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应激性溃疡形成过程中脆弱大鼠的能量消耗。

Energy expenditure during stress ulcer formation in vulnerable rats.

作者信息

Greenberg D, Ackerman S H

机构信息

Department of Psychiatry, Cornell University Medical College, White Plains, New York.

出版信息

Am J Physiol. 1989 Feb;256(2 Pt 2):R403-7. doi: 10.1152/ajpregu.1989.256.2.R403.

Abstract

Rat pups separated early from their mothers at day 15 become vulnerable to hypothermia and gastric erosion formation when food deprived and physically restrained on postnatal day 30 (S.H. Ackerman, M. A. Hofer, and H. Weiner, Science Wash. DC. 201: 373-376, 1978, and Gastroenterology 75: 649-654, 1978). We tested the hypothesis that this hypothermia is associated with a decrease in oxidative metabolism. We measured O2 consumption of 30-day-old rat pups that had been previously separated at either day 15 (15w) or day 21 (21w). When food was available, 15w rats used as much O2 as 21w rats. When rats were food deprived or food deprived and restrained, 15w rats used significantly less O2 than 21w rats, implying less heat production. We hypothesized that this decrease in heat production during food deprivation and/or restraint was due to impaired thermogenesis resulting from inadequate release of endogenous norepinephrine (NE), which is a stimulant of brown adipose tissue- (BAT) mediated thermogenesis. To test this hypothesis we administered exogenous NE to 15w to 21w rats. Exogenous NE failed to increase O2 consumption in 21w or 15w rats when injected during either food deprivation or restraint. We concluded that 30-day-old 15w rats have decreased oxidative metabolism during food deprivation and restraint and therefore become hypothermic. This decreased oxidative metabolism does not appear to be attributable to insufficient endogenous NE, since it is not reversed by the addition of exogenous NE. We suggest that a decrease in oxidative metabolism may explain susceptibility to stress ulcers in a number of previously reported experimental models.

摘要

出生后第15天就与母亲早早分离的幼鼠,在出生后第30天若被剥夺食物并受到身体束缚,就容易出现体温过低和胃糜烂(S.H. 阿克曼、M.A. 霍弗和H. 韦纳,《科学》,华盛顿特区,201: 373 - 376, 1978年,以及《胃肠病学》,75: 649 - 654, 1978年)。我们检验了这样一个假设,即这种体温过低与氧化代谢的降低有关。我们测量了30日龄幼鼠的耗氧量,这些幼鼠此前分别在第15天(15w)或第21天(21w)与母亲分离。当有食物时,15w组的大鼠与21w组的大鼠耗氧量相同。当大鼠被剥夺食物或既被剥夺食物又受到束缚时,15w组的大鼠耗氧量明显低于21w组的大鼠,这意味着产热更少。我们推测,在食物剥夺和/或束缚期间产热减少是由于内源性去甲肾上腺素(NE)释放不足导致产热受损,内源性去甲肾上腺素是棕色脂肪组织(BAT)介导的产热的刺激物。为了验证这一假设,我们给15w到21w的大鼠注射外源性NE。在食物剥夺或束缚期间注射外源性NE时,外源性NE未能增加21w或15w大鼠的耗氧量。我们得出结论,30日龄的15w大鼠在食物剥夺和束缚期间氧化代谢降低,因此体温过低。这种氧化代谢降低似乎并非归因于内源性NE不足,因为添加外源性NE并不能使其恢复。我们认为,氧化代谢降低可能解释了许多先前报道的实验模型中对应激性溃疡的易感性。

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