Chang Yen, Liang Huang-Chien, Wei Hao-Ji, Chu Chih-Ping, Sung Hsing-Wen
Division of Cardiovascular Surgery, Veterans General Hospital-Taichung, Taiwan, Republic of China.
J Biomed Mater Res A. 2004 May 1;69(2):323-33. doi: 10.1002/jbm.a.30003.
It was noted in our previous study that acellular tissues can provide a natural microenvironment for host cell migration and proliferation to accelerate tissue regeneration. The purpose of this study was to further investigate the tissue regeneration patterns in acellular bovine pericardia fixed with glutaraldehyde or genipin as a biological patch to repair a defect in the pulmonary trunk in a canine model. The implanted samples were retrieved at distinct durations postoperatively. The structural remodeling of retrieved samples was then examined. It was found that the degree of inflammatory reaction observed for the genipin-fixed acellular patch was significantly less than its glutaraldehyde-fixed counterpart. At 1 month postoperatively, intimal thickening was found on the inner surfaces of both studied groups. The intimal thickening observed on the glutaraldehyde-fixed acellular patch was significantly thicker than its genipin-fixed counterpart. An intact layer of endothelial cells was found on the intimal thickening of the genipin-fixed acellular patch, whereas endothelial cells did not universally and totally cover the entire surface of the glutaraldehyde-fixed acellular patch. Additionally, fibroblasts with neocollagen fibrils and myofibroblasts were observed in the acellular patches for both studied groups, an indication of tissue regeneration. This phenomenon was more prominent for the genipin-fixed acellular patch than its glutaraldehyde-fixed counterpart. At 6 months postoperatively, foci of chondroid and/or bony metaplasia were found in each retrieved sample for both studied groups. The observed adverse response of chondroid metaplasia may be attributed to a compliance mismatch at the implanted site of the canine pulmonary trunk after implantation or a lack of angiogenesis in the regenerated tissue observed at 1 month postoperatively. Bony metaplasia may then develop as in other chondroid tissues. It was reported that ischemia is a usual cause of metaplasia.
我们之前的研究指出，脱细胞组织可为宿主细胞迁移和增殖提供天然微环境，以加速组织再生。本研究的目的是进一步研究用戊二醛或京尼平固定的脱细胞牛心包作为生物补片修复犬模型肺动脉干缺损时的组织再生模式。在术后不同时间段取出植入的样本，然后检查取出样本的结构重塑情况。结果发现，京尼平固定的脱细胞补片的炎症反应程度明显低于戊二醛固定的补片。术后1个月，两个研究组的内表面均出现内膜增厚。戊二醛固定的脱细胞补片上观察到的内膜增厚明显厚于京尼平固定的补片。在京尼平固定的脱细胞补片的内膜增厚处发现了完整的内皮细胞层，而内皮细胞并未普遍且完全覆盖戊二醛固定的脱细胞补片的整个表面。此外，在两个研究组的脱细胞补片中均观察到带有新胶原纤维的成纤维细胞和平滑肌成纤维细胞，这表明有组织再生。这种现象在京尼平固定的脱细胞补片中比在戊二醛固定的补片中更为明显。术后6个月，两个研究组的每个取出样本中均发现了软骨样和/或骨化生灶。观察到的软骨样化生的不良反应可能归因于植入后犬肺动脉干植入部位的顺应性不匹配，或术后1个月在再生组织中观察到的血管生成不足。然后骨化生可能会像在其他软骨样组织中一样发展。据报道，缺血是化生的常见原因。
