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ATP-MgCl₂ 改善缺血再灌注后的线粒体功能。

Improved mitochondrial function following ischemia and reflow by ATP-MgCl2.

作者信息

Chaudry I H, Ohkawa M, Clemens M G

出版信息

Am J Physiol. 1984 May;246(5 Pt 2):R799-804. doi: 10.1152/ajpregu.1984.246.5.R799.

Abstract

To determine whether infused ATP-MgCl2 affects mitochondrial adenine nucleotide translocase (ANT) activity, free fatty acids (FFAs), and Ca2+ levels, total hepatic ischemia in rats was produced for 90 min after which blood flow was allowed to return to the liver. Immediately on reflow, the animals received intravenously 0.5 ml of either saline, ATP-MgCl2 (12.5 mumol), or dopamine (6 mg/kg). Three hours after ischemia and reflow, hepatic mitochondrial FFAs and Ca2+ levels increased; however, ATP-MgCl2 infusion significantly lowered FFAs and restored Ca2+ levels. The depressed mitochondrial ANT activity was somewhat improved but not restored by circulatory support with dopamine; however, ATP-MgCl2 infusion following ischemia restored that activity. Thus the present results suggest that the improved organ function that occurs with ATP-MgCl2 infusion following ischemia may be mediated through an improvement in ischemia-induced mitochondrial function.

摘要

为了确定输注ATP-MgCl2是否会影响线粒体腺嘌呤核苷酸转位酶(ANT)活性、游离脂肪酸(FFA)和Ca2+水平,对大鼠进行了90分钟的全肝缺血,之后恢复肝脏血流。再灌注即刻,动物静脉注射0.5 ml生理盐水、ATP-MgCl2(12.5 μmol)或多巴胺(6 mg/kg)。缺血再灌注3小时后,肝线粒体FFA和Ca2+水平升高;然而,输注ATP-MgCl2可显著降低FFA并恢复Ca2+水平。线粒体ANT活性降低,多巴胺循环支持虽有所改善但未恢复该活性;然而,缺血后输注ATP-MgCl2可恢复该活性。因此,目前的结果表明,缺血后输注ATP-MgCl2所出现的器官功能改善可能是通过改善缺血诱导的线粒体功能来介导的。

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