Pharmacological control of soluble tissue factor and monocyte for the inhibition of the extrinsic coagulation pathway during cardiopulmonary bypass in monkeys

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Administration of high-dose heparin causes massive release of TFPI from vascular endothelial cells. We purposed to provide evidence to clarify the role of TFPI (with or without PDE IV inhibitor) in attenuation of TF-dependent thrombin generation during primate CPB. In the primate CPB model, plasma TFPI was enhanced by pre-heparinization, and levels of thrombin generation were reduced by inhibition of extrinsic pathway when compared with control group. PDE IV inhibitor reduced monocyte function and thrombin generation. Massive release of plasma TFPI induced by early heparin administration may attenuate TF-dependent thrombin generation during clinical CPB.