In vivo hemostatic capability of a novel Tetra-PEG hydrogel

TetraStat is a novel synthetic sealant created with a tetra-armed polyethylene glycol (PEG) hydrogel. It has no risk of infection from biological pathogens and has a hemostatic mechanism independent of the blood coagulation pathway and controllable gelation. We evaluated the hemostatic effect of TetraStat in ex vivo and in vivo experiments for future clinical application. In ex vivo experiments using a circulatory system filled with phosphate-buffered saline under high pressure, needle punctures were astricted with TetraStat and two commercially available hemostatic agents (SURGICEL and TachoSil). For in vivo experiments, rat vena cavae were punctured with 14, 18, and 20 gauge needles, and hemorrhage occurred for several seconds. A porous PEG sponge soaked with TetraStat was applied as a hemostatic system for the massive hemorrhage. In the ex vivo experiment, punctures were sealed completely after 1 min astriction with TetraStat gel; in contrast, SURGICEL and TachoSil failed to seal the hole. In vivo experiments demonstrated that TetraStat successfully caused hemostasis in the punctured vena cava within 1 min of application in a dose-dependent manner. For SURGICEL and TachoSil, successful hemostasis occurred after 5 min astriction but was less frequent after 1 min astriction. Ex vivo and in vivo experiments revealed TetraStat’s high hemostatic ability under high pressure and in rat vena cava injuries under massive hemorrhage. A porous PEG sponge soaked with TetraStat is a promising advancement in hemostatic systems.

Microfibrillar Elastic Polymer Wrapping of Rat Vena Cava for the Study of Engineered Arterial Vein Grafts

The autologous saphenous vein graft remains the graft of choice for 95% of surgeons performing coronary artery or peripheral bypass procedures. Within the first 5 years after implantation, 20%–40% of arterial vein grafts (AVG) fail due to intimal hyperplasia (IH)1. This adverse pathological response by AVGs may be in part due to their abrupt exposure to the significantly elevated circumferential wall stress associated with the arterial system2. We believe that if an AVG is given an ample opportunity to adapt and remodel to the stresses of the arterial environment, cellular injury may be reduced, thus limiting the initiating mechanisms of IH.