Tanaka N, Kita T, Kasai K, Nagano T
Department of Forensic Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Virchows Arch. 1994;424(3):273-7. doi: 10.1007/BF00194611.
After the intravenous administration of lipopolysaccharide at a dose of 3.0 mg/100 g to rats, immunoreactive sites for tumour necrosis factor (TNF) and peptide leukotrienes (LTs) were examined in the heart and lung. Immunoreaction for TNF is preferentially localized on the apical endothelial cell surface of the vessels and in lysosomes of inflammatory and interstitial cells. Lysosomes of cardiac muscle cells which undergo degeneration are also reactive. Peptide LTs in inflammatory cells give almost the same reactions as those for TNF. However, the production of peptide LTs occurs uniquely in cardiac muscle cells in the media of the pulmonary vein, although lysosomes of intracardiac muscle cells which undergo degeneration do not show immunoreactivity. These results suggest that the degeneration of cardiac muscle cells may be induced not only by endogenous TNF but also by peptide LTs which are produced in muscle cells of the venous media and are transported to the myocardium via the coronary circulation.
给大鼠静脉注射剂量为3.0毫克/100克的脂多糖后,检测了心脏和肺中肿瘤坏死因子(TNF)和肽白三烯(LTs)的免疫反应位点。TNF的免疫反应优先定位在血管的顶端内皮细胞表面以及炎症和间质细胞的溶酶体中。发生变性的心肌细胞的溶酶体也有反应。炎症细胞中的肽LTs与TNF的反应几乎相同。然而,肽LTs仅在肺静脉中层的心肌细胞中产生,尽管发生变性的心脏内肌细胞的溶酶体没有显示免疫反应性。这些结果表明,心肌细胞的变性可能不仅由内源性TNF诱导,还可能由静脉中层肌肉细胞产生并通过冠状动脉循环转运至心肌的肽LTs诱导。