Reversible diminished calcitonin secretion in the rat during chronic hypercalcemia.
Reversible diminished calcitonin secretion in the rat during chronic hypercalcemia.
复制标题
慢性高钙血症期间大鼠降钙素分泌可逆性减少。
作者：
F. Raue;I. Deutschle;C. Küntzel;R. Ziegler
血清降钙素（CT）浓度的短暂增加是由急性静脉钙（Ca）负荷引起的，而在慢性高钙血症状态下，血清CT水平以及甲状腺的CT含量是模棱两可的。采用高钙沃克癌肉瘤256 （HWCS 256）致肿瘤模型、慢性口服钙和慢性口服1,25(OH)2D3模型对CT分泌进行了检测。在HWCS 256大鼠中，肿瘤移植后第4天，即血清Ca升高前1天，血清CT水平从0.21 +/- 0.11 ng/ml的基础值上升至最高0.42 +/- 0.20 ng/ml。第二天（第5天）血清CT水平再次下降。在甲状腺切除、甲状旁腺自体移植HWCS 256的大鼠中，血清Ca比完整大鼠早1天升高。用外源性CT注射替代CT使高钙血症延迟一天。钙负荷后血清CT水平下降（三角CT）；甲状腺CT含量由9.4 +/- 1.1 ng/mg wet wt降至1.0 +/- 0.3 ng/mg wet wt，同时伴有高钙血症。此外，慢性腹腔注射钙诱导CT对钙负荷（δ CT）的反应降低，甲状腺CT含量从9.32 +/- 0.58 ng/mg湿wt降至3.84 +/- 0.33 ng/mg湿wt。停止给钙4天后，这些变化不再存在。在125 (OH)2D3诱导的慢性高钙血症中，基础血清CT水平没有显著变化，而血清Ca在第4天升高到11.8 +/- 0.46 mg/dl。急性钙负荷后的CT降低，125 (OH)2D3给药期间甲状腺的CT含量也降低。在停用1,25(OH)2D3后，这些变化是可逆的。在慢性高钙血症期间，观察到甲状腺CT含量的可逆性耗尽和CT对急性钙刺激的反应减弱，而基础血清CT水平保持不变。
A transient increase in serum calcitonin (CT) concentration is induced by an acute iv calcium (Ca) load, whereas in the chronic hypercalcemic state, serum CT levels, as well as CT content of the thyroid, are equivocal. The secretion of CT was tested in three models of hypercalcemia in rats: tumor induced by the hypercalcemic Walker carcinosarcoma 256 (HWCS 256), chronic parenteral Ca administration, and chronic 1,25(OH)2D3 administration. In rats with HWCS 256, serum CT levels increased from basal values of 0.21 +/- 0.11 ng/ml to a maximum of 0.42 +/- 0.20 ng/ml on day 4 after tumor transplantation, 1 day before serum Ca increased. The serum CT levels declined again the following day (day 5). In thyroidectomized, parathyroid autotransplated rats with HWCS 256, serum Ca increased 1 day earlier than in intact rats. Substitution of CT by exogenous CT injections delayed the hypercalcemia for one day. Ca loading was followed by a decreased serum CT level (delta CT); the CT content of the thyroid fell from 9.4 +/- 1.1 ng/mg wet wt to 1.0 +/- 0.3 ng/mg wet wt. While hypercalcemia was present. Also chronic intraperitoneal Ca administration induced a decrease in the CT response to a Ca load (delta CT) and a decrease in thyroid CT content from 9.32 +/- 0.58 ng/mg wet wt to 3.84 +/- 0.33 ng/mg wet wt. These changes were no longer present 4 days after stopping Ca administration. In chronic hypercalcemia induced by 1,25(OH)2D3 administration, basal serum CT levels did not vary significantly, whereas serum Ca increased to 11.8 +/- 0.46 mg/dl on day 4. CT after an acute Ca load was diminished, as was CT content of the thyroid during 1,25(OH)2D3 administration. These changes were reversible after stopping 1,25(OH)2D3 administration. During chronic hypercalcemia a reversible exhaustion of CT content of the thyroid and a diminished CT response to acute Ca stimulation was observed, while basal serum CT levels remained unchanged.