Thompson C H, Kemp G J, Radda G K
MRC Biochemical and Clinical Magnetic Resonance Unit, Oxford Radcliffe Hospital, UK.
Nephron. 1996;72(2):253-6. doi: 10.1159/000188850.
The secondary hyperparathyroidism of chronic renal failure has been implicated in the pathogenesis of metabolic abnormalities in skeletal muscle. We studied the muscle metabolism in a model of hyperparathyroidism (Wistar rats injected with parathyroid hormone or saline for 4 days). 31P magnetic resonance spectroscopy allowed measurements of the concentration of cytosolic metabolically active inorganic phosphate [Pi] at rest and the rates of oxidative and anaerobic adenosine triphosphate turnover during exercise and recovery. Parathyroid hormone caused significant reductions in plasma [Pi] and intracellular [Pi], but had no effect upon oxidative or glycogenolytic adenosine triphosphate turnover.
慢性肾衰竭的继发性甲状旁腺功能亢进与骨骼肌代谢异常的发病机制有关。我们在甲状旁腺功能亢进模型（向Wistar大鼠注射甲状旁腺激素或生理盐水，持续4天）中研究了肌肉代谢。31P磁共振波谱能够测量静息时胞质中代谢活性无机磷酸盐[Pi]的浓度，以及运动和恢复过程中氧化和无氧三磷酸腺苷周转的速率。甲状旁腺激素导致血浆[Pi]和细胞内[Pi]显著降低，但对氧化或糖原分解性三磷酸腺苷周转没有影响。
