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维生素D过多症诱导的Wistar大鼠动脉钙化的超微结构研究

Ultrastructural study of hypervitaminosis D induced arterial calcification in Wistar rats.

作者信息

Kingma J G, Roy P E

机构信息

Quebec Heart Institute, Laval Hospital, Quebec.

出版信息

Artery. 1988;16(1):51-61.

PMID:3207390
Abstract

Hypervitaminosis D produces extensive vascular alterations which are similar to Monckeberg's calcinosis. The present study was undertaken to examine early changes in vascular ultrastructure of rats receiving tap water supplemented with either calcium chloride or a relatively low dosage of irradiated ergocalciferol ad libitum for 21 days. Untreated rats received normal tap water ad libitum. A significant increase in serum calcium levels was obtained in hypervitaminosis D treated rats. Calcium deposits were seen near the internal elastic lamina, within new elastic elements and around degenerating smooth muscle cell fragments in the extracellular organic matrix of hypervitaminosis D treated rats. Calcium deposits were not detected in vascular sections from untreated rats or those receiving calcium chloride. A complex pathogenesis of vascular lesions produced by hypervitaminosis is suggested. One possible pathogenic mechanism for calcification of elastic matrix may be via altered microfibrils. Our data support this hypothesis and indicate that much lower levels of vitamin D administration, compared to other reports, produce considerable vascular calcinosis in this experimental preparation. Several hypotheses regarding possible mechanisms of pathologic calcification are discussed.

摘要

维生素D过多症会导致广泛的血管改变,类似于蒙克贝格氏钙质沉着症。本研究旨在检查自由饮用添加氯化钙或相对低剂量辐照麦角钙化醇的自来水21天的大鼠血管超微结构的早期变化。未处理的大鼠自由饮用正常自来水。维生素D过多症处理的大鼠血清钙水平显著升高。在维生素D过多症处理的大鼠的细胞外有机基质中,在内弹性膜附近、新的弹性元件内以及退化的平滑肌细胞碎片周围可见钙沉积。在未处理的大鼠或接受氯化钙的大鼠的血管切片中未检测到钙沉积。提示维生素D过多症导致血管病变的发病机制复杂。弹性基质钙化的一种可能致病机制可能是通过微原纤维的改变。我们的数据支持这一假设,并表明与其他报告相比,在本实验制剂中给予低得多的维生素D水平会产生相当程度的血管钙化。讨论了关于病理性钙化可能机制的几种假设。

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