Myocardial manganese elevation and proton relaxivity enhancement with manganese dipyridoxyl diphosphate.: Ex vivo assessments in normally perfused and ischemic guinea pig hearts
Myocardial manganese elevation and proton relaxivity enhancement with manganese dipyridoxyl diphosphate.: Ex vivo assessments in normally perfused and ischemic guinea pig hearts
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DOI：
10.1002/(sici)1099-1492(199910)12:6
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发表时间：
1999-10-01
影响因子：
2.9
通讯作者：
Jynge, P
中科院分区：
文献类型：
--
作者：
Brurok, H;Skoglund, T;Jynge, P
二磷酸二吡啶锰(MnDPDP)是肝脏MRI造影剂的活性成分。通过代谢，MnDPDP释放Mn2+，Mn2+被肝细胞吸收和保留。这项研究检测了MnDPDP是否增加了正常心肌中的锰含量和增强了质子松弛能力，但在冠脉血管减少和代谢受损的缺血心肌中却没有。以正常流量或低流量灌流豚鼠离体心，造成全心次全缺血。测定心肌细胞三磷酸腺苷(ATP)和锰含量，T_1和T_2。在正常血流状态下，加入MnDPDP(3000 mU/L)后，组织中的锰含量由对照的4.1 mU/100g干重增加到70.4 mU/100g干重，而低流量灌流时，组织中的锰含量仅为16.6 mU/100g干重，而长时间的缺血(35分钟和90分钟)使组织中的锰含量降至对照水平。正常和低流量灌流时T-1缩短与心肌Mn升高密切相关。使用像MnDPDP这样的释放Mn2+的造影剂可以揭示T-1与冠脉流量、细胞锰摄取和滞留、离子通道功能和代谢的不同变化模式，从而有望成为评价冠心病患者心肌功能和生存能力的一种有前景的原则。版权所有(C)1999 John Wiley&Sons，Ltd.
Manganese (Mn) dipyridoxyl diphosphate (MnDPDP) is the active component of a contrast medium for liver MRI. By being metabolized, MnDPDP releases Mn2+, which is taken up and retained in hepatocytes. The study examined whether MnDPDP elevates Mn content and enhances proton relaxivity in normal myocardium, but not in ischemic myocardium with reduced coronary how and impaired metabolism. Isolated guinea pig hearts were perfused at normal flow or low flow, inducing global subtotal ischemia. Ventricular ATP and Mn contents, T-1 and T-2 were measured. At normal flow tissue Mn content increased from the control level of 4.1 to 70.4 mu mol/100g dry wt with MnDPDP (3000 mu M), while low-flow perfusion with MnDPDP (3000 mu M) resulted in a Mn content of 16.6 mu mol/100 g dry wt. Prolonged ischemia (35 and 90 min) reduced tissue Mn down to the control level. T-1 shortening closely paralleled myocardial Mn elevations during both normal and low-flow perfusion. The use of a Mn2+-releasing contrast agent like MnDPDP may be a promising principle in MRI assessments of myocardial function and viability in coronary heart disease by revealing a differential pattern of changes in T-1 relative to coronary flow, cell Mn uptake and retention, ion channel function and metabolism. Copyright (C) 1999 John Wiley & Sons, Ltd.