Evaluation of Local Ischemia, General Anoxia, and Vasodilators in Reactive Hyperemia

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Abstract
The relationship of local Ischemia, general anoxia and vasodilator metabolites to the production of reactive hyperemia was studied in the vasculature of the hind limb of the dog. Oxygen tension of the circulating blood was reduced to extremely low values by the techniques of progressive reduction of respiration rates down to zero, and inhalation of pure nitrogen at normal respiration rates. In no instance was the reactive hyperemia influenced by these conditions. Very short occlusive periods, i. e., 3 seconds, produced hyperemic responses. It is doubtful if this short occlusion could produce significant concentrations of known vasodilator metabolites or reduction in O2 tension in the occluded vasculature areas. Venous occlusion, in contrast to arterial occlusion, does not produce a hyperemic response. When a venous occlusion precedes or is made simultaneous with an arterial occlusion, the resulting hyperemia is much less than with arterial occlusion alone. Relatively large amounts of lactic acid, i. e., 0.6 cc of a 3% solution, injected directly into the femoral circulation were required to produce a relatively small increase in blood flow. Compounds known to antagonize the action of histamine and serotonin were ineffective in altering the hyperemic response. These data indicate lactic acid, histamine, and serotonin are probably not involved in the basic mechanism of reactive hyperemia.