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- W2348659212 abstract "The hypothesis of the authors is that the increase infibrin monomer would be due to a preexisting imbalancebetween available factor XIII and thrombin.Thrombin proteolytically cleaves fibrinogen to solublefibrin monomers, which are incorporated into a cross-linked and thus stabilized or nonsoluble fibrin networkin the presence of appropriate amounts of activatedfactor XIII. Thrombin also cleaves the A subunit of factorXIII to generate the enzymatically active factor XIII(FXIIIa), capable of cross-linking fibrin monomers into afibrin strand (fig. 1). The authors hypothesize that arelative imbalance of thrombin in respect to activatablefactor XIII would result in an accumulation of fibrinmonomers due to the inadequate incorporation of mono-mers into a stable fibrin network. They further hypoth-esize that in patients with preoperatively elevated fibrinmonomers, the surgical procedure may lead to an accen-tuation of the above-described imbalance that may beassociated with increased perioperative blood loss." @default.
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- W2348659212 date "2009-01-01" @default.
- W2348659212 modified "2023-09-27" @default.
- W2348659212 title "Are Fibrin Monomers and Factor XIII the Missing Link" @default.
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