University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Eur J Nucl Med Mol Imaging. 2010 Oct;37(10):1909-17. doi: 10.1007/s00259-010-1495-0. Epub 2010 Jul 24.
(99m)Tc-glucarate is an infarct-avid imaging agent. However, patients may have mixtures of normal, irreversibly injured, stunned, and hibernating myocardium. The purposes were to determine (99m)Tc-glucarate uptake and clearance kinetics in these four conditions, and its ability to determine the extent of injury.
Twenty-two perfused rat hearts were studied: controls (n = 5), stunned (n = 5; 20-min no-flow followed by 5-min reflow), hibernating (n = 6; 120-min low flow at 4 ml/min), and ischemic-reperfused (n = 6; 120-min no-flow followed by reflow). (99m)Tc-glucarate was then infused. Tracer activity was monitored using a NaI scintillation detector and a multichannel analyzer. Creatine kinase, electron microscopy, and triphenyltetrazolium chloride determined viability.
(99m)Tc-glucarate 10-min myocardial uptake was significantly greater in ischemic-reperfused (2.50 +/- 0.09) (cpm, SEM) than in control (1.74 +/- 0.07), stunned (1.68 +/- 0.11), and hibernating (1.59 +/- 0.11) (p < 0.05). Tracer retention curves for ischemic-reperfused were elevated at all time points as compared with the other groups. (99m)Tc-glucarate 60-min myocardial uptake was significantly greater in ischemic-reperfused (7.60 +/- 0.63) than in control (1.98 +/- 0.15), stunned (1.79 +/- 0.08), and hibernating (2.33 +/- 0.15) (p < 0.05). The 60-min well-counted tracer activity ratio of ischemic-reperfused to control was 9:1 and corroborated the NaI detector results. Creatine kinase, triphenyltetrazolium chloride, and electron microscopy all demonstrated significantly greater injury in ischemic-reperfused compared to the other groups. An excellent correlation was observed between viability markers and tracer activity (r = 0.99 triphenyltetrazolium chloride; r = 0.90 creatine kinase).
(99m)Tc-glucarate activity continually and progressively increased in irreversibly injured myocardium. (99m)Tc-glucarate uptake was strongly correlated with myocardial necrosis as determined by three independent assessments of viability. There were minimal and similar (99m)Tc-glucarate uptakes in control, stunned, and hibernating myocardium.
（99m）Tc-葡庚酸盐是一种梗塞性成像剂。然而，患者可能存在正常、不可逆损伤、顿抑和冬眠心肌的混合物。目的是确定这四种情况下（99m）Tc-葡庚酸盐摄取和清除动力学及其确定损伤程度的能力。
研究了 22 个灌注大鼠心脏：对照组（n=5）、顿抑组（n=5；20 分钟无血流后 5 分钟再灌注）、冬眠组（n=6；4 毫升/分钟低流量 120 分钟）和缺血再灌注组（n=6；120 分钟无血流后再灌注）。然后输注（99m）Tc-葡庚酸盐。使用碘化钠闪烁探测器和多道分析器监测示踪剂活性。肌酸激酶、电子显微镜和三苯基四唑氯化物测定活力。
缺血再灌注组（2.50 +/- 0.09）（cpm，SEM）在 10 分钟时心肌摄取（99m）Tc-葡庚酸盐明显高于对照组（1.74 +/- 0.07）、顿抑组（1.68 +/- 0.11）和冬眠组（1.59 +/- 0.11）（p < 0.05）。与其他组相比，缺血再灌注组的示踪剂保留曲线在所有时间点均升高。缺血再灌注组（7.60 +/- 0.63）在 60 分钟时心肌摄取（99m）Tc-葡庚酸盐明显高于对照组（1.98 +/- 0.15）、顿抑组（1.79 +/- 0.08）和冬眠组（2.33 +/- 0.15）（p < 0.05）。缺血再灌注组与对照组的 60 分钟经计数示踪剂活性比值为 9:1，与碘化钠探测器结果相符。肌酸激酶、三苯基四唑氯化物和电子显微镜均显示缺血再灌注组的损伤明显大于其他组。活力标志物与示踪剂活性之间存在极好的相关性（r = 0.99 三苯基四唑氯化物；r = 0.90 肌酸激酶）。
不可逆损伤心肌中（99m）Tc-葡庚酸盐活性持续且逐渐增加。（99m）Tc-葡庚酸盐摄取与通过三种独立的活力评估确定的心肌坏死密切相关。对照组、顿抑组和冬眠组的（99m）Tc-葡庚酸盐摄取量均较小且相似。
