In our experience, the outcome of the popliteal artery aneurysm repair was comparable in the emergent and elective settings. Aggressive tibial reconstruction plays a crucial role in the treatment of popliteal artery aneurysms, especially in those presenting with acute limb ischemia. Thrombolytic therapy is infrequently required in the acute setting, although it may be useful in patients with no identifiable outflow target vessel on initial arteriogram.

Although minor amputations can lead to limb preservation in most patients, the performance of a revascularization subsequent to amputation, transmetatarsal as the initial amputation, and end-stage renal disease are poor prognostic indicators. Inferior long-term patient survival is most closely associated with renal insufficiency and conversion to major amputation early after the initial procedure.

Inframalleolar bypass to plantar artery branches and the lateral tarsal artery, even in patients with a previously failed revascularization, can be undertaken with acceptable patency and limb salvage rates. Early graft failure, however, is higher, whereas patency and limb salvage rates are lower, compared with bypass to the dorsalis pedis artery. The use of saphenous vein as a conduit results in the best patency for plantar or lateral tarsal bypass procedures.

Limb reflux time as determined by color-flow-assisted duplex scans correlated significantly with the air plethysmographic variable accepted as a measure of the severity of venous reflux, the venous filling index. This study confirms the validity of total limb reflux times in the quantification of chronic venous insufficiency.

Abstract-Kininogens have recently been shown to possess antiadhesive, anticoagulant, and profibrinolytic properties and can inhibit platelet activation at low thrombin concentrations. To test whether kininogens have antithrombotic properties in vivo, we devised a model of limited arterial injury confined to removal of the endothelium. Brown-Norway Katholiek strain rats with an absence of low-and high-molecular-weight kininogen due to a single point mutation, A163T, were compared in the thrombosis model to the wild-type animals, which were otherwise genetically identical. Despite an equivalent vascular injury, the mean time (ϮSEM) for a 90% decrease in flow measured by laser Doppler was 38.4Ϯ17 minutes in the kininogen-deficient rats compared with 194Ϯ29 minutes in the wild-type animals (PϽ0.002). Key Words: arterial thrombosis Ⅲ kininogens Ⅲ antithrombotic Ⅲ fibrinolysis Ⅲ rats K ininogens are plasma proteins first recognized as the precursors of a peptide, bradykinin, which was liberated by plasma kallikrein. 1 Bradykinin can reproduce many inflammatory changes, including edema, pain, vasodilation, and increased vascular permeability. A deficiency of plasma high-(HK) and low-(LK) molecular-weight kininogens 2 in humans does not lead to a hemorrhagic disorder, despite a marked prolongation of the activated partial thromboplastin time. In fact, cloning 3 and delineation of the structurefunction relationships of kininogen have revealed new properties of this protein, including cysteine protease inhibition, 4 modulation of thrombin-induced platelet aggregation, 5 antiadhesive properties, 6 and profibrinolytic potential. 7 HK and LK have been divided into domains D1, D2, and D3, which compose the common heavy-chain N-terminal to domain D4, which contains the bradykinin sequence. LK contains a small domain, D5 L , whereas HK contains the large domains D5 H and D6, which compose the light chains. 3 The ability of D2 of the kininogens to inhibit platelet calpain 4 has been linked to an inhibition of thrombin-induced platelet aggregation, 8 whereas inhibition of the binding of thrombin to platelets by D3 of kininogens has led to a 10-fold shift in the doseresponse curve of thrombin-induced platelet activation. 9 HK can compete for fibrinogen binding to neutrophils 10 by competing for a site on the integrin Mac-1 11 and thus, limit the adhesion of neutrophils to artificial and biological surfaces. Peptides from D6 of HK can downregulate urokinasedependent plasminogen activation on human endothelial cells 7 by inhibiting the binding of prekallikrein to HK.All of these studies suggest that HK should serve as an antithrombotic protein. Conversely, individuals deficient in HK should manifest a prothrombotic state. Unfortunately, HK deficiency is a rare condition, and only a very small number of individuals have been observed in a serial fashion. Therefore, to test this hypothesis, we decided to use a well-defined animal model. Fortunately, a natural "knockout" exists in the Katholiek strain of the Brown-Norway rat. These rat...