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用2-环辛基-2-羟乙胺降低大鼠脑内肾上腺素水平会诱发高血糖症。

Decreasing brain epinephrine levels with 2-cyclooctyl-2-hydroxyethylamine induces hyperglycemia in rats.

作者信息

Chu P C, Lin M T, Leu S Y

出版信息

Neuroendocrinology. 1985 Sep;41(3):181-5. doi: 10.1159/000124175.

Abstract

Intraperitoneal administration of 2-cyclooctyl-2-hydroxyethyl-amine (CONH; 25-75 mg/kg) produced dose-related reductions in the epinephrine (EPI) concentrations in both the hypothalamic and brainstem regions, but not in the adrenal glands. The reductions in the hypothalamic and brainstem EPI concentrations in rats anesthetized with pentobarbital sodium were accompanied by parallel increases in blood glucose. These data suggest that CONH induces its hyperglycemia action at least in part by altering central EPI biosynthesis. This hyperglycemic was antagonized by spinal transection or adrenalectomy, but not by vagotomy. This indicates that CONH increases the adrenal-sympathetic efferent activity and leads to hyperglycemia in rats.

摘要

腹腔注射2-环辛基-2-羟乙胺(CONH;25 - 75毫克/千克)可使下丘脑和脑干区域的肾上腺素(EPI)浓度呈剂量依赖性降低,但对肾上腺无此作用。用戊巴比妥钠麻醉的大鼠,下丘脑和脑干EPI浓度降低的同时,血糖水平平行升高。这些数据表明,CONH至少部分通过改变中枢EPI生物合成来诱导其高血糖作用。这种高血糖作用可被脊髓横断或肾上腺切除术拮抗,但不能被迷走神经切断术拮抗。这表明CONH增加了肾上腺交感传出活动并导致大鼠高血糖。

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