Inhibition of Carbohydrate Oxidation During the First Minute of Reperfusion After Brief Ischemia: NMR Detection of Hyperpolarized 13CO2 and H13CO3-

Inhibition of Carbohydrate Oxidation During the First Minute of Reperfusion After Brief Ischemia: NMR Detection of Hyperpolarized 13CO2 and H13CO3-
复制标题

DOI:
10.1002/mrm.21760
复制
发表时间:
2008-11-01
影响因子:
3.3
通讯作者:
Malloy, Craig R.
Malloy, Craig R.
中科院分区:
医学3区
文献类型:
--
作者:
Merritt, Matthew E.;Harrison, Crystal;Malloy, Craig R.

文献摘要

被引文献

相似文献

用~(31)P NMR和~(13)C NMR研究离体大鼠心脏。提供超极化[1-C]丙酮酸盐以控制含氧量正常的心脏,并以1-s时间分辨率监测[1 - 13 C]乳酸盐、[1- 13 C]丙氨酸、(CO2)-C-13和(HCO 3-)-C-13的产生。心脏还经受10分钟的全脑缺血,随后再灌注。在缺血期后3分钟内,血压、心率、耗氧量、[ATP]、[磷酸肌酸]和pH值恢复。在再灌注的前90秒,[1 -C-13]丙氨酸和[1 -C-13]乳酸迅速出现,表明丙酮酸通过主要局限于胞质溶胶的两种酶,丙氨酸氨基转移酶和乳酸脱氢酶代谢。未检出(CO2)-C-13和(HCO 3-)-C-13。缺血及再灌注后期,丙酮酸脱氢酶产物(CO_2)-C-13和(HCO_3)-C-13-易于检测。使用这种多核核磁共振方法,我们确定,在第一个90秒的再灌注PDH流量基本上是零,并在20分钟内恢复可逆性损伤的心肌。Magn Reson Med 60:1029-1036,2008. (C)2008 Wiley-Liss,Inc.
Isolated rat hearts were studied by P-31 NMR and C-13 NMR. Hyperpolarized [1-C]pyruvate was supplied to control normoxic hearts and production of [1-13C]lactate, [1-13C]alanine, (CO2)-C-13 and (HCO3-)-C-13 was monitored with 1-s temporal resolution. Hearts were also subjected to 10 min of global ischernia followed by reperfusion. Developed pressure, heart rate, oxygen consumption, [ATP], [phosphocreatine], and pH recovered within 3 min after the ischemic period. During the first 90 s of reperfusion, [1 -C-13]alanine and [1 -C-13]lactate appeared rapidly, demonstrating metabolism of pyruvate through two enzymes largely confined to the cytosol, alanine aminotransferase, and lactate dehydrogenase. (CO2)-C-13 and (HCO3-)-C-13 were not detected. Late after ischernia and reperfusion, the products of pyruvate dehydrogenase, (CO2)-C-13 and (HCO3)-C-13- were easily detected. Using this multinuclear NMR approach, we established that during the first 90 s of reperfusion PDH flux is essentially zero and recovers within 20 min in reversibly-injured myocardium. Magn Reson Med 60:1029-1036, 2008. (C) 2008 Wiley-Liss, Inc.