Correlation between [5-3H]glucose and [U-14C]deoxyglucose as markers of glycolysis in reperfused myocardium.

Liedtke, A. J.; Renstrøm, Britta; Nellis, S. H.

doi:10.1161/01.res.71.3.689

Cited by 26 publications

(19 citation statements)

References 51 publications

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“…In postischaemic rat hearts, glucose uptake continued at a similar rate to pre-ischaemic conditions, while 18 FDG-6-P accumulation decreased [6]. In another study in pig myocardium, increased glucose uptake post ischaemia was not reflected in the observed DG-6-P accumulation rate [7].…”

Section: Introductionmentioning

confidence: 79%

“…Glucose tracer uptake under the same conditions was confined to either 18 FDG [19,20] or 2-DG [22], or was not examined [10,18,21,23]. Similarly, in studies investigating dual or triple glucose tracer uptake, protocols have varied in species, buffer composition and ischaemic time, and none have investigated concurrent changes in transporter distribution [6,24,25]. Therefore in this study, we examined the accumulation of both 18 FDG-6-P and 14 C-DG-6-P in the same hearts, and GLUT 1 and GLUT 4 distribution in a parallel set of hearts to establish the role of the glucose transporters in mediating the relative accumulation of these tracers.…”

Section: Discussionmentioning

confidence: 99%

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Dissociation of glucose tracer uptake and glucose transporter distribution in the regionally ischaemic isolated rat heart: application of a new autoradiographic technique

et al. 2002

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Fluorine-18 fluoro-2-deoxyglucose ((18)FDG) and carbon-14 2-deoxyglucose ((14)C-2-DG) are both widely used tracers of myocardial glucose uptake and phosphorylation. We have recently shown, using positron emission tomography (PET) and nuclear magnetic resonance, that ischaemia-reperfusion (I-R) causes differential changes in their uptake. We describe here the novel application of an autoradiographic technique allowing the investigation of this phenomenon at high resolution, using tracer concentrations of both analogues in the dual-perfused isolated rat heart. We also investigate the importance of glucose transporter (GLUT 1 and GLUT 4) distribution in governing the observed phosphorylated analogue accumulation. Hearts ( n=5) were perfused with Krebs buffer for 40 min, made regionally zero-flow ischaemic for 40 min and reperfused for 60 min with Krebs containing tracer (18)FDG (200 MBq) and tracer (14)C-2-DG (0.37 MBq). Hearts were then frozen and five sections (10 micro m) were cut per heart, fixed and exposed on phosphor storage plates for 18 h (for (18)FDG) and then for a further 9 days (for (14)C-2-DG). Quantitative digital images of tracer accumulation were obtained using a phosphor plate reader. The protocol was repeated in a second group of hearts and GLUT 1 and GLUT 4 distribution analysed. Post-ischaemic accumulation of (18)FDG-6-P was inhibited by 38.2%+/-1.7% and (14)C-DG-6-P by 19.0%+/-2.2%, compared with control ( P<0.05). After placing seven "lines of interrogation" across each heart section and analysing the phosphorylated tracer accumulation along them, a transmural gradient of both tracers was observed; this was highest at the endocardium and lowest at the epicardium. GLUT 4 translocated to the sarcolemma in the ischaemic/reperfused region (from 24%+/-3% to 59%+/-5%), while there was no cellular redistribution of GLUT 1. We conclude that since decreased phosphorylated tracer accumulation occurs after ischaemia-reperfusion, despite greater externalisation of GLUT 4, hexokinase or the affinities of the GLUT transporters are changed under these conditions.

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Section: Introductionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Dissociation of glucose tracer uptake and glucose transporter distribution in the regionally ischaemic isolated rat heart: application of a new autoradiographic technique

et al. 2002

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“…Liedtke et al showed that myocardial accumulation of 14C-deoxyglucose does not reflect glycolysis during reperfusion (14). They suggested that the myocardial kinetics of deoxyglucose are not specific for myocardial glucose metabolism.…”

Section: Discussionmentioning

confidence: 99%

Efficacy and Limitation of F-18-fluorodeoxyglucose Positron Emission Tomography during Fasting to Assess Myocardial Viability in the Acute Phase of Myocardial Infarction.

