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胃前食物诱发刺激在大鼠无全身脱水情况下引发饮水行为。

Pregastric food-contingent stimulation elicits drinking in the absence of systemic dehydration in the rat.

作者信息

Kraly F S

机构信息

Department of Psychology, Colgate University, Hamilton, NY 13346.

出版信息

Physiol Behav. 1990 Dec;48(6):841-4. doi: 10.1016/0031-9384(90)90237-x.

Abstract

Adult male Sprague-Dawley rats surgically fitted with a stainless steel gastric cannula were prepared following 24-h food deprivation for sham feeding liquid diet with open gastric fistula. Sham feeding (pregastric food-contingent stimulation) of 5, 10, 20 or 40 ml of liquid diet elicited water intake that was not in proportion to volume of liquid diet sham fed. Rats sham feeding between 1 and 68 ml of sweetened milk showed no evidence of cellular or extracellular dehydration as measured by plasma osmolality and hematocrit, respectively. Subcutaneous injection of 100 mg/kg captopril, a dose sufficient to block conversion of angiotensin I to angiotensin II in brain and periphery, inhibited drinking elicited by sham feeding without effect on sham feeding. These results demonstrate that pregastric food-contingent stimulation elicits water intake that is not in proportion to amount of liquid diet sham fed and that occurs in the apparent absence of systemic dehydration. That such drinking could depend upon endogenous angiotensin II provokes consideration of a role for angiotensin II in the mediation of a pregastric (perhaps histaminergic) mechanism that initiates drinking in advance of postprandial dehydration.

摘要

对成年雄性斯普拉格-道利大鼠进行手术,安装不锈钢胃插管,在禁食24小时后,为其准备用于假饲流食的开放性胃瘘。假饲(胃前食物相关刺激)5、10、20或40毫升流食所引发的水摄入量与假饲的流食体积不成比例。分别通过血浆渗透压和血细胞比容测量发现,假饲1至68毫升甜牛奶的大鼠没有细胞内或细胞外脱水的迹象。皮下注射100毫克/千克卡托普利(足以阻断脑和外周组织中血管紧张素I转化为血管紧张素II的剂量)可抑制假饲引发的饮水,但对假饲没有影响。这些结果表明,胃前食物相关刺激引发的水摄入量与假饲的流食量不成比例,且在明显没有全身性脱水的情况下发生。这种饮水可能依赖内源性血管紧张素II,这引发了人们对血管紧张素II在介导胃前(可能是组胺能)机制中的作用的思考,该机制在餐后脱水之前引发饮水。

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