| Title | Tranexamic acid - an Alternative to Aprotinin in Fibrin-Based Cardiovascular Tissue Engineering. | | Author(s) | Cholewinski E, Dietrich M, Flanagan TC, Schmitz-Rode T, Jockenhoevel S | | Institution | Aachen, Germany; eva.cholewinski@rwth-aachen.de. | | Source | Tissue Eng Part A 2009 Jun 4. | | Abstract | Recent clinical trials have led the worldwide suspension of aprotinin, the most commonly-used anti-fibrinolytic agent in fibrin-based tissue engineering. For future clinical applications of fibrin-based scaffolds, a suitable, alternative fibrinolysis inhibitor must be identified. The present study aimed to evaluate tranexamic acid (t-AMCA) as an alternative fibrinolysis inhibitor to aprotinin for cardiovascular tissue engineering applications. The effects of various concentrations of t-AMCA (30-160microg/ml) and aprotinin on fibrin gel-lysis were spectrophotometrically quantified in vitro. Cytotoxic effects of t-AMCA and aprotinin on carotid artery-derived cells, in addition to their influence on fibrin gel mechanical strength, were examined. Furthermore, the influence of t-AMCA vs. aprotinin on 3-D-fibrin-based constructs was analysed using light microscopy, SEM and TEM. The results demonstrated that neither t-AMCA (30-160 microg/ml) nor aprotinin elicited cytotoxic effects on cultured cells. Although aprotinin showed reduced fibrinolysis in the presence of plasmin compared to t-AMCA, no significant difference was obtained under 'standard' culture conditions. Additionally, t-AMCA had no negative influence on the mechanical stability of fibrin gels, which also demonstrated excellent cell morphology, tissue development and ultrastructure. The results from the present study demonstrate that t-AMCA may be a suitable alternative to aprotinin for controlling the in vitro degradation rate of fibrin-based tissue-engineered constructs. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 19496679 |
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