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急性心肌梗死脂质代谢的组织化学研究

Histochemical study on lipid metabolism in acute myocardial infarction.

作者信息

Sakurai I, Tosaka A, Yamada T, Masubuchi K

出版信息

Acta Pathol Jpn. 1978 Sep;28(5):669-75. doi: 10.1111/j.1440-1827.1978.tb00906.x.

Abstract

As a part of the series of studies on lipid metabolism in ischemic myocardium, the present study was attempted to analyse 29 infarcted hearts with acute or scar lesions by a routine histopathology and lipid histochemistry. The time after the onset of attack till death ranged from one day to years. Sixteen were of the acute form, less than 2 month-old, and 13 were of the chronic scarred form. Within the first day, fat deposition appeared in the survived muscle cells around the infarcts reaching the peak from 2 days to one week, but necrotized cells never contained fat droplets. Macrophages in granulation tissue in periphery of the infarcts tended to have significant fat droplets usually in 10 days to one month. Fat disappeared from the survived muscle cells and also from the scar later than 2 months. The survived cells around the infarcts might be degenerated with fat, probably triglyceride, which accumulated by a relative ischemia not severe enough to produce coagulation necrosis, and they bear some relationship with extension or limitation of size of infarcts.

摘要

作为缺血心肌脂质代谢系列研究的一部分,本研究试图通过常规组织病理学和脂质组织化学方法分析29例有急性或瘢痕病变的梗死心脏。发病至死亡的时间从1天到数年不等。16例为急性形式,发病不到2个月,13例为慢性瘢痕形式。在发病后的第一天内,梗死灶周围存活的心肌细胞中出现脂肪沉积,在2天至1周达到峰值,但坏死细胞中从未含有脂肪滴。梗死灶周边肉芽组织中的巨噬细胞通常在10天至1个月时倾向于含有大量脂肪滴。脂肪在2个月后从存活的心肌细胞以及瘢痕中消失。梗死灶周围存活的细胞可能会因脂肪(可能是甘油三酯)而发生变性,这些脂肪是由相对缺血积聚而成,缺血程度不足以导致凝固性坏死,并且它们与梗死灶大小的扩展或局限存在一定关系。

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