In 1954 Ejrup and Hiertonn recorded a case of stenosis of the popliteal artery caused by a cyst arising from the adventitia, and this case and three similar ones were described by Hiertonn, Lindberg, and Rob (1957) as " cystic degeneration of the popliteal artery." The cardinal features they described were those of a localized arterial disease of young adult males causing intermittent claudication of sudden onset, which was successfully treated by resection of the affected arterial segment with autogenous vein graft or arterial homograft replacement. This condtion is rare, and of the 32 cases described in the literature 24 have involved the popliteal artery (Sutton, 1962;Hamming and Vink, 1965; and others). It has also been described in the external iliac artery (Atkins and Key, 1946;Jacquet and Meyer-Burgdorff, 1960), the radial artery (Parkes, 1961; Bdckstrbm, Linell, and Ostberg, 1965), and the ulnar artery (Parkes, 1961), andHiertonn (1966) Arteriogram showing posterior displacement of the popliteal artery due to the cyst. tion with the knee joint. On incising the cyst a quantity of thick " jelly " extruded. The cyst wall was partially excised, after which the popliteal artery pulsated normally. Postoperatively the popliteal and posterior tibial pulses were normal, and he was asymptomatiL for about one year.He then had recurrence of claudication at 400 yards (365 metres), and on examination it was found that the popliteal cyst had recurred and was pushing the popliteal artery posteriorly so that the popliteal pulse was more easily palpable than normal and there was an audible bruit. Arteriography showed postero-medial displacement of the artery (Fig. 1). Ten millilitres of viscous homogeneous gel with a pinkish hue was aspirated from the cyst and he again became asymptomatic.411'
Fibrinolytic activity in human blood develops after the occurrence of viscous metamorphosis (VM) of platelets. Freshly drawn venous blood was held at room temperature until spontaneous VM of platelets occurred and then introduced into oxalate solution to prevent coagulation. As compared to the control (blood added to anticoagulant before VM) plasma of such samples exhibited increased fibrinolytic activity, detected by increased serial thrombin times. Clots from platelet-rich plasma exhibited an increase in the convergence of branches of the thrombelastograph and a decrease in weight after incubation for 24 hr or more. The increase in branch convergence was roughly proportional to the platelet count and was reduced or absent in thrombocytopenic blood or platelet-poor plasma. Dimethylsulfoxide blocked VM and prevented branch convergence (without preventing clot retraction). Epsilon-aminocaproic acid, an inhibitor of plasminogen activator, blocked or inhibited fibrinolytic activity without arresting VM. This evidence suggests that platelets contain significant proactivator or activator of plasminogen (or a factor which initiates their activity) which is released when VM occurs.
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