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胎盘干绒毛闭塞性血管病(作者译)

[Obliterative angiopathy of placental stem villi (author's transl)].

作者信息

Bender H G, Werner C, Kortmann H R, Becker V

出版信息

Arch Gynakol. 1976 Sep 17;221(2):145-59. doi: 10.1007/BF00667144.

Abstract

Out of 136 placentas with vascular obliterations, 25 cases were placentas of children born alive, in 92 cases the placentas belonged to children born dead. In 19 cases we had no data on the baby. In placentas of babies born alive, the same vascular changes (subtotal and total obliterations, septal partitions of vascular lumina) were found as in those of dead-born children, although considerably less severe. Vascular obliterations should not be considered as post-mortal alterations of the placenta blood vessels, since only quantitative differences could be proved. Septum-like partitions are hardly ever found in placentas of babies born alive, in dead-born babies they are more frequent. They seem to present recanalizations, and are understood as a compensation mechanism for a placental insufficiency caused by vascular obliterations. The accentuated collagenization of the placental periphery, noticed in placentas of babies born alive, is being interpreted as the consequence of an impaired blood circulation, caused by partial and total vascular obliterations. The high collagen rate in the placental periphery in placentas of the dead-born is probably a reaction to the diminished fetal circulation. Endangitis obliterations in 73 placentas out of 4600 pregnancies of cases with late abortions, premature deliveries, perinatal death, underweigh and small for gestational age babies, impaired adaptation in newborns of mothers with proteinuria and hypertension speak strongly for assuming that endangitis obliterans presents a form of placental insufficiency. Endangitis obliterans of the placental blood-vessels has, however, been discovered frequently after Rubella infection in early pregnancy. The etiological factors of the endovascular process can be multiple, the morphological and the pathophysiological reactions are the same.

摘要

在136例存在血管闭塞的胎盘中,25例为活产儿的胎盘,92例为死产儿的胎盘。19例中我们没有关于婴儿的资料。在活产儿的胎盘中,发现了与死产儿相同的血管变化(部分和完全闭塞、血管腔的间隔分隔),尽管程度要轻得多。血管闭塞不应被视为胎盘血管的死后改变,因为只能证明存在数量上的差异。在活产儿的胎盘中几乎从未发现过隔膜样分隔,而在死产儿中则更为常见。它们似乎是再通现象,被认为是血管闭塞导致胎盘功能不全的一种代偿机制。在活产儿的胎盘中观察到的胎盘周边胶原化加剧,被解释为部分和完全血管闭塞导致血液循环受损的结果。死产儿胎盘周边的高胶原率可能是对胎儿循环减少的一种反应。在4600例晚期流产、早产、围产期死亡、低体重和小于孕周婴儿的病例妊娠中,有73例胎盘出现闭塞性动脉内膜炎,这有力地表明闭塞性动脉内膜炎是胎盘功能不全的一种形式。然而,胎盘血管的闭塞性动脉内膜炎在妊娠早期风疹感染后经常被发现。血管内病变的病因可能是多方面的,但其形态学和病理生理学反应是相同的。

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