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在福尔马林固定、石蜡包埋组织中检测早期心肌梗死

Detection of early myocardial infarction in formalin-fixed, paraffin-embedded tissue.

作者信息

Fujiwara H, Fujiwara T, Tanaka M, Onodera T, Miyazaki S, Wu D J, Matsuda M, Sasayama S, Kawai C

机构信息

Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.

出版信息

Am J Cardiovasc Pathol. 1988;2(1):57-61.

PMID:3207489
Abstract

Whether the early infarct area in formalin-fixed, paraffin-embedded tissue could be delineated by the immunohistochemical method using myoglobin-antibody was studied in 23 pig hearts without collateral circulation. Five hearts were examined at 20 minutes, 2 hours, 4 hours, and 6 hours after occlusion of the distal one third of the left anterior descending coronary artery, respectively. Three pigs were killed 24 hours after occlusion. Heart rate and aortic pressure before and after occlusion did not change in any groups. The subepicardial and subendocardial regional blood flows were reduced to almost zero in all hearts after occlusion (0.88 +/- 0.10 to 0.02 +/- 0.02 mL/g/min). Slight myoglobin defects in the ischemic tissue were noted in the five pigs examined 2 hours after occlusion and definite myoglobin defects were detected in all pigs examined at 4, 6, and 24 hours after occlusion. Nitrotetrazorium blue stain of myocardial tissue before formalin fixation showed slight demarcation of the ischemic area at 4 hours after occlusion and definite demarcation at 6 and 24 hours after occlusion. Slight demarcation was noted at 2 hours after occlusion in Masson trichrome stain and 4 hours after occlusion in the hematoxylin-eosin stain. However, definite demarcation of the ischemic area was seen in Masson trichrome stain only at 24 hours after occlusion and was not noted in hematoxylin-eosin stain even at 24 hours after occlusion. Our previous electron microscopic study revealed that, in the pig heart, irreversible cellular damage was transmurally seen at two hours after occlusion of the coronary artery. Therefore, a definite myoglobin defect reflects irreversible cellular damage such as infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在23个无侧支循环的猪心脏中,研究了使用肌红蛋白抗体的免疫组织化学方法能否勾勒出福尔马林固定、石蜡包埋组织中的早期梗死区域。分别在左前降支冠状动脉远端三分之一闭塞后20分钟、2小时、4小时和6小时检查5个心脏。闭塞后24小时处死3头猪。所有组闭塞前后的心率和主动脉压均无变化。闭塞后所有心脏的心外膜下和心内膜下区域血流几乎降至零(从0.88±0.10降至0.02±0.02 mL/g/min)。在闭塞后2小时检查的5头猪中,缺血组织中发现轻微的肌红蛋白缺陷,在闭塞后4小时、6小时和24小时检查的所有猪中均检测到明确的肌红蛋白缺陷。福尔马林固定前心肌组织的硝基四氮唑蓝染色显示,闭塞后4小时缺血区域有轻微分界,闭塞后6小时和24小时有明确分界。在马森三色染色中,闭塞后2小时有轻微分界,苏木精-伊红染色中闭塞后4小时有轻微分界。然而,缺血区域的明确分界仅在闭塞后24小时的马森三色染色中可见,即使在闭塞后24小时的苏木精-伊红染色中也未观察到。我们之前的电子显微镜研究表明,在猪心脏中,冠状动脉闭塞后两小时可透壁观察到不可逆的细胞损伤。因此,明确的肌红蛋白缺陷反映了诸如梗死等不可逆的细胞损伤。(摘要截短于250字)

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引用本文的文献

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Int J Clin Exp Pathol. 2009 Sep 20;3(1):98-105.
2
Antidiabetic drug miglitol inhibits myocardial apoptosis involving decreased hydroxyl radical production and Bax expression in an ischaemia/reperfusion rabbit heart.抗糖尿病药物米格列醇抑制心肌细胞凋亡,这与缺血/再灌注兔心脏中羟自由基生成减少和Bax表达降低有关。
Br J Pharmacol. 2004 Jul;142(6):983-90. doi: 10.1038/sj.bjp.0705863. Epub 2004 Jun 21.
3
High frequency of spontaneous acute myocardial infarction due to small coronary artery disease in dead (NZWxBXSB)F1 male mice.
死亡的(新西兰白兔×棕色施氏小鼠)F1代雄性小鼠因小冠状动脉疾病导致自发性急性心肌梗死的频率较高。
Am J Pathol. 1989 Dec;135(6):989-99.
4
Clinicopathological study of myocardial infarction with normal or nearly normal extracardiac coronary arteries. Quantitative analysis of contraction band necrosis, coagulation necrosis, hemorrhage, and infarct size.心外膜冠状动脉正常或近乎正常的心肌梗死的临床病理研究。收缩带坏死、凝固性坏死、出血及梗死面积的定量分析。
Heart Vessels. 1990;6(1):55-62. doi: 10.1007/BF02301880.