Pyridinolcar-bamate; Anginin (B23) is a venous bradykinin antagonist, which antagonizes competitively and reversibly the venoconstrictive effect of bradykinin and its active homologues. This compound also to antagonizes the congestion, exudation and hemorrhage induced by bradykinin and its active homologues and to remove the edematous change from experimental atheroma and to promote the normal fibrous healing of atheroma. This compound has also exhibited clinically a beneficial effect in the atherosclerotic diseases of the brain and the heart, however, the evaluation of the effectiveness of this kind of drug in these morbid conditions had to depend upon rather the indirect evidences. In order to see directly the effect of pyridinolcarbamate on the arterial lesion the atherosclerosis of extremities seems much more suitable. The authors have first attempted this compound in the treatment of atherosclerotic occlusion in lower extremities of 2 hospitalized patients; 33 years old and 57 years old men. The first patient aged 33 years suffered from a marked cyanosis of his right foot with a history of 6 months and the pulsations of right popliteal, posterior tibial and dorsal pedal arteries were completely absent and arteriography revealed the complete obstruction of popliteal artery immediately above the knee joint. Pyridinolcarbamate was given 1 g daily and on the 3rd day of the medication the cyanosis disappeared dramatically and the intermittent claudication exhibited a slight improvement. On the 14th day of the medication the right dorsal pedal pulsation was recognized and on the 15th day the pulsation became visible through the skin and at the same time the pulsation of right popliteal artery began to be recognized. The volume of pulsation increased gradually but relatively rapidly and concomitantly with the remarkable improvement of intermittent claudication and on the 25th day of the treatment there was no difference of skin temperature between right and left foot and the pulsation exhibited almost normal volume in dorsal pedal artery. On the 26th day the pulsation of his right posterior tibial artery also reappeared. Under the medication of this compound no relapse and no untoward effects of the drug have been noted for 3 months period of the observation. The second case aged 57 years suffered from intermittent claudication and the absence of the pulsation of bilateral popliteal, dorsal pedal and posterior tibial arteries and the arteriography revealed the occlusion of the middle part of the right femoral artery. The treatment with pyridinolcarbamate for 2 weeks in a daily dose of one g induced a slight improvement of intermittent claudication and on the end of third week a marked improvement was noted and at the same time the pulsation of his right dorsal pedal artery reappeared. His intermittent claudication exhibited a marked improvement concomitantly with the appearance of his dorsal pedal artery. A definite shortening in crest time in plethysmogram was noted in the bilateral second toes on the 130th day of the treatment. Thereafter his condition has been continuously good and he had no relapse and no untoward effects of the drug during the whole observation period of 5 months. The effect of pyridinolcarbamate seems to originate from the improvement of atheromatous changes by the compound in these patients.