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[胎膜早破时胎膜抗张强度降低机制的评估]

[Evaluation of the mechanism of decreased tensile strength of fetal membrane in premature rupture of membrane].

作者信息

Lai R S

机构信息

81th Hospital of PLA, Nanjing.

出版信息

Zhonghua Fu Chan Ke Za Zhi. 1993 Sep;28(9):520-3, 567-8.

PMID:8313741
Abstract

Pathological morphology, thickness, tensile strength, coefficient variation of elasticity and immunohistochemical characteristics of fetal membrane in 246 cases of premature rupture of membrane (PROM) and 30 cases of control were investigated. The results showed that fetal membrane of PROM group appeared to be thinner, mainly composing of chorionic membrane lacking of mature development of fibroid component. The thickness of fetal membrane at the rupture site (54 +/- 11 microns) in PROM group was significantly thinner than that (208 +/- 94 microns) in control. The difference of tensile and elasticity strength of fetal membrane between 2 groups was highly significant. According to the findings of some immunohistochemical indices such as collagen type IV, FN, vimentin, MNF116, hCG and desmin, different component including collagenic fibers, basal membrane, fibroblastic cells, myofibroblastic cells and trophoblastic cells in fetal membrane and villus of PROM group revealed either dysplasia or aging. The mechanism of changes in biophysical characteristics of fetal membrane in PROM caused by noninfectious factors has been evaluated mainly.

摘要

对246例胎膜早破(PROM)患者及30例对照者的胎膜进行病理形态学、厚度、拉伸强度、弹性系数变异及免疫组化特征研究。结果显示,PROM组胎膜变薄,主要由缺乏成熟纤维成分发育的绒毛膜组成。PROM组破裂部位胎膜厚度(54±11微米)明显薄于对照组(208±94微米)。两组胎膜拉伸强度和弹性强度差异极显著。根据IV型胶原、FN、波形蛋白、MNF116、hCG和结蛋白等免疫组化指标结果,PROM组胎膜及绒毛中包括胶原纤维、基底膜、成纤维细胞、肌成纤维细胞和滋养层细胞在内的不同成分均显示发育异常或老化。主要评估了非感染因素导致PROM胎膜生物物理特性改变的机制。

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