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Enoxaparin does not affect network formation of adipose tissue–derived microvascular fragments

Dermal substitutes are frequently used for the initial coverage of extensive skin defects. The seeding of these implants with adipose tissue–derived microvascular fragments (ad‐MVF) has recently been shown to accelerate their vascularization and incorporation. In the present study we analyzed whether these processes are affected by a thromboprophylactic therapy with the low molecular weight heparin (LMWH) enoxaparin (enox). Green fluorescent protein (GFP)+ ad‐MVF were isolated from enox‐ (8 mg/kg s.c.) and vehicle‐treated (0.9% NaCl s.c.) (C57BL/6‐Tg(CAG‐EGFP)1Osb/J mice and seeded onto Integra matrices. Subsequently, these were implanted into full‐thickness skin defects within dorsal skinfold chambers of enox‐ and vehicle‐treated C57BL/6 wild‐type mice. Repetitive stereomicroscopy and intravital fluorescence microscopy over 2 weeks as well as histological and immunohistochemical analyses on day 14 revealed that enox does not inhibit the reassembly of ad‐MVF into new microvascular networks. In addition, treatment with the anticoagulative compound did not promote implant‐induced hemorrhage formation. Accordingly, Integra matrices in enox‐ and vehicle‐treated animals exhibited a comparable final microvessel density, fraction of GFP+ blood vessels originating from seeded ad‐MVF, collagen fiber content, and epithelialization. These novel findings demonstrate that the seeding of dermal substitutes with ad‐MVF may be applied also during thromboprophylactic therapy without affecting implant vascularization and bleeding risk.