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羊膜囊穿刺诱导大鼠发育缺陷的发病机制。

Pathogenesis of developmental defects induced in the rat by amniotic sac puncture.

作者信息

Kennedy L A, Persaud T V

出版信息

Acta Anat (Basel). 1977;97(1):23-35. doi: 10.1159/000144714.

Abstract

The morphogenesis of developmental defects induced by aminotic sac puncture was studied at the gross and microscopic levels. In fetuses recovered from 15 min to 48 h after amniocentesis, a pattern of hemorrhagic lesions, excessive accumulation of interstitial fluid, followed by tissue necrosis and leading ultimately to the reduction of amputation of distal limb segments and morphological changes in the head, was observed. These changes were indicative of venous stasis, hypervolemia and embryonic oxygen deficiency. Intrauterine compression of the fetus and the obstruction of the fetomaternal circulation were considered to be the primary etiological factors in amniocentesis-induced anomalies which included hemorrhagic lesions, limb reductions and amputations, deformities of the head and abdominal regions, generalized edema and postural moulding.

摘要

在大体和微观水平上研究了羊膜腔穿刺诱导的发育缺陷的形态发生。在羊膜穿刺术后15分钟至48小时恢复的胎儿中,观察到一种出血性病变模式,间质液过度积聚,随后组织坏死,最终导致远端肢体节段的截断和头部形态变化。这些变化表明静脉淤滞、血容量过多和胚胎缺氧。胎儿的宫内压迫和母胎循环的阻塞被认为是羊膜穿刺诱导异常的主要病因,这些异常包括出血性病变、肢体缩短和截断、头部和腹部区域的畸形、全身性水肿和姿势塑形。

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