Kamio A, Taguchi T, Shiraishi M, Shitama K, Fukushima K, Takebayashi S
Acta Pathol Jpn. 1979 Jul;29(4):545-62. doi: 10.1111/j.1440-1827.1979.tb00923.x.
The early fine structural changes in the arteries of rats induced by excess vitamin D3 perorally or parenterally were essentially similar, except the latter had a more prominent toxic effect to the vascular wall. The ultrastructural features, incidental to calcification, included the appearance of increased ground substance with a separation of collagenous and elastic fibrils, and degenerative changes in smooth muscle cells. Atherosclerosis was greatly accelerated at the sites of vascular injury when cholesterol, cholic acid and thiouracil were added to the basal diet. Calcification was initially observed in relation to elastic fibrils or degenerated cells in the upper and middle layers of the arteries, although there were few such deposits in the thickened intima of the coronary arteries. Calcium deposition could not be a direct effect of hypercalcemia, but the functional activity of smooth muscle cells did seem to promote the mineralization of calcium and phosphate. Furthermore, vitamin D-induced sclerosis did not prevent intimal thickening of the arteries when vitamin D3 was withdrawn.
经口或非经口给予过量维生素D3诱导的大鼠动脉早期精细结构变化基本相似，只是后者对血管壁的毒性作用更显著。钙化相关的超微结构特征包括基质增多、胶原纤维和弹性纤维分离，以及平滑肌细胞的退行性变化。当在基础饮食中添加胆固醇、胆酸和硫脲嘧啶时，血管损伤部位的动脉粥样硬化进程大大加速。钙化最初在动脉中层和上层的弹性纤维或退变细胞处观察到，尽管在冠状动脉增厚的内膜中此类沉积物很少。钙沉积并非高钙血症的直接作用，但平滑肌细胞的功能活性似乎确实促进了钙和磷的矿化。此外，当停用维生素D3时，维生素D诱导的硬化并不能阻止动脉内膜增厚。
