López Ignacio, Aguilera-Tejero Escolástico, Estepa José Carlos, Rodríguez Mariano, Felsenfeld Arnold J
Departamento de Medicina y Cirugía Animal, Universidad de Córdoba, 14014 Córdoba, Spain.
Am J Physiol Endocrinol Metab. 2004 May;286(5):E780-5. doi: 10.1152/ajpendo.00473.2003. Epub 2004 Jan 13.
Recently, we showed that both acute metabolic acidosis and respiratory acidosis stimulate parathyroid hormone (PTH) secretion in the dog. To evaluate the specific effect of acidosis, ionized calcium (iCa) was clamped at a normal value. Because iCa values normally increase during acute acidosis, we now have studied the PTH response to acute metabolic and respiratory acidosis in dogs in which the iCa concentration was allowed to increase (nonclamped) compared with dogs with a normal iCa concentration (clamped). Five groups of dogs were studied: control, metabolic (clamped and nonclamped), and respiratory (clamped and nonclamped) acidosis. Metabolic (HCl infusion) and respiratory (hypoventilation) acidosis was progressively induced during 60 min. In the two clamped groups, iCa was maintained at a normal value with an EDTA infusion. Both metabolic and respiratory acidosis increased (P < 0.05) iCa values in nonclamped groups. In metabolic acidosis, the increase in iCa was progressive and greater (P < 0.05) than in respiratory acidosis, in which iCa increased by 0.04 mM and then remained constant despite further pH reductions. The increase in PTH values was greater (P < 0.05) in clamped than in nonclamped groups (metabolic and respiratory acidosis). In the nonclamped metabolic acidosis group, PTH values first increased and then decreased from peak values when iCa increased by > 0.1 mM. In the nonclamped respiratory acidosis group, PTH values exceeded (P < 0.05) baseline values only after iCa values stopped increasing at a pH of 7.30. For the same increase in iCa in the nonclamped groups, PTH values increased more in metabolic acidosis. In conclusion, 1) both metabolic acidosis and respiratory acidosis stimulate PTH secretion; 2) the physiological increase in the iCa concentration during the induction of metabolic and respiratory acidosis reduces the magnitude of the PTH increase; 3) in metabolic acidosis, the increase in the iCa concentration can be of sufficient magnitude to reverse the increase in PTH values; and 4) for the same degree of acidosis-induced hypercalcemia, the increase in PTH values is greater in metabolic than in respiratory acidosis.
最近,我们发现急性代谢性酸中毒和呼吸性酸中毒均可刺激犬甲状旁腺激素(PTH)的分泌。为评估酸中毒的特定作用,将离子钙(iCa)维持在正常水平。由于急性酸中毒时iCa值通常会升高,我们现在研究了iCa浓度允许升高(非钳制)的犬与iCa浓度正常(钳制)的犬对急性代谢性和呼吸性酸中毒的PTH反应。研究了五组犬:对照组、代谢性(钳制和非钳制)和呼吸性(钳制和非钳制)酸中毒组。在60分钟内逐渐诱导代谢性(输注盐酸)和呼吸性(低通气)酸中毒。在两个钳制组中,通过输注乙二胺四乙酸(EDTA)将iCa维持在正常水平。代谢性和呼吸性酸中毒均使非钳制组的iCa值升高(P<0.05)。在代谢性酸中毒中,iCa的升高是渐进性的,且幅度大于呼吸性酸中毒(P<0.05),呼吸性酸中毒时iCa升高0.04 mM,随后尽管pH值进一步降低但保持恒定。钳制组的PTH值升高幅度大于非钳制组(代谢性和呼吸性酸中毒)(P<0.05)。在非钳制的代谢性酸中毒组中,当iCa升高>0.1 mM时,PTH值先升高,然后从峰值下降。在非钳制的呼吸性酸中毒组中,仅在pH值为7.30时iCa值停止升高后,PTH值才超过(P<0.05)基线值。对于非钳制组中相同幅度的iCa升高,代谢性酸中毒时PTH值升高更多。总之,1)代谢性酸中毒和呼吸性酸中毒均刺激PTH分泌;2)代谢性和呼吸性酸中毒诱导过程中iCa浓度的生理性升高降低了PTH升高的幅度;3)在代谢性酸中毒中,iCa浓度的升高幅度足以逆转PTH值的升高;4)对于相同程度的酸中毒诱导的高钙血症,代谢性酸中毒时PTH值的升高幅度大于呼吸性酸中毒。