Lopez Ignacio, Rodriguez Mariano, Felsenfeld Arnold J, Estepa Jose Carlos, Aguilera-Tejero Escolastico
Departamento de Medicina y Cirugía Animal, Universidad de Córdoba, Córdoba, Spain.
J Bone Miner Res. 2003 Aug;18(8):1478-85. doi: 10.1359/jbmr.2003.18.8.1478.
Acute alkalosis may directly affect PTH secretion. The effect of acute metabolic and respiratory alkalosis was studied in 20 dogs. PTH values were lower in the metabolic (5.6 +/- 0.8 pg/ml) and respiratory (1.8 +/- 0.6 pg/ml) alkalosis groups than in the control group (27 +/- 5 pg/ml). Acute alkalosis is an independent factor that decreases PTH values during normocalcemia and delays the PTH response to hypocalcemia.
We recently showed that acute metabolic and respiratory acidosis stimulated PTH secretion. This study was designed to evaluate whether acute metabolic and respiratory alkalosis suppressed parathyroid hormone (PTH) secretion.
Three groups of 10 dogs were studied: control, acute metabolic alkalosis, and acute respiratory alkalosis. Metabolic alkalosis was induced with an infusion of sodium bicarbonate and respiratory alkalosis by hyperventilation. Calcium chloride was infused to prevent alkalosis-induced hypocalcemia during the first 60 minutes. During the next 30 minutes, disodium EDTA was infused to induce hypocalcemia and to evaluate the PTH response to hypocalcemia. Because the infusion of sodium bicarbonate resulted in hypernatremia, the effect of hypernatremia was studied in an additional group that received hypertonic saline.
After 60 minutes of a normocalcemic clamp, PTH values were less (p < 0.05) in the metabolic (5.6 +/- 0.8 pg/ml) and respiratory (1.8 +/- 0.6 pg/ml) alkalosis groups than in the control group (27 +/- 5 pg/ml); the respective blood pH values were 7.61 +/- 0.01, 7.59 +/- 0.02, and 7.39 +/- 0.02. The maximal PTH response to hypocalcemia was similar among the three groups. However, the maximal PTH response was observed after a decrease in ionized calcium of 0.20 mM in the control group but not until a decrease of 0.40 mM in the metabolic and respiratory alkalosis groups. In contrast to the metabolic alkalosis group, hypernatremia (157 +/- 2 mEq/liter) in the hypertonic saline group was associated with an increased PTH value (46 +/- 4 pg/ml). Finally, the half-life of intact PTH was not different among the control and two alkalosis groups.
Acute metabolic and respiratory alkalosis markedly decreased PTH values during normocalcemia and delayed the PTH response to hypocalcemia. Whether acute metabolic and respiratory alkalosis affect PTH and calcium metabolism in such settings as the postprandial alkaline tide (metabolic alkalosis) and acute sepsis (respiratory alkalosis) deserves to be evaluated in future studies.
急性碱中毒可能直接影响甲状旁腺激素（PTH）分泌。对20只犬研究了急性代谢性和呼吸性碱中毒的影响。代谢性碱中毒组（5.6±0.8 pg/ml）和呼吸性碱中毒组（1.8±0.6 pg/ml）的PTH值低于对照组（27±5 pg/ml）。急性碱中毒是在血钙正常时降低PTH值并延迟PTH对低钙血症反应的独立因素。
我们最近发现急性代谢性和呼吸性酸中毒刺激PTH分泌。本研究旨在评估急性代谢性和呼吸性碱中毒是否抑制甲状旁腺激素（PTH）分泌。
研究了三组，每组10只犬：对照组、急性代谢性碱中毒组和急性呼吸性碱中毒组。通过输注碳酸氢钠诱导代谢性碱中毒，通过过度通气诱导呼吸性碱中毒。在最初60分钟内输注氯化钙以预防碱中毒诱导的低钙血症。在接下来30分钟内，输注乙二胺四乙酸二钠以诱导低钙血症并评估PTH对低钙血症的反应。由于输注碳酸氢钠导致高钠血症，在另一组接受高渗盐水的犬中研究了高钠血症的影响。
在血钙正常钳夹60分钟后，代谢性碱中毒组（5.6±0.8 pg/ml）和呼吸性碱中毒组（1.8±0.6 pg/ml）的PTH值低于对照组（27±5 pg/ml）（p<0.05）；各自的血pH值分别为7.61±0.01、7.59±0.02和7.39±0.02。三组对低钙血症的最大PTH反应相似。然而，对照组在离子钙降低0.20 mM后观察到最大PTH反应，而代谢性和呼吸性碱中毒组直到离子钙降低0.40 mM才观察到最大PTH反应。与代谢性碱中毒组相反，高渗盐水组的高钠血症（157±2 mEq/升）与PTH值升高（46±4 pg/ml）相关。最后，对照组和两个碱中毒组中完整PTH的半衰期无差异。
急性代谢性和呼吸性碱中毒在血钙正常时显著降低PTH值并延迟PTH对低钙血症的反应。急性代谢性和呼吸性碱中毒在诸如餐后碱潮（代谢性碱中毒）和急性脓毒症（呼吸性碱中毒）等情况下是否影响PTH和钙代谢值得在未来研究中评估。
