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大鼠松节油诱导应激期间颈交感神经系统在钙稳态变化中的作用。

Involvement of the cervical sympathetic nervous system in the changes of calcium homeostasis during turpentine oil-induced stress in rats.

作者信息

Stern J E, Ladizesky M G, Keller Sarmiento M I, Cardinali D P

机构信息

Departamento de Fisiología, Facultad de Medicina, Universidad de Buenos Aires, Argentina.

出版信息

Neuroendocrinology. 1993 Mar;57(3):381-7. doi: 10.1159/000126383.

Abstract

Hypocalcemia is a common finding during stress. The objective of this study was to examine: (a) the changes in circulating calcium, parathyroid hormone (PTH) and calcitonin (CT) concentration in rats stressed by being given a subcutaneous injection of turpentine oil, and (b) the involvement of the sympathetic cervical pathway in stress-induced changes of calcium homeostasis. Four hours after receiving turpentine oil or vehicle, rats were subjected either to hypocalcemia, by being given EDTA intraperitoneally, or to hypercalcemia, by being injected CaCl2 intraperitoneally. Significant changes in serum calcium (10% decrease), serum PTH (28% increase) and CT levels (40% decrease) were observed in stressed rats. EDTA administration brought about a significantly greater hypocalcemia, and a higher PTH secretory response in turpentine oil-stressed rats. During stress, the increase of serum calcium after CaCl2 was significantly smaller, and the rise of CT was greater than in controls. In the case of CT the changes were still observed in rats subjected to superior cervical ganglionectomy (SCGx) 14 days earlier. In the case of PTH, the increase found in stressed rats, but not the augmented response after EDTA, was blunted by SCGx. The potentiation of hypocalcemia brought about by turpentine oil was no longer observed in SCGx rats. In vehicle-treated controls, SCGx delayed PTH response to hypocalcemia, but did not affect the increased response of CT to CaCl2 challenge. The results indicate that a number of changes in calcium homeostasis arise during turpentine oil stress in rats. SCGx was effective to modify the set point for PTH release, but played a minor role in affecting the augmentation of CT release during stress.

摘要

低钙血症是应激期间常见的表现。本研究的目的是检测:(a)皮下注射松节油诱导应激的大鼠循环钙、甲状旁腺激素(PTH)和降钙素(CT)浓度的变化;(b)交感颈神经通路在应激诱导的钙稳态变化中的作用。给予松节油或赋形剂4小时后,大鼠腹腔注射乙二胺四乙酸(EDTA)造成低钙血症,或腹腔注射氯化钙造成高钙血症。应激大鼠血清钙显著降低(10%)、血清PTH显著升高(28%)、CT水平显著降低(40%)。给予EDTA后,松节油应激大鼠出现显著更低的血钙水平及更高的PTH分泌反应。应激期间,氯化钙注射后血清钙的升高显著小于对照组,CT的升高则大于对照组。对于CT,在14天前接受颈上神经节切除术(SCGx)的大鼠中仍观察到变化。对于PTH,应激大鼠中发现的升高,但EDTA注射后的增强反应,在SCGx后减弱。SCGx大鼠未观察到松节油引起的低钙血症增强。在给予赋形剂的对照组中,SCGx延迟了PTH对低钙血症的反应,但不影响CT对氯化钙激发的增强反应。结果表明,大鼠在松节油应激期间钙稳态出现了一些变化。SCGx有效地改变了PTH释放的设定点,但在影响应激期间CT释放的增强方面作用较小。

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