Carry M M, Mrak R E, Murphy M L, Peng C F, Straub K D, Fody E P
Division of Medicine, John L. McClellan Memorial Veterans Hospital, Little Rock, Arkansas.
Am J Cardiovasc Pathol. 1989;2(4):335-44.
Coronary reperfusion following myocardial ischemia may result in further damage to injured myocytes, as judged by their ultrastructural appearance. Ruthenium red is an inorganic dye with calcium flux-inhibiting properties which protects ischemic myocardium against reperfusion damage, as judged by biochemical indices of mitochondrial function. In this study, we produced myocardial ischemia in pigs by means of reversible coronary artery occlusion. The pigs were infused with either ruthenium red or nitroprusside (an after-load reducing agent with no known calcium flux-inhibiting properties) prior to and during coronary reperfusion. During reperfusion, both ruthenium red and nitroprusside produced similar lowering of mean arterial pressure, while mean arterial pressure rose in pigs not receiving these drugs. Myocardial samples from the ischemic reperfused region were examined by electron microscopy. Ischemic damage to nuclei, mitochondria, and myofibrils and glycogen depletion were graded independently on a three-point scale by two investigators. For each of the organelles studied, ischemic damage was significantly less for treated animals than for controls. This protective effect was similar for both ruthenium red-treated animals and nitroprusside-treated animals. These results suggest that the protective effects of ruthenium red treatment are attributable to its afterload reducing properties rather than to inhibition of transmembrane calcium flux in cardiac fibers.
根据超微结构表现判断，心肌缺血后的冠状动脉再灌注可能会导致受损心肌细胞进一步损伤。钌红是一种具有钙通量抑制特性的无机染料，根据线粒体功能的生化指标判断，它可保护缺血心肌免受再灌注损伤。在本研究中，我们通过可逆性冠状动脉闭塞在猪身上制造心肌缺血。在冠状动脉再灌注之前及期间，给猪输注钌红或硝普钠（一种已知不具有钙通量抑制特性的后负荷降低剂）。在再灌注期间，钌红和硝普钠均使平均动脉压出现类似程度的降低，而未接受这些药物的猪的平均动脉压则升高。对缺血再灌注区域的心肌样本进行电子显微镜检查。两名研究人员以三点量表独立对细胞核、线粒体、肌原纤维的缺血损伤及糖原消耗进行分级。对于所研究的每个细胞器，治疗组动物的缺血损伤均显著轻于对照组。钌红治疗组动物和硝普钠治疗组动物的这种保护作用相似。这些结果表明，钌红治疗的保护作用归因于其降低后负荷的特性，而非抑制心脏纤维中的跨膜钙通量。
