INHIBITION OF CALCIFICATION OF GLUTARALDEHYDE PRETREATED PORCINE AORTIC-VALVE CUSPS WITH SODIUM DODECYL-SULFATE - PREINCUBATION AND CONTROLLED-RELEASE STUDIES
INHIBITION OF CALCIFICATION OF GLUTARALDEHYDE PRETREATED PORCINE AORTIC-VALVE CUSPS WITH SODIUM DODECYL-SULFATE - PREINCUBATION AND CONTROLLED-RELEASE STUDIES
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DOI：
10.1002/jbm.820271203
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发表时间：
1993-12-01
期刊：
影响因子：
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通讯作者：
LEVY, RJ
中科院分区：
文献类型：
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作者：
HIRSCH, D;DRADER, J;LEVY, RJ
由戊二醛预处理的牛心包或猪主动脉瓣（PAV）制成的生物人工心脏瓣膜的钙化是这些器械失效的常见原因。在迄今为止考虑的所有策略中，只有使用十二烷基硫酸钠（SDS）等化合物的清洁剂预孵育才能抑制循环绵羊生物瓣膜置换术中的PAV生物瓣膜矿化。本研究旨在表征SDS预孵育的作用机制。运输和材料表征研究的结果表明，SDS对PAV具有相对较高的亲和力，在37 ℃下24小时内的最大摄取量为167.1 +/- 6.8 μ g SDS/mg组织，分配系数为19.3。SDS的PAV扩散为1.95 +/- 0.35 10（-6）cm（2）/sec。SDS对PAV的主要作用是提取磷脂。SDS预处理组织中的残留有机磷酸盐为2.22 +/- 0.72 nmol/mg组织，而对照未处理组为18.52 +/- 2.1 nmol/mg组织。与对照组（177.8 +/- 6.0 μ g/mg）相比，PAV标本在1% SDS溶液中孵育24 h可显著抑制3周龄雄性大鼠皮下植入物21天后的钙化（PAV Ca 2 + = 18.0 +/- 11.8 μ g/mg）。相比之下，与非药物硅胶基质对照（Ca 2 += 173.0 +/- 6.6 μ g/mg）相比，30% SDS硅橡胶聚合物的联合植入（局部持续SDS给药）在21天植入体内未阻碍PAV钙化。因此，我们得出结论，SDS抑制PAV钙化的机制是由于预孵育过程中发生的物质效应，而不是通过持续SDS给药促进的。(C)1993年，John Wiley and Sons，Inc.
Calcification of bioprosthetic heart valves fabricated from glutaraldehyde pretreated bovine pericardium or porcine aortic valves (PAV) is a frequent cause of the failure of these devices. Of all strategies considered thus far, only detergent preincubations using compounds such as sodium dodecyl sulfate (SDS) inhibited PAV bioprosthetic mineralization in circulatory sheep bioprosthetic valve replacements. The present study sought to characterize the mechanism of action of SDS preincubation. Results of transport and material characterization studies showed that SDS had a relatively high affinity for PAV, with a maximum uptake of 167.1 +/- 6.8 mu g SDS/mg tissue over 24h at 37 degrees C with a partition coefficient of 19.3. The PAV diffusion of SDS was 1.95 +/- 0.35 10(-6) cm(2)/sec. The principal effect of SDS on PAV was phospholipid extraction. The residual organic phosphate in the SDS pretreated tissue was 2.22 +/- 0.72 nmol/mg tissue compared to the control untreated group with 18.52 +/- 2.1 nmol/mg tissue. Incubations of PAV specimens in a 1% SDS solution for 24 h significantly inhibited calcification after 21 days in subdermal implants in 3-week-old male rats (PAV Ca2+ = 18.0 +/- 11.8 mu g/mg) compared to control (177.8 +/- 6.0 mu g/mg). In contrast, coimplants of 30% SDS silicone rubber polymers, for regional sustained SDS administration, did not impede PAV calcification in 21 day implants Ca2+ = 166.0 +/- 14.0 mu g/mg compared to the nondrug silicone matrix controls, Ca2+ = 173.0 +/- 6.6 mu g/mg). Thus, we conclude that the mechanisms of SDS inhibition of PAV calcification is due to material effects which occur during preincubation, and is not facilitated by sustained SDS administration. (C) 1993 John Wiley and Sons, Inc.