Matthews C, Heimberg K W, Ritz E, Agostini B, Fritzsche J, Hasselbach W
Kidney Int. 1977 Apr;11(4):227-35. doi: 10.1038/ki.1977.35.
In the fragmented sarcoplasmic reticulum from skeletal muscle of rabbits with experimental uremia, defective calcium ion transport is found. An impairment of all parameters is observed (initial rate of uptake, storing capacity with and without oxalate, and concentrating ability). In vivo administration of 1,25-dihydroxycholecalciferol (1,25-(OH)2-vitamin D3)(2 X 27 ng X kg of body wt-1 X day-1 and 6 X 27 ng X kg-1 X day-1, respectively) improved the kinetic parameters. The low dose improved storing capacity, and the higher dose, in addition to the storing capacity, also corrected concentrating ability and the initial rate of uptake. It is concluded that active calcium transport in the sarcoplasmic reticulum is impaired by uremia and that this defect is responsive to the administration of 1,25-(OH)2-vitamin D3.
在实验性尿毒症兔骨骼肌的破碎肌浆网中,发现钙离子转运存在缺陷。观察到所有参数均受损(摄取初始速率、有无草酸盐时的储存能力以及浓缩能力)。分别以1,25 - 二羟胆钙化醇(1,25 - (OH)₂ - 维生素D₃)(2×27 ng×kg体重⁻¹×天⁻¹和6×27 ng×kg⁻¹×天⁻¹)进行体内给药,改善了动力学参数。低剂量改善了储存能力,而高剂量除了改善储存能力外,还纠正了浓缩能力和摄取初始速率。得出的结论是,尿毒症会损害肌浆网中的活性钙转运,且这种缺陷对1,25 - (OH)₂ - 维生素D₃的给药有反应。