually to complete stasis. Stasis begins in the venules and spreads throughout the vascular bed. As stasis develops the packed blood cells produce wide dilations in all vessels in the injured area. Hemoconcentration is the apparent cause of stasis following local cold injury.
Submitted on January 16, 1957
This article has been cited by other articles:
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S. M. Gulati, B. M.L. Kapur, and J. R. Talwar Oxyphenbutazone (Antiinflammatory Agent) in the Management of Cold Injury Angiology, July 1, 1969; 20(7): 367 - 373. [Abstract] [PDF] |
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