Spectroscopic and metabolic effects of MnCl2 and MnDPDP on the isolated and perfused rat heart.
Spectroscopic and metabolic effects of MnCl2 and MnDPDP on the isolated and perfused rat heart.
复制标题
MnCl2 和 MnDPDP 对离体和灌注大鼠心脏的光谱和代谢影响。
DOI：
--
复制
发表时间：
1997
影响因子：
6.7
通讯作者：
Robert N Muller
中科院分区：
文献类型：
--
作者：
L. Elst;J. Colet;Robert N Muller
理由和目标
一些研究表明，肝胆磁共振成像造影剂二吡啶二磷酸锰 (MnDPDP) 会部分释放其金属离子，并表现出由游离锰离子 (Mn++) 引起的心血管效应。在目前的研究中，通过器官的机械功能和 P-31 核磁共振的相对展宽来监测离体大鼠心脏对 Mn 的细胞内化。
方法
大鼠心脏灌注氯化锰（MnCl2；15 和 25 µM）或 MnDPDP（25 µM）。监测磷酸肌酸和三磷酸腺苷峰的线宽、高度和表面的变化。通过心率、左心室压力和冠状动脉血流同时监测心脏功能。
结果
由于原子核和离子之间强烈的标量顺磁相互作用，Mn++ 的流入导致三磷酸腺苷和磷酸肌酸的 P-31 共振显着展宽。与相同浓度的 MnDPDP 相比，MnCl2 诱导更明显且剂量依赖性的谱线展宽以及冠状血管舒张。钙通道阻滞剂（硝苯地平和维拉帕米）和 EDTA 抑制 MnCl2 流入。同样，维拉帕米、EDTA 和 DPDP 可以减少 MnDPDP 引起的改变。
结论
MnDPDP 的影响较小，但与 MnCl2 引起的影响相同。它们被钙通道阻滞剂（维拉帕米和硝苯地平）和过量的强螯合剂（如 DPDP 或 EDTA）抑制，证实它们源自造影剂部分释放的 Mn++。
RATIONALE AND OBJECTIVES
Several works have shown that the hepatobiliary magnetic resonance imaging contrast agent manganese dipyridoxyl diphosphate (MnDPDP) partly releases its metallic ion and exhibits cardiovascular effects that are supposed to arise from the free manganese ions (Mn++). In the current study, the cellular internalization of Mn by the isolated rat heart is monitored through the mechanical function of the organ and the relative broadening of the P-31 nuclear magnetic resonances.
METHODS
Rat hearts were perfused with manganese chloride (MnCl2; 15 and 25 microM) or MnDPDP (25 microM). Variations of the linewidths, heights, and surfaces of phosphocreatine and adenosine triphosphate peaks were monitored. Cardiac function was monitored simultaneously through heart rate, left ventricular pressure, and coronary flow.
RESULTS
Influx of Mn++ induces a significant broadening of the P-31 resonances of adenosine triphosphate and phosphocreatine because of a strong scalar paramagnetic interaction between the nuclei and the ion. Compared with MnDPDP administered at the same concentration, MnCl2 induced a more pronounced and dose-dependent line broadening as well as a coronary vasodilation. Calcium channel blockers (nifedipine and verapamil) and EDTA inhibit MnCl2 influx. Similarly, verapamil, EDTA, and DPDP reduce the alterations provoked by MnDPDP.
CONCLUSIONS
The effects of MnDPDP are smaller but of the same type than those induced by MnCl2. Their inhibition by calcium channel blockers (verapamil and nifedipine) and by an excess of strong chelators such as DPDP or EDTA confirms that they originate from a partial release of Mn++ by the contrast agent.
使用 54Mn 测量离体成年大鼠心脏细胞的 Ca 通道活性。
影响因子：
3.9
作者：
Haworth,RA;Goknur,AB;Berkoff,HA
通讯作者：
Berkoff,HA