In vitro Endothelialization and Platelet Adhesion on Titaniferous Upgraded Polyether and Polycarbonate Polyurethanes.

Polycarbonateurethanes (PCU) and polyetherurethanes (PEU) are used for medical devices, however their bio- and haemocompatibility is limited. In this study, the effect of titaniferous upgrading of different polyurethanes on the bio- and haemocompatibility was investigated by endothelial cell (EC) adhesion/proliferation and platelet adhesion (scanning electron microscopy), respectively. There was no EC adhesion/proliferation and only minor platelet adhesion on upgraded and pure PCU (Desmopan). PEUs (Texin 985, Tecothane 1085, Elastollan 1180A) differed in their cyto- and haemocompatibility. While EC adhesion depended on the type of PEU, any proliferative activity was inhibited. Additional titaniferous upgrading of PEU induced EC proliferation and increased metabolic activity. However, adherent ECs were significantly activated. While Texin was highly thrombotic, only small amounts of platelets adhered onto Tecothane and Elastollan. Additional titaniferous upgrading reduced thrombogenicity of Texin, preserved haemocompatibility of Elastollan, and increased platelet activation/aggregation on Tecothane. In conclusion, none of the PUs was cytocompatible; only titaniferous upgrading allowed EC proliferation and metabolism on PEUs. Haemocompatibility depended on the type of PU.

Nanocoating with titanium reduces iC3b- and granulocyte-activating immune response against glutaraldehyde-fixed bovine pericardium: a new technique to improve biologic heart valve prosthesis durability?

OBJECTIVES: An IgG and granulocyte-activating immune response with secondary dystrophic calcification might be the reason glutaraldehyde (GA)-fixed xenograft valves fail, especially in young patients, who are more immunocompetent than the elderly. Titanium nanocoating on GA-fixed bovine pericardium was tested for its ability to prevent major immunoreactions. METHODS: The immune activity of platelets from GA-fixed bovine pericardium with different treatment procedures was evaluated using the blood from 5 human donors: group I (n = 5), GA fixed as the control; group 2 (n = 5), detoxified with 10% citric acid; group 3 (n = 5), 10% citric acid, aldehyde-dehydrogenase, and a physical plasma treatment; and group 4 (n = 5), treated the same as group 3, but with an additional titanium coat 30 nm in thickness. Titanium deposition was visualized using scanning electron microscopy. IgG deposits (iC3b) were shown by immunostaining and documented as colored pixels (red). The pixels were evaluated electronically. Attracted granulocytes (polymorphonuclear leukocytes) were counted in front of the titanium-coated surface. RESULTS: IC3b deposits and polymorphonuclear leukocytes within control group 1 were defined as 100%; in group 2, iC3b was 149% ± 34% and polymorphonuclear leukocytes were 89%, in group 3, IC3b was 102% ± 24% and polymorphonuclear leukocytes were 47%; and in group 4, IC3b had decreased to 38.49% ± 21% (P < .05) and polymorphonuclear leukocyte activation had decreased to 6.3% (P ≤ .01). CONCLUSIONS: Titanium coating significantly reduced the iC3b and granulocyte activating immune response of GA-fixed pericardium. Therefore, it might prevent relevant immunorejection and increase the durability of GA-fixed bioprosthetic heart valves.

Detoxification and endothelialization of glutaraldehyde-fixed bovine pericardium with titanium coating: a new technology for cardiovascular tissue engineering.

BACKGROUND: Endothelial cell seeding of glutardialdehyde-fixed biological heart valves is hypothesized to improve biocompatibility and durability; however, the toxicity of glutardialdehyde prevents its use as a biological coating. Therefore, different detoxification strategies are applied, including surface coating with titanium, before in vitro endothelialization of glutaraldehyde-fixed bovine pericardium as the base material for prosthetic heart valves. METHODS AND RESULTS: Bovine pericardium was fixed with 0.25% glutardialdehyde. Detoxification was performed with citric acid, aldehyde dehydrogenase, and plasma deposition with titanium at low temperatures of 30 degrees C to 35 degrees C. Toxic glutaraldehyde ligands were quantified photometrically, and the vitality of seeded cells was tested to validate detoxification methods. Detoxification agents and titanium coating were applied before seeding with human endothelial cells. Endothelial cells were visualized by electron microscopic surface scanning. To evaluate cell adhesion, shear stress was applied by a flow of 5 L/min over 24 hours. Compared with untreated glutaraldehyde-fixed samples, treatment with the different agents reduced free aldehyde groups gradually (citric acid 5% < citric acid 10% < titanium < aldehyde dehydrogenase). A combination of citric acid 10%, aldehyde dehydrogenase, and titanium coating resulted in a reduction of free aldehyde ligands to 17.3+/-4.6% (P < or = 0.05) and demonstrated a vitality of seeded cells of 94+/-6.7% (P < or = 0.05). This procedure yielded a completely confluent layer of regular human endothelial cells (n=5). After application of shear stress for 24 hours on these endothelial layers, cell vitality was 81%. CONCLUSIONS: Titanium coating combined with chemical procedures yielded significant detoxification and complete endothelialization of conventional glutaraldehyde-fixed pericardium. This new technique might improve glutardialdehyde-fixed cardiovascular bioimplants for better biocompatibility and longer durability.