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心脏脂肪酸结合蛋白作为早期心肌损伤死后检测的标志物。

Heart fatty acid binding protein as a marker for postmortem detection of early myocardial damage.

作者信息

Meng Xiangzhi, Ming Mei, Wang Enyin

机构信息

Department of Forensic Medicine, Medical College, Wuhan University, Wuhan 430071, PR China.

出版信息

Forensic Sci Int. 2006 Jun 27;160(1):11-6. doi: 10.1016/j.forsciint.2005.08.008. Epub 2005 Sep 22.

Abstract

Depletion of heart fatty acid binding protein (H-FABP) from cardiomyocytes with varying post-ischemia intervals was studied in acute myocardial infarction (AMI) model of rat, and 22 human autopsy cases were studied with streptavidin-peroxidase conjugated method (S-P). It was observed that as early as 15 min after ischemia, the depletion of H-FABP could be detected in model rats. With the ischemic time prolonged, the depletion of H-FABP was more and more evident. In all human cases with myocardial infarction, absent H-FABP staining could be found in infarcted area. And in some suspected early myocardial infarction cases, depletion of H-FABP staining could be demonstrated in areas that showed normal hematoxylin-eosin (HE) staining. The blood samples from model rats before ligation, at varying post-ischemia intervals and various postmortem time were measured for plasma concentration of H-FABP with enzyme-linked immuno-sorbent assay (ELISA) method. At 15 min after myocardial ischemia, the concentration of H-FABP was 4 times higher (546.0+/-85.3 microg/l) than that of the baseline level (103.7+/-94.1 microg/l). With the continuation of ischemic time, the concentration of H-FABP increased and peaked at 4 h (1953.5+/-405.3 microg/l), then decreased. The plasma concentration of H-FABP decreased slightly with postmortem time, but was still significant higher at any postmortem intervals than that of baseline level within 48 h after death. The results suggest that H-FABP staining can detect very early ischemic damages in human myocardium and the elevated plasma concentration of H-FABP in rat was an indicator of AMI, which was not affected by autolysis.

摘要

在大鼠急性心肌梗死(AMI)模型中,研究了不同缺血后间隔时间内心肌细胞中心脏脂肪酸结合蛋白(H-FABP)的消耗情况,并采用链霉亲和素-过氧化物酶偶联法(S-P)对22例人类尸检病例进行了研究。结果发现,在缺血后15分钟,模型大鼠中即可检测到H-FABP的消耗。随着缺血时间延长,H-FABP的消耗越来越明显。在所有心肌梗死的人类病例中,梗死区域均未发现H-FABP染色。在一些疑似早期心肌梗死的病例中,在苏木精-伊红(HE)染色正常的区域也可显示H-FABP染色的消耗。采用酶联免疫吸附测定(ELISA)法对模型大鼠在结扎前、不同缺血后间隔时间和不同死后时间的血样进行H-FABP血浆浓度测定。心肌缺血15分钟时,H-FABP浓度比基线水平(103.7±94.1μg/l)高4倍(546.0±85.3μg/l)。随着缺血时间的持续,H-FABP浓度升高,并在4小时达到峰值(1953.5±405.3μg/l),随后下降。H-FABP血浆浓度随死后时间略有下降,但在死后48小时内的任何间隔时间仍显著高于基线水平。结果表明,H-FABP染色可检测人类心肌中非常早期的缺血损伤,大鼠血浆中H-FABP浓度升高是AMI的一个指标,且不受自溶影响。

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