Cuisinier-Gleizes P, George A, Thomasset M, Mathieu H
C R Acad Hebd Seances Acad Sci D. 1975 May 12;280(18):2145-8.
Chronic metabolic acidosis entails hyperparathyroidism and osteopathy. In order to elucidate the role of the thyroparathyroids in this bone lesion production the effects of acidic diet for 7 weeks were studied in parathyroidectomized (PTX), thyroparathyroidectomized (TPTX) and shamoperated (Sh-O) growing rats. In all animals urinary excretion of calcium, phosphate, ammonium and titrable acidity was similarly increased. The rise in hydroxyproline excretion and urinary 85-sr (that was injected previous to acidic feeding) was more marked in PTX and TPTX rats. Moreover, in these animals the serum calcium level was increased, the blood pH was decreased. According to these data, an acidic diet intake that is not sufficient to elicit a fall in blood pH of normal young rats can induce severe acidosis in chronically parathyroidectomized or thyroparathyroidectomized animals; moreover the bone resorption appears more marked. It is concluded that parathyroids are involved in the extra-cellular fluid defense mechanism against acidosis by a no bone resorptive mechanism. We hypothesize that the parathyroids permit the necessary and adequate supply of bicarbonates by the bone to maintain blood pH homeostasis.
慢性代谢性酸中毒会引发甲状旁腺功能亢进和骨病。为了阐明甲状腺旁腺在这种骨病变产生中的作用,我们对甲状旁腺切除(PTX)、甲状腺旁腺切除(TPTX)和假手术(Sh - O)的生长大鼠进行了为期7周的酸性饮食影响研究。在所有动物中,钙、磷、铵和可滴定酸度的尿排泄量均同样增加。羟脯氨酸排泄量和尿85 - 锶(在酸性喂养前注射)的升高在PTX和TPTX大鼠中更为明显。此外,在这些动物中,血清钙水平升高,血液pH值降低。根据这些数据,正常幼鼠摄入不足以引起血液pH值下降的酸性饮食,可在慢性甲状旁腺切除或甲状腺旁腺切除的动物中诱发严重酸中毒;而且骨吸收似乎更明显。结论是甲状旁腺通过一种无骨吸收机制参与细胞外液抗酸中毒防御机制。我们推测甲状旁腺允许骨骼提供必要且充足的碳酸氢盐以维持血液pH值稳态。