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人体盐负荷诱导的循环因子对血浆血管加压素细胞化学测定的干扰。

Interference in the cytochemical assay of plasma vasopressin by a circulating factor induced by salt-loading in man.

作者信息

Baylis P H, Pippard C, Burd J M

出版信息

J Endocrinol. 1986 Dec;111(3):495-9. doi: 10.1677/joe.0.1110495.

Abstract

Infusion of hypertonic saline into six normal volunteers caused an increase in plasma osmolality from 286.8 +/- 1.7 (mean +/- S.E.M.) to 307.6 +/- 2.6 mosmol/kg (P less than 0.001), a 7.1% increase in estimated blood volume, a rise in plasma immunoreactive arginine vasopressin (AVP) concentrations from 1.3 +/- 0.2 to 12.7 +/- 3.6 pmol/l (P less than 0.001) but no change in plasma AVP concentrations (2.1 +/- 0.9 and 1.9 +/- 1.3 pmol/l) as measured by a cytochemical technique based on the ability of AVP to stimulate rat renal medullary Na+/K+-ATPase activity. Addition of synthetic AVP to plasma obtained before, during and after hypertonic saline infusion also failed to stimulate Na+/K+-ATPase activity. The results suggest that infusion of hypertonic saline interfered with the cytochemical assay for AVP by inhibiting AVP-stimulated medullary Na+/K+-ATPase activity. We conclude that the use of this cytochemical method to detect plasma AVP has severe limitations under these experimental conditions.

摘要

向六名正常志愿者输注高渗盐水后,血浆渗透压从286.8±1.7(均值±标准误)升高至307.6±2.6毫摩尔/千克(P<0.001),估计血容量增加7.1%,血浆免疫反应性精氨酸加压素(AVP)浓度从1.3±0.2升高至12.7±3.6皮摩尔/升(P<0.001),但基于AVP刺激大鼠肾髓质Na+/K+-ATP酶活性的细胞化学技术检测显示血浆AVP浓度无变化(分别为2.1±0.9和1.9±1.3皮摩尔/升)。在高渗盐水输注前、输注期间和输注后获取的血浆中添加合成AVP,也未能刺激Na+/K+-ATP酶活性。结果表明,输注高渗盐水通过抑制AVP刺激的髓质Na+/K+-ATP酶活性干扰了AVP的细胞化学测定。我们得出结论,在这些实验条件下,使用这种细胞化学方法检测血浆AVP存在严重局限性。

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