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葡萄糖输注对大鼠肝脏原位核心冷却新模型中通过磁共振波谱检测的磷酸单酯和三磷酸腺苷水平的影响。

Influence of glucose infusion on levels of phosphomonoesters and adenosine triphosphate as detected by magnetic resonance spectroscopy in a new model of core-cooling of the rat liver in situ.

作者信息

Iriyama K, Azuma T, Osawa T, Tsuchibashi T, Kitagawa T, Suzuki H

机构信息

Second Department of Surgery, Mie University School of Medicine, Tsu, Japan.

出版信息

JPEN J Parenter Enteral Nutr. 1993 Jan-Feb;17(1):77-81. doi: 10.1177/014860719301700177.

Abstract

This preliminary study was undertaken to ascertain whether our newly developed model of the cold ischemic rat liver in situ is applicable to studies designed to assess the metabolism of nutrients. Ischemia of the whole liver of 12 Wistar rats was induced by clamping all supply and drainage vessels. The ischemic liver was perfused in situ. The duration of ischemia of the liver was 20 minutes. Saline was infused into six rats throughout the experiment (group A). An intravenous infusion of glucose at a rate of 0.75 g/h per rat was begun immediately after the induction of blood-reflow to the liver (group B, n = 6). Six rats (group C) did not undergo the procedure for induction of hepatic ischemia and received glucose at the same rate as rats in group B. Changes in hepatic levels of sugar phosphates (phosphomonoesters [PMEs]), inorganic phosphorus, and beta-positioned phosphorus in adenosine triphosphate (beta-ATP) were monitored by 31P magnetic resonance spectroscopy. Ischemia caused a significant increase in levels of PMEs and a decrease in levels of beta-ATP. The infusion of glucose caused a further increase in levels of PMEs and a further decrease in levels of beta-ATP in group B. In contrast, in group C such infusion did not induce any changes in levels of PMEs or beta-ATP. In group A, PMEs and beta-ATP returned to basal levels 5 hours after the induction of blood-reflow to the liver. The changes in levels of PMEs were similar to those in levels of inorganic phosphorus in all groups.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本初步研究旨在确定我们新开发的大鼠肝脏原位冷缺血模型是否适用于评估营养物质代谢的研究。通过夹闭所有供血和引流血管诱导12只Wistar大鼠的全肝缺血。对缺血肝脏进行原位灌注。肝脏缺血持续时间为20分钟。在整个实验过程中,向6只大鼠输注生理盐水(A组)。在肝脏恢复血流后立即开始以每只大鼠0.75 g/h的速率静脉输注葡萄糖(B组,n = 6)。6只大鼠(C组)未进行肝脏缺血诱导操作,并以与B组大鼠相同的速率接受葡萄糖。通过31P磁共振波谱监测肝内磷酸糖(磷酸单酯[PMEs])、无机磷和三磷酸腺苷β位磷(β-ATP)水平的变化。缺血导致PMEs水平显著升高,β-ATP水平降低。在B组中,葡萄糖输注导致PMEs水平进一步升高,β-ATP水平进一步降低。相比之下,在C组中,这种输注未引起PMEs或β-ATP水平的任何变化。在A组中,肝脏恢复血流5小时后,PMEs和β-ATP恢复到基础水平。所有组中PMEs水平的变化与无机磷水平的变化相似。(摘要截短于250字)

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