Colet J M, Cetiner E, Hedlund B E, Muller R N
Department of Organic Chemistry, University of Mons-Hainaut, Belgium.
Magn Reson Med. 1996 Nov;36(5):753-7. doi: 10.1002/mrm.1910360514.
Reperfusion of an ischemic organ can lead to microcirculatory impairment caused, in part, by the generation of reactive free radicals. The iron-catalyzed formation of these deleterious substances can be counteracted by strong metal chelators like deferoxamine. In this study, the protective effect of deferoxamine conjugate was evaluated by assessment of the hepatic microcirculation in the post-ischemic phase. Assessment of the microvasculature was performed by MRI on the isolated perfused rat liver. The restriction of sinusoids subsequent to reperfusion injury was demonstrated by the use of a particulate superparamagnetic contrast agent trapped in the microvasculature. The protective effect of conjugated deferoxamine was evaluated by both MRI and release of alanine aminotransferase. Contrast-enhanced MRI demonstrated a marked impairment of the microcirculation subsequent to the unprotected reperfusion of the ischemic tissue. This injury was attenuated by deferoxamine conjugated to hydroxyethyl-starch (HES-DFO).
缺血器官的再灌注可导致微循环障碍,部分原因是活性自由基的产生。铁催化形成这些有害物质的过程可被强力金属螯合剂(如去铁胺)抵消。在本研究中,通过评估缺血后阶段的肝脏微循环来评价去铁胺缀合物的保护作用。通过磁共振成像(MRI)对离体灌注大鼠肝脏的微血管系统进行评估。使用捕获在微血管系统中的颗粒超顺磁性造影剂来证明再灌注损伤后肝血窦的狭窄。通过MRI和丙氨酸转氨酶的释放来评估缀合去铁胺的保护作用。对比增强MRI显示,缺血组织未受保护的再灌注后微循环明显受损。与羟乙基淀粉缀合的去铁胺(HES-DFO)减轻了这种损伤。