Sympathetic nervous system and adrenal medullary responses to ischemic injury in mice.

Sympathetic nervous system and adrenal medullary responses to ischemic injury in mice.
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交感神经系统和肾上腺髓质对小鼠缺血性损伤的反应。

DOI:
10.1152/ajpendo.1983.245.1.e67
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发表时间:
1983
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Landsberg,L
Landsberg,L
中科院分区:
--
文献类型:
--
作者:
Young,JB;Fish,S;Landsberg,L

文献摘要

被引文献

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急性、严重的创伤常伴有低血压、体温过低和代谢率降低,尽管尿和血浆中的儿茶酚胺水平升高。由于在其他几种情况下记录的交感神经系统(SNS)抑制和肾上腺髓质刺激的组合可以解释这些观察结果,因此在急性损伤的后肢缺血模型中独立检查了小鼠的SNS和肾上腺髓质功能。SNS活性通过测量心脏中的[3H]去甲肾上腺素(NE)周转率和肾上腺髓质分泌(通过消耗肾上腺儿茶酚胺含量)来评估。在9个独立的实验中,在第一个10小时后终止的2.5小时后肢缺血期间,心脏NE营业额平均减少了23%(P小于0.05)在受伤的小鼠。同时,损伤组肾上腺儿茶酚胺含量下降37%(P <0.05),而对照组无明显变化。与急性反应相反,存活3天的小鼠的SNS活性比对照组高59%。因此,NE营业额的减少和肾上腺儿茶酚胺含量的耗竭表明,SNS抑制和肾上腺髓质刺激构成了严重损伤模型中的急性交感肾上腺反应。由于肾上腺切除小鼠损伤后24小时内的存活率下降,尽管糖皮质激素治疗,肾上腺髓质儿茶酚胺可能有助于严重损伤动物的存活。此外,由于SNS在血压和产热的调节中起着重要作用,因此伤后数小时内SNS活性的减少可能导致创伤后低血压和低代谢。
Acute, severe injury is frequently attended by hypotension, hypothermia, and decreased metabolic rate despite elevated urine and plasma catecholamine levels. Because the combination of sympathetic nervous system (SNS) suppression and adrenal medullary stimulation documented in several other situations could account for these observations, SNS and adrenal medullary function were examined independently in mice in the hindlimb ischemia model of acute injury. SNS activity was assessed by the measurement of [3H]norepinephrine (NE) turnover in heart and adrenal medullary secretion by depletion of adrenal catecholamine content. In nine separate experiments during the first 10 h after termination of a 2.5-h period of hindlimb ischemia, cardiac NE turnover was reduced an average of 23% (P less than 0.05) in injured mice. At the same time, adrenal catecholamine content fell 37% (P less than 0.05) in injured animals but not in controls. In contrast to the acute reaction, SNS activity in mice surviving 3 days was 59% greater than in controls. Thus, the reduction in NE turnover and depletion of adrenal catecholamine content suggest that SNS suppression and adrenal medullary stimulation constitute the acute sympathoadrenal response in this model of severe injury. Because survival within the first 24 h after injury was decreased in adrenalectomized mice despite glucocorticoid treatment, adrenal medullary catecholamines may contribute to survival in severely injured animals. Furthermore, because the SNS plays an important role in the regulation of blood pressure and heat production, the diminution in SNS activity in the hours after injury may contribute to posttraumatic hypotension and hypometabolism.