Myeloperoxidase Activity as a Quantitative Marker of Polymorphonuclear Leukocyte Accumulation into an Experimental Myocardial Infarct—The Effect of Ibuprofen on Infarct Size and Polymorphonuclear Leukocyte Accumulation
Myeloperoxidase Activity as a Quantitative Marker of Polymorphonuclear Leukocyte Accumulation into an Experimental Myocardial Infarct—The Effect of Ibuprofen on Infarct Size and Polymorphonuclear Leukocyte Accumulation
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髓过氧化物酶活性作为实验性心肌梗塞多形核白细胞积聚的定量标志物——布洛芬对梗塞面积和多形核白细胞积聚的影响
DOI：
10.1097/00005344-198511000-00022
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发表时间：
1985
影响因子：
3
通讯作者：
A. Parke
中科院分区：
文献类型：
--
作者：
G. Allan;P. Bhattacherjee;C. Brook;N. Read;A. Parke
摘要：多形核白细胞（PMN）在犬心肌梗死（MI）闭塞/再灌注模型中的积累已经用PMN特异性酶髓过氧化物酶（MPO）的分光光度法进行了定量分析。在麻醉的比格犬左冠状动脉前降支闭塞1小时后再灌注1小时，梗死心肌的MPO活性是正常心肌的4倍。梗死心肌MPO活性随冠状动脉再灌注呈时间相关性增高，在冠状动脉再灌注后5小时积聚最多。缺血心肌中MPO活性的时间相关性升高与组织学切片观察到的PMN积累密切相关，从而支持了该方法的特异性。用布洛芬（12.5 mg/kg静脉注射）对狗进行预处理，并没有改变MPO含量，因此梗死心肌的PMN侵袭，这一发现在光镜下得到了证实。然而，布洛芬预处理增加了心肌梗死面积（从11.5%增加到37.4%,p < 0.01），增加了出血性梗死和心室颤动的发生率。总之，我们的研究表明，MPO可以作为PMN在心肌梗死中积累的一个敏感和定量的标志。此外，我们已经证明，PMN以一种时间依赖性的方式快速浸润损伤的心肌，这种积累不受布洛芬预处理的影响。
Summary: The accumulation of polymorphonuclear leukocytes (PMN) into a canine occlusion/reperfusion model of myocardial infarction (MI) has been quantitated using a spectrophotometric assay for the PMN-specific enzyme myeloperoxidase (MPO). In anaesthetised beagle dogs subjected to 1 h of occlusion of the left anterior descending coronary artery followed by coronary reperfusion for 1 h, MPO activity was found in fourfold greater amounts in infarcted myocardium as opposed to normal myocardium. MPO activity in infarcted myocardium increased with coronary reperfusion in a time-related manner, the greatest accumulation occurring at 5 h of coronary reperfusion. The time-related increase in MPO activity in ischemic myocardium was closely correlated with the observed accumulation of PMN as assessed by histological sectioning, thus supporting the specificity of the method. Pretreatment of dogs with ibuprofen (12.5 mg/kg i.v.) did not alter the MPO content and therefore PMN invasion of infarcted myocardium, a finding confirmed by light microscopy. However, pretreatment with ibuprofen increased myocardial infarct size (from 11.5 to 37.4%, p < 0.01) and increased the incidence of haemorrhagic infarction and ventricular fibrillation. In conclusion, our studies demonstrate that MPO can be used as a sensitive and quantitative marker of PMN accumulation into an evolving MI. Furthermore, we have demonstrated that PMNs rapidly infiltrated injured myocardium in a time dependent manner and this accumulation was unaffected by ibuprofen pretreatment.