Correlation between [5-3H]glucose and [U-14C]deoxyglucose as markers of glycolysis in reperfused myocardium.
Correlation between [5-3H]glucose and [U-14C]deoxyglucose as markers of glycolysis in reperfused myocardium.
复制标题
[5-3H]葡萄糖和[U-14C]脱氧葡萄糖作为再灌注心肌糖酵解标记物之间的相关性。
DOI：
10.1161/01.res.71.3.689
复制
发表时间：
1992
影响因子：
20.1
通讯作者：
Nellis,SH
中科院分区：
文献类型：
--
作者：
Liedtke,AJ;Renstrom,B;Nellis,SH
在体外灌流的、完整的工作猪心脏上进行了研究，以确定在心肌中，微量标记的脱氧葡萄糖是否可以作为暴露于轻到中度局部缺血后再灌注时糖酵解流量的准确标志物。在主要研究中，比较了两组心脏，根据全血灌流液中的葡萄糖水平进行区分(正常血糖心脏[组I]，血糖为7.4+/-0.2 Mumol/ml，n=7；高血糖心脏[组II]，血糖为12.9+/-0.5 Mumol/ml，n=8)。两组均将冠状动脉前降支血流减少60%，持续30分钟，然后再灌流40分钟。两组在复流过程中都注意到了适度和可比的局部机械震颤。根据有氧灌流期间稳态输注[5-3H]葡萄糖释放的3H2O估计的葡萄糖利用率不高，但在再灌流期间，两组中的每一组都显著高于有氧值，其中II组心脏的利用率是I组心脏的两倍(p<0.041或p<0.090)。在两组患者中，乳酸净萃取物在复流方面具有可比性，这表明在这一特定情况下，高血糖II组心脏优先增强葡萄糖氧化。再灌流心肌中[U-14C]2-脱氧葡萄糖组织放射性蓄积的变化不能跟踪这些趋势。~(14)C标记的放射性在动物中的可变性是显著的，并且基本上掩盖了任何辨别糖酵解趋势的能力，如有氧和再灌流间隔之间的氚葡萄糖所描述的那样。经线性回归分析，~(14)C标记脱氧葡萄糖的斜率与~3H标记葡萄糖的斜率不一致或不敏感。组织糖原水平在再流早期恢复缓慢，在再灌流结束时仍明显低于有氧水平。提示冠脉再灌流和高血糖对心肌糖酵解流量的测定有影响。标记的脱氧葡萄糖仅被认为是外源葡萄糖利用的标志，在相对较低的葡萄糖流量条件下，似乎是描述这些事件的不敏感试剂。
Studies were conducted in extracorporeally perfused, intact, working pig hearts to determine whether, in heart muscle, trace-labeled deoxyglucose serves as an accurate marker of glycolytic flux in reperfusion after exposures to mild to moderate regional ischemia. In the main study, two groups of hearts were compared, as distinguished by levels of glucose in the whole-blood perfusate (euglycemic hearts [group I], blood glucose of 7.4 +/- 0.2 mumol/ml, n = 7; hyperglycemic hearts [group II], blood glucose of 12.9 +/- 0.5 mumol/ml, n = 8). Both groups were subjected to a 60% reduction in anterior descending coronary flow for 30 minutes followed by reperfusion for 40 minutes. Modest and comparable regional mechanical stunning during reflow was noted in both groups. Glucose utilization, as estimated from the release of 3H2O from the steady-state infusion of [5-3H]glucose during aerobic perfusion, was modest but during reperfusion was noted to increase significantly above aerobic values in each of the two groups, with a doubling of rates in group II hearts compared with group I hearts (p less than 0.041 or p less than 0.090). Net lactate extraction was comparable in reflow in both groups, suggesting in this specific instance a preferential enhancement of glucose oxidation in hyperglycemic group II hearts. Shifts in accumulation of tissue radioactivity of [U-14C]2-deoxyglucose in reperfused myocardium were not able to track these trends. The variability of 14C-labeled radioactivity among animals was marked and essentially masked any ability to discern trends in glycolysis as described by tritiated glucose between the aerobic and reperfusion intervals. When the data were arrayed by linear regression analysis, the slopes derived from 14C-labeled deoxyglucose were either discordant or insensitive to those described by 3H-labeled glucose. Tissue glycogen levels were slow to recover in early reflow and at end reperfusion were still significantly depressed from aerobic levels. The present data indicate that coronary reperfusion and hyperglycemia have influence in determining glycolytic flux in myocardium. Labeled deoxyglucose, considered solely as a marker of exogenous glucose utilization, appears to be an insensitive agent in describing these events at conditions of relatively low glucose flux.