The role of glutaraldehyde-induced cross-links in calcification of bovine pericardium used in cardiac valve bioprostheses.

The role of glutaraldehyde-induced cross-links in calcification of bovine pericardium used in cardiac valve bioprostheses.
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DOI：
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发表时间：
1987-04
期刊：
The American journal of pathology
影响因子：
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通讯作者：
G. Golomb;F. Schoen;M. S. Smith;J. Lindén;M. Dixon;R. Levy
G. Golomb;F. Schoen;M. S. Smith;J. Lindén;M. Dixon;R. Levy
中科院分区：
其他
文献类型：
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作者：
G. Golomb;F. Schoen;M. S. Smith;J. Lindén;M. Dixon;R. Levy

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钙化是用戊二醛（GLUT）预处理的组织源性心脏瓣膜置换失败的主要原因。本研究的目的是确定谷氨酰胺诱导的交联在牛心包组织钙化中的作用。通过不同的孵育pH得到不同水平的3H-GLUT掺入，并通过氨基酸分析和对胶原酶消化的抗性来确定蛋白质修饰。用大鼠皮下植入物研究交联组织的钙化。低GLUT摄取（小于150 nm/mg）由于有限的交联（赖氨酸+羟赖氨酸= 26.1残基/1000个氨基酸[AA]），导致最小的钙化（Ca2+， 12.8微克/mg）和稳定性（消化后剩余重量4%）。相反，过量的供过于求诱导了更多的交联（Lys + Hyl = 8.2个残基/1000 AA），从而提高了稳定性（95%残基wt）；这些组织钙化严重（Ca2+， 93.5微克/毫克）。超过临界水平两到三倍的GLUT掺入并没有进一步增强钙化。由此可见，GLUT的掺入量控制了交联的程度，而交联的程度又直接决定了组织的稳定性和钙化。
Calcification is the principal cause of failure of tissue-derived cardiac valve replacements pretreated with glutaraldehyde (GLUT). The objective of this study was to determine the role of GLUT-induced cross-links in bovine pericardial tissue calcification. Various levels of 3H-GLUT incorporation were obtained by varying incubation pH, and protein modification was determined by amino acid analysis and resistance to collagenase digestion. Calcification of cross-linked tissue was studied using subdermal implants in rats. Low GLUT uptake (less than 150 nm/mg) resulted in minimal calcification (Ca2+, 12.8 micrograms/mg) and stability (4% residual weight following digestion) due to a limited crosslinking (lysine + hydroxylysine = 26.1 residues/1000 amino acids [AA]). In contrast, higher GLUT uptake induced more cross-links (Lys + Hyl = 8.2 residues/1000 AA) and consequent higher stability (95% residual wt); such tissues calcified severely (Ca2+, 93.5 micrograms/mg). Incorporation of GLUT two to three times beyond a critical level did not further enhance calcification. It is concluded that the amount of GLUT incorporated controls the extent of cross-links, which in turn directly determines tissue stability and calcification.