et al. 1998

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Objective: The present study was designed to determine the ability of positron emission tomography (PET) to assess myocardial viability and ischemia in acute myocardial infarction (MI) after reperfusion therapy (thrombolysis and/or coronary angioplasty). Methods: PETwith fluorine-18-labeled fluorodeoxyglucose (FDG) under fasting conditions and thallium-201 singlephoton emission computed tomography (TL) were analyzed in 21 patients one week following MI. Myocardial viability was also assessed by regional wall motion using serial analysis of 2-D echocardiography or left ventriculography. Results: Marked uptake of FDGtogether with a residual perfusion defect were observed in the infarct region in all patients one week post ML However, in 9 of the 21 patients, the infarct-related coronary artery had no significant stenosis after reperfusion therapy and remained patent in one month post MI suggesting no myocardial ischemia. In contrast, in 4 of the 21 patients the regional wall motion was akinetic and there was a complete defect observed with TL imaging at one month post MI, indicating no viability in the infarct region. Conclusions: PET using fasting FDGat one week post MI had a limitation to predict myocardial viability or ischemia. (Internal Medicine 37: 653-661, 1998)

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“…In experimental models, myocardium subjected to repetitive stunning shows prolonged but reversible down-regulation of glucose uptake and oxidative metabolism despite restoration of the myocardial flow [12,13,14]. In contrast, however, regional glucose uptake in post-ischaemic myocardium has also been reported to be increased [6,7,8,9] or unchanged [10,11]. In the heart, glucose transport is mediated via insulin-sensitive glucose transporter proteins similar to those in skeletal muscle [53].…”

Section: Myocardial Glucose Uptakementioning

confidence: 99%

“…In post-ischaemic myocardial stunning, reported changes in glucose metabolism are not uniform and range from increased regional glucose uptake [6,7,8,9], through unaltered glucose uptake [10,11] to reduced glucose uptake [12,13,14]. Conflicting results have also been published on fatty acid metabolism in post-ischaemic myocardium [15,16,17,18].…”

Section: Introductionmentioning

confidence: 99%

125I-BMIPP and 18F-FDG uptake in a transgenic mouse model of stunned myocardium

Verberne

Sloof

Beets

et al. 2003

Eur J Nucl Med Mol Imaging

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Reported metabolic patterns in myocardial stunning are not uniform. We investigated relative myocardial perfusion, glucose and fatty acid uptake using a technetium-99 hexakis-2-methoxyisobutyl-isonitrile (MIBI), fluorine-18 2-fluoro-2-deoxyglucose (FDG) and iodine-125 15-(p-iodo-phenyl)-3(R,S)-methylpentadecanoic acid (BMIPP) mixture, in a recently developed transgenic (TR) mouse model which mimics stunned myocardium. Twenty-seven mice - 14 TR and 13 age-matched wild type controls (C) - were divided into four groups: TR-fed, TR-fasted, C-fed and C-fasted. Animals were sacrificed 2 h after injection, tissue samples counted and percent-injected dose/gram tissue (% id/g) calculated for each radioisotope. Tissues were also Folch extracted and 125I incorporation into the various lipid pools (TG, triglycerides; DG, diglycerides; FFA, free fatty acids; PL, phospholipids) was determined by thin-layer chromatography (TLC). The pooled data for each of the four groups (TR-fed vs C-fed and TR-fed vs C-fasted) showed no differences in myocardial blood flow (% MIBI id/g), glucose uptake (% FDG id/g) or fatty acid uptake (% BMIPP id/g). Only minor differences were observed in the incorporation of 125I-BMIPP into the myocardial TG, DG, FFA and PL lipid pools. However, significantly decreased myocardial FDG uptake was observed in a subset of fasted mice - four out of ten TR-fasted mice (3.4% vs 20.5% id/g) and three out of nine C-fasted mice (5.5% vs 30.6% id/g). The transgenic mouse model of stunned myocardium shows normal myocardial perfusion and overall intact myocardial glucose and myocardial fatty acid uptake as determined with clinically applicable radiolabelled analogues. These data are in line with the hypothesis that the contractile inefficiency in stunned myocardium is not linked to metabolic alterations but is associated with an insufficient chemical to mechanical energy coupling.

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Correlation between [5-3H]glucose and [U-14C]deoxyglucose as markers of glycolysis in reperfused myocardium.

Cited by 26 publications

References 51 publications

Dissociation of glucose tracer uptake and glucose transporter distribution in the regionally ischaemic isolated rat heart: application of a new autoradiographic technique

Dissociation of glucose tracer uptake and glucose transporter distribution in the regionally ischaemic isolated rat heart: application of a new autoradiographic technique

Efficacy and Limitation of F-18-fluorodeoxyglucose Positron Emission Tomography during Fasting to Assess Myocardial Viability in the Acute Phase of Myocardial Infarction.

125I-BMIPP and 18F-FDG uptake in a transgenic mouse model of stunned myocardium

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