Abstract
Summary and Conclusions
1. In 6 subjects reactive hyperemia was produced in the legs by release of arterial occlusion maintained for from one-half to 10 minutes. Blood flow in the foot and distal portion of the leg was measured with a venous occlusion plethysmograph. The initial inflow rate immediately following release of arterial occlusion is taken as representative of the degree of vasodilatation resulting from the occlusion.
2. After administration of effective amounts of antihistaminic drugs the reactive hyperemia was not diminished.
3. The mechanism of reactive hyperemia has not been shown to be due to release of histamine or “H-substance.” It is as yet unexplained.
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