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锝-99m甲氧基异丁基异腈的动力学是否受细胞代谢和活力的影响?

Are the kinetics of technetium-99m methoxyisobutyl isonitrile affected by cell metabolism and viability?

作者信息

Beanlands R S, Dawood F, Wen W H, McLaughlin P R, Butany J, D'Amati G, Liu P P

机构信息

Nuclear Cardiology Laboratory, Toronto Hospital, Canada.

出版信息

Circulation. 1990 Nov;82(5):1802-14. doi: 10.1161/01.cir.82.5.1802.

Abstract

To investigate the role of cell viability and metabolism on the myocardial kinetics of a new tracer, technetium-99m-methoxyisobutyl isonitrile (Tc-99m-MIBI), 250 microCi/l Tc-99m-MIBI was infused in isolated rat hearts under constant flow conditions. The hearts were studied after inducing irreversible damage by cytochrome c oxidase inhibitor sodium cyanide (n = 8) or sarcolemmal membrane detergent Triton X-100 (n = 8). The control hearts (n = 6) received no toxins. Mean Tc-99m-MIBI peak accumulation activity was significantly reduced after cyanide (51.1 +/- 44.2% of control, p less than 0.01) and Triton (13.8 +/- 2.7% of control, p less than 0.001) administration. Kinetic studies also showed marked reduction in accumulation rates and marked increase in clearance rates for cyanide (p less than 0.01) and Triton (p less than 0.01) groups compared with controls. Potential changes in regional flow distribution were assessed using microspheres. When peak accumulation activity was corrected for these changes, there remained significant differences between the groups. In the cyanide and Triton groups, irreversible cell injury was confirmed by creatine kinase and lactate dehydrogenase release, triphenyl tetrazolium chloride staining, and electron microscopy. All the cells were viable in the control group. We conclude that the accumulation and clearance kinetics of Tc-99m-MIBI are significantly affected by cell viability. Tc-99m-MIBI kinetics appear to be dependent on sarcolemmal integrity and to a lesser extent on aerobic metabolism.

摘要

为研究细胞活力和代谢在新型示踪剂锝-99m-甲氧基异丁基异腈(Tc-99m-MIBI)心肌动力学中的作用,在恒流条件下向离体大鼠心脏注入250微居里/升的Tc-99m-MIBI。在用细胞色素c氧化酶抑制剂氰化钠(n = 8)或肌膜去污剂 Triton X-100(n = 8)诱导不可逆损伤后对心脏进行研究。对照心脏(n = 6)未接受毒素处理。给予氰化物后,Tc-99m-MIBI的平均峰值蓄积活性显著降低(为对照的51.1 +/- 44.2%,p < 0.01),给予 Triton后也显著降低(为对照的13.8 +/- 2.7%,p < 0.001)。动力学研究还显示,与对照组相比,氰化物组(p < 0.01)和 Triton组(p < 0.01)的蓄积率显著降低,清除率显著升高。使用微球评估区域血流分布的潜在变化。当对这些变化校正峰值蓄积活性后,各组之间仍存在显著差异。在氰化物组和 Triton组中,通过肌酸激酶和乳酸脱氢酶释放、氯化三苯基四氮唑染色及电子显微镜证实存在不可逆细胞损伤。对照组所有细胞均存活。我们得出结论,Tc-99m-MIBI的蓄积和清除动力学受细胞活力显著影响。Tc-99m-MIBI动力学似乎依赖于肌膜完整性,在较小程度上依赖于有氧代谢。

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