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March 1936


Author Affiliations

From the Department of Surgery of the University of Chicago.

Arch Surg. 1936;32(3):528-543. doi:10.1001/archsurg.1936.01180210157008

It has been known for a little more than fifty years that after local asphyxia there occurs a local vasodilatation, which is nearly a maximal response of the vessels involved provided that the asphyxia has been of sufficiently long duration. The immediate cause of this vasodilatation is unknown. This phenomenon is of frequent occurrence and is of great value to the tissues from a protective standpoint, since it is obvious that in terrestrial life the standing, sitting or lying posture must lead to anemia of the weight-bearing tissues and therefore to a reactive vascular dilatation whenever the static force has been of appreciable duration, perhaps longer than one second.1 It is obvious that a local anemia is accompanied by increased loss of heat provided that the surrounding climate is cooler than the temperature of the anemic part. This paper is concerned with a quantitative study of the thermal effects

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