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新生绵羊出生时游离和硫酸结合儿茶酚胺的反应。

Free and sulfoconjugated catecholamine responses at birth in newborn sheep.

作者信息

Oyama K, Padbury J, Martinez A, Chappell B, Stein H, Blount L, Buhl E

机构信息

Perinatal Research Laboratories, University of California, Los Angeles Harbor Medical Center, Torrance 90509.

出版信息

Am J Physiol. 1992 Jul;263(1 Pt 1):E23-7. doi: 10.1152/ajpendo.1992.263.1.E23.

Abstract

There have been little data on catecholamine sulfoconjugation in developing animals or humans. We studied the differences in free and sulfoconjugated catecholamines at birth in newborn sheep. Baseline concentrations of sulfoconjugated norepinephrine and epinephrine were the predominant form of circulating catecholamine, representing 77 +/- 4 and 65 +/- 12% of total circulating catecholamines, respectively. At birth the free epinephrine concentration increased 10-fold (49 +/- 27 to 653 +/- 21 pg/ml, respectively), and plasma free norepinephrine concentration rose 4-fold (307 +/- 92 to 1,178 +/- 389 pg/ml). In contrast, there was only a transient twofold increase in the sulfoconjugated epinephrine. There was no increase in the sulfoconjugated form of norepinephrine. These data demonstrate that, while the near-term newborn sheep has a well-developed mechanism for sulfoconjugation of circulating catecholamines, this does not occur rapidly. During the logarithmic increases of circulating catecholamines at birth, there are not commensurate increases in the concentration of sulfoconjugated norepinephrine or epinephrine. Thus sulfoconjugation does not appear to represent a significant mechanism for inactivation of the high circulating levels of catecholamines seen at birth.

摘要

关于发育中的动物或人类体内儿茶酚胺硫酸结合作用的数据很少。我们研究了新生绵羊出生时游离和硫酸结合型儿茶酚胺的差异。硫酸结合型去甲肾上腺素和肾上腺素的基线浓度是循环儿茶酚胺的主要形式,分别占总循环儿茶酚胺的77±4%和65±12%。出生时,游离肾上腺素浓度增加了10倍(分别从49±27 pg/ml增至653±21 pg/ml),血浆游离去甲肾上腺素浓度升高了4倍(从307±92 pg/ml增至1178±389 pg/ml)。相比之下,硫酸结合型肾上腺素仅短暂增加了两倍。硫酸结合型去甲肾上腺素没有增加。这些数据表明,虽然接近足月的新生绵羊具有完善的循环儿茶酚胺硫酸结合机制,但这种结合过程并不迅速。在出生时循环儿茶酚胺呈对数增加期间,硫酸结合型去甲肾上腺素或肾上腺素的浓度并没有相应增加。因此,硫酸结合似乎并不是出生时所见高循环水平儿茶酚胺失活的重要机制。

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