Abstract
Intermittent claudication is the presenting symptom of the great majority of patients with arterial occlusion in the legs, whether it be due to arteriosclerosis, thromboangiitis obliterans or past embolism. Despite all the vasodilator drugs, blocking of sympathetic ganglions and sympathectomy, the mechanical methods, intra-arterial injections and even multiple transfusions, at least half the patients with intermittent claudication cannot walk better after treatment than before treatment. In a study of a group of ischemic patients who continued to complain of inability to walk more than a block or two without stopping, it became evident that in these patients with major arterial occlusion the collateral vessels, even when maximally dilated, cannot supply sufficient blood to the calf muscles to permit continuous walking without pain. Since treatment directed toward increasing the blood supply so often fails to improve claudication, the idea suggested itself that perhaps one could reduce the demand of the calf
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