Chanda J, Kuribayashi R, Abe T
Department of Cardiovascular Surgery, Akita University School of Medicine, Japan.
Biomaterials. 1997 Aug;18(16):1109-13. doi: 10.1016/s0142-9612(97)00033-1.
Calcific degeneration is the main cause of failure of glutaraldehyde-treated xenograft heart valve substitutes implanted in humans. Coupling of heparin through an intermediate surface-bound substrate containing amino groups showed complete prevention of calcification of glutaraldehyde-treated porcine pericardium implanted subdermally in weanling rats for 5 months (heparin bonded pericardium: calcium, 0.625 +/- 0.24 mg g(-1); glutaraldehyde-only-treated pericardium: calcium, 228.32 +/- 37.39 mg g(-1); P < 0.0001). Conceivably, inactivation of unpaired aldehyde moieties present in bioprostheses after exposure to glutaraldehyde by amino compounds followed by blocking the potential binding sites of the graft with a surface modifying agent like heparin would be the key steps in the prevention of calcification and degeneration of glutaraldehyde-treated biological tissue grafts.
钙化变性是植入人体的戊二醛处理异种移植心脏瓣膜替代物失效的主要原因。通过含氨基的中间表面结合底物偶联肝素，可完全防止戊二醛处理的猪心包在断奶大鼠皮下植入5个月后发生钙化（肝素结合心包：钙含量为0.625±0.24mg/g；仅用戊二醛处理的心包：钙含量为228.32±37.39mg/g；P<0.0001）。可以想象，用氨基化合物使生物假体在暴露于戊二醛后存在的未配对醛基失活，然后用肝素等表面改性剂封闭移植物的潜在结合位点，将是预防戊二醛处理的生物组织移植物钙化和变性的关键步骤。
