Adrenomedullary function in the neonatal rat: responses to acute hypoxia.
Adrenomedullary function in the neonatal rat: responses to acute hypoxia.
复制标题
新生大鼠的肾上腺髓质功能：对急性缺氧的反应。
DOI：
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发表时间：
1985
期刊：
影响因子：
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通讯作者：
T. Slotkin
中科院分区：
文献类型：
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作者：
F. Seidler;T. Slotkin
研究了新生大鼠肾上腺髓质释放儿茶酚胺的机制，以及这些胺在机体抵抗急性缺氧的能力中的作用。直到出生后第一周结束，大鼠肾上腺的内脏神经支配才发挥功能。然而，缺氧导致 1 日龄大鼠和 8 日龄动物的肾上腺儿茶酚胺消耗。用胆碱能受体阻断剂进行预处理并不能阻止第 1 天的儿茶酚胺反应，但在老年动物中却可以阻止；这些结果表明，消耗机制在 1 日龄动物中不是神经源性的，但在 8 日龄动物中是神经源性的。缺氧应激释放的去甲肾上腺素和肾上腺素的比例在两个年龄段也不同，神经源性机制优先释放肾上腺素，而非神经源性机制则不优先释放肾上腺素。神经源性机制对非神经源性肾上腺髓质反应的个体发生替代与内脏神经功能的发生直接相关。加速神经元连接发育的治疗（新生儿甲状腺功能亢进、母亲应激）导致非神经源性反应过早丧失。在交感神经功能发育之前，肾上腺儿茶酚胺在使新生儿能够在缺氧中生存方面发挥着主要作用。干扰肾上腺胺的释放总是会增加缺氧期间的死亡率。相比之下，干扰交感神经释放儿茶酚胺并不影响 1 日龄大鼠耐受缺氧的能力，表明低 PO2 条件下的生存并不依赖于该发育阶段的交感神经支配。在交感神经功能发育和非神经源性肾上腺髓质反应消失后，新生大鼠部分依赖于来自交感神经末梢的儿茶酚胺；第 8 天给予溴苄铵会显着损害缺氧期间的存活率。干扰肾上腺素受体功能也会干扰新生大鼠承受低 PO2 的能力。 1 日龄时，苯氧苯扎明或 ICI-118551（而非阿替洛尔）缩短了缺氧期间的存活时间。第 8 天时，只有苯氧苯扎明做到了这一点。（摘要截断为 400 字）
The mechanism of release of catecholamines from the adrenal medulla of neonatal rats was examined, together with the role of these amines in the ability of the organism to withstand acute O2 deprivation. Splanchnic innervation of the rat adrenal is non‐functional until the end of the first postnatal week. Nevertheless, hypoxia caused depletion of adrenal catecholamines in 1‐day‐old rats as well as in 8‐day‐old animals. Pre‐treatment with cholinergic receptor blocking agents did not prevent the catecholamine response at 1 day but did in older animals; these results indicate that the depletion mechanism is not neurogenic in 1‐day‐old animals but is neurogenic in 8‐day‐old animals. The proportions of noradrenaline and adrenaline released by hypoxic stress also differed at the two ages, with preferential release of adrenaline by the neurogenic mechanism but not by the non‐neurogenic one. The ontogenetic replacement of non‐neurogenic adrenomedullary responses by the neurogenic mechanism was directly related to the onset of splanchnic nerve function. Treatments which accelerated the development of neuronal connexions (neonatal hyperthyroidism, maternal stress) caused premature loss of the non‐neurogenic response. Prior to the development of sympathetic nerve function, adrenal catecholamines plays a predominant role in enabling the neonate to survive hypoxia. Interference with the release of adrenal amines invariably increased mortality during hypoxia. In contrast, interference with sympathetic neural release of catecholamines did not affect the ability of 1‐day‐old rats to withstand hypoxia, indicating that survival during low PO2 conditions is not dependent on the sympathetic innervation at that stage of development. After functional development of the sympathetic nerves and disappearance of non‐neurogenic adrenomedullary responses, the neonatal rats became partially dependent upon catecholamines derived from sympathetic terminals; administration of bretylium at 8 days significantly compromised survival during hypoxia. Interference with adrenergic receptor function also interfered with the ability of neonatal rats to withstand low PO2. At 1 day of age, either phenoxybenzamine or ICI‐118551, but not atenolol, shortened the survival time during hypoxia. At 8 days, only phenoxybenzamine did so.(ABSTRACT TRUNCATED AT 400 WORDS)
DOI：
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发表时间：
1982
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
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作者：
Lau,C;Burke,SP;Slotkin,TA
通讯作者：
Slotkin,TA