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By Gregory Cheng

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2000. 31: 396–495. [89] Greaves M. Antiphospholipid antibodies and thrombosis. Lancet 1999;353:1348e53. [90] Levine JS, Branch DW, Rauch J. The antiphospholipid syndrome. N Engl J Med 2002;346: 752e63. The “primary” antiphospholipid syndrome: major clinical and serological features. Medicine (Baltimore) 1989;68:366e74. [92] Vianna JL, Khamashta MA, Ordi-Ros J, et al. Comparison of the primary and secondary antiphospholipid syndrome: a European Multicenter Study of 114 patients. Am J Med 1994;96:3e9.

Our study results demonstrate that IPC used alone did not increase TFPI in plasma and didn‘t produce hypocoagulation effect during laparoscopic fundoplication. Most circulating TFPI is bound to lipoproteins. TFPI is also found in platelet α-granules and on the endothelium cell surface. TFPI bound to the endothelium is released with therapeutic doses of heparin or low molecular weight heparin, suggesting that TFPI binds to endogenous glycosaminoglycans on the endothelium wall surface. Our clinical data suggest that LMWH, administered 1 h before operation, together with IPC induce more favorable hypocoagulation profile compared with LMWH alone.

Thus, in the anesthetized patient, venous return from the legs depends mainly on the pressure gradient between the venules (12-18 mm Hg) and the right atrium (4-5 mm Hg). It is expected that the introduction of a pressure barrier between legs venules and the right atrium impedes venous return. Venous thrombosis is major causes of morbidity and mortality. Venous thrombosis leads to pulmonary embolism, which can be fatal, and to postphlebitic syndrome. Venous thrombosis occurs when procoagulant stimuli overwhelm natural protective mechanisms.

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