Measurement of regional glucose metabolic rates in reperfused myocardium.
Measurement of regional glucose metabolic rates in reperfused myocardium.
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再灌注心肌中局部葡萄糖代谢率的测量。
DOI：
10.1152/ajpheart.1991.261.6.h2058
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Schelbert,HR
中科院分区：
文献类型：
--
作者：
Buxton,DB;Schelbert,HR
用[18F]氟脱氧葡萄糖（FDG）和正电子发射断层扫描测量闭胸麻醉犬冠状动脉内球囊闭塞3小时后正常组织和缺血后组织的局部心肌葡萄糖利用率。假设再灌注组织中的集总常数不变，使用Sokoloff模型估计葡萄糖代谢率。根据闭塞血流图像和死后组织学将心肌区分为正常、可逆性损伤或含有梗死。微球测量的闭塞血流在可逆性损伤区减少38%，在梗死区减少74%，在灌注后1小时分别恢复到91%和66%。灌注后1个月，可逆性损伤区血流正常，但梗死区血流下降60%。基线时葡萄糖利用率均匀，平均为0.8 mmol .g-1 min-1。冠状动脉左前降支闭塞后再灌注3小时后，正常心肌的区域葡萄糖代谢率相对于基线增加了60%，但缺血后区域没有增加，导致正常心肌的FDG摄取相对于缺血后增强。灌注后24小时，正常远端组织的葡萄糖代谢率下降至基线水平的46%，可能反映了血浆游离脂肪酸水平的增加，但在可逆性损伤的心肌中没有明显改变，导致相对于正常心肌，可逆性损伤的FDG摄取增加。随后，正常区和缺血后区葡萄糖代谢无显著差异。当正常心肌糖代谢率较低时，缺血后组织糖代谢率的相对增强时间延长。各条件下心肌葡萄糖利用率与FDG磷酸化速率常数hg相关（r = 0.88）。
Regional myocardial glucose utilization was measured with [18F]fluorodeoxyglucose (FDG) and positron emission tomography in normal and postischemic tissue after 3 h of intracoronary balloon occlusion in closed-chest chronically instrumented anesthetized dogs. Estimates of glucose metabolic rates were made using the Sokoloff model, assuming the lumped constant to be unchanged in reperfused tissue. Myocardial sectors were classified as normal, reversibly injured, or infarct containing based on occlusion blood flow images and postmortem histology. Occlusion flow, measured by microspheres, was reduced by 38% in reversibly injured and 74% in infarct-containing sectors, recovering to 91 and 66%, respectively, 1 h postreperfusion. One month postreperfusion, flow was normal in reversibly injured sectors but remained depressed at 60% in infarct-containing sectors. Glucose utilization at baseline was homogeneous, averaging 0.8 mumol.g-1.min-1. After 3 h of reperfusion following occlusion of the left anterior descending coronary artery, regional glucose metabolic rate was increased 60% relative to baseline in normal myocardium but not in postischemic sectors, leading to an enhancement of FDG uptake in normal relative to postischemic myocardium. At 24 h postreperfusion, the glucose metabolic rate decreased in normal remote tissue to 46% of baseline levels, probably reflecting increased plasma free fatty acid levels, but was not significantly altered in reversibly injured myocardium, leading to enhanced FDG uptake in reversibly injured relative to normal myocardium. Subsequently, glucose metabolism in normal and postischemic sectors was not significantly different. Prolonged relative enhancement of glucose metabolic rate in postischemic tissue was found when the glucose metabolic rate in normal myocardium was low. Myocardial glucose utilization correlated with hg, the rate constant for FDG phosphorylation under all conditions (r = 0.88).