Nilsson S
Department of Diagnostic Radiology, Uppsala University Hospital, Sweden.
Acta Radiol Suppl. 1995;397:1-44.
To assess the usefulness of Dy-DTPA-BMA-induced signal reduction, as an indicator of myocardial viability, myocardial infarction was induced in 17 domestic pigs by ligating a diagonal branch of the left anterior descending coronary artery (LAD). In 6 pigs, Dy-DTPA-BMA (1 mmol/kg b.w.) was administered 4 hours after induction of ischaemia. In 5 additional pigs, Gd-DTPA-BMA (0.3 mmol/kg b.w.) and Dy-DTPA-BMA (1 mmol/kg b.w.) were simultaneously injected after 4 hours of ischaemia to ascertain whether Dy-DTPA-BMA counteracted the signal enhancement effect of Gd-DTPA-BMA. A further 6 pigs with infarctions, not administered contrast medium, served as controls. All pigs were sacrificed after 6 hours of ischaemia, and the extirpated hearts were investigated with MR (ex vivo). The concentrations of Dy and Gd were determined in tissue samples from infarcted and non-ischaemic myocardium. The extracellular concentrations of both contrast media were monitored over time during 2 hours in the double-contrast group (in vivo), using a microdialysis technique and analysed by inductively coupled plasma atomic emission spectrometry (ICP-AES). The infarctions demonstrated a high SI in the proton density- and T2-weighted sequences, in both the Dy-DTPA-BMA and control groups, although the former group demonstrated a 3-fold greater concentration of Dy in infarcted compared with non-ischaemic myocardium. Dy-DTPA-BMA did not counteract the Gd-DTPA-BMA-induced enhancement of the infarcted tissue despite a 3-fold higher concentration. This lack of detectable susceptibility effects of Dy may be caused by a loss of cell membrane integrity in the infarcts, resulting in a homogeneous intra- and extracellular distribution of the contrast agent. This hypothesis of an expanded volume of distribution in infarcted tissue was further supported by the microdialysis data, demonstrating a similar extracellular concentration of contrast agents in infarcted and non-ischaemic myocardium, despite a proven 3-fold greater concentration in infarcted tissue samples. To investigate whether Gd-DTPA-BMA-enhanced MR imaging (ex vivo) permits differentiation between reperfused and non-reperfused myocardial infarction, and whether Dy-DTPA-BMA-enhanced MR imaging enables a differentiation between reversible and irreversible myocardial injury following reperfusion, myocardial infarction was induced in 24 domestic pigs (divided into 4 groups) by placing a patched ligature around a diagonal branch of the LAD. Four additional hearts were reperfused after 2 min of brief occlusion, not long enough to cause irreversible injury.(ABSTRACT TRUNCATED AT 250 WORDS)
为评估镝-二乙三胺五乙酸-苄基甲酯（Dy-DTPA-BMA）诱导的信号降低作为心肌存活指标的有效性，通过结扎左前降支冠状动脉（LAD）的对角支，在17头家猪中诱导心肌梗死。6头猪在缺血诱导后4小时给予Dy-DTPA-BMA（1 mmol/kg体重）。另外5头猪在缺血4小时后同时注射钆-二乙三胺五乙酸-苄基甲酯（Gd-DTPA-BMA，0.3 mmol/kg体重）和Dy-DTPA-BMA（1 mmol/kg体重），以确定Dy-DTPA-BMA是否抵消Gd-DTPA-BMA的信号增强作用。另外6头梗死但未给予造影剂的猪作为对照。所有猪在缺血6小时后处死，取出的心脏用磁共振成像（离体）进行研究。测定梗死心肌和非缺血心肌组织样本中的镝和钆浓度。在双造影组（体内），使用微透析技术在2小时内随时间监测两种造影剂的细胞外浓度，并通过电感耦合等离子体原子发射光谱法（ICP-AES）进行分析。在Dy-DTPA-BMA组和对照组中，梗死灶在质子密度加权和T2加权序列中均显示高信号强度，尽管前一组梗死心肌中的镝浓度比非缺血心肌高3倍。尽管Dy-DTPA-BMA浓度高3倍，但它并未抵消Gd-DTPA-BMA诱导的梗死组织信号增强。Dy缺乏可检测到的磁化率效应可能是由于梗死灶细胞膜完整性丧失，导致造影剂在细胞内和细胞外均匀分布。微透析数据进一步支持了梗死组织中分布容积扩大的这一假设，该数据表明梗死心肌和非缺血心肌中的造影剂细胞外浓度相似，尽管在梗死组织样本中已证实前者浓度高3倍。为研究Gd-DTPA-BMA增强磁共振成像（离体）是否能区分再灌注和未再灌注的心肌梗死，以及Dy-DTPA-BMA增强磁共振成像是否能区分再灌注后可逆和不可逆的心肌损伤，通过在LAD的对角支周围放置带补丁结扎线，在24头家猪（分为4组）中诱导心肌梗死。另外4颗心脏在短暂闭塞2分钟后进行再灌注，时间不足以造成不可逆损伤。（摘要截取自250字）
