Ostrovskiĭ A A, Nikitin V S
Vopr Pitan. 1987 Sep-Oct(5):57-61.
The influence of vitamin B1-deficiency on the ultrastructure of the cellular elements in the focus of aseptic inflammation in the skeletal muscles was studied in white mice, 2 and 3 days after the infliction of a mechanical trauma. Food B1-hypovitaminosis was induced by keeping the animals on a thiamine-deficient ration during 30 days. Oxythiamine hypovitaminosis was simulated by subcutaneous injections of vitamin B1 antimetabolite--oxythiamine, in a dose of 10 mg/kg, every 12 h, during 10 days. Both types of hypovitaminosis induced similar reactions of the cellular elements. The volume fraction of lysosomes and phagosomes in the macrophage cytoplasma decreased, the volume density of mitochondria increased, differentiation of fibroblasts was delayed. No significant changes were detected in the ultrastructure of neutrophilic granulocytes, eosinophils and lymphocytes. Decrease of macrophage phagocytic activity is one of the main factors in the mechanism of delay of necrotic mass resorption and inhibition of the following development of reparative processes.
在白色小鼠遭受机械创伤2天和3天后，研究了维生素B1缺乏对骨骼肌无菌性炎症病灶中细胞成分超微结构的影响。通过让动物在30天内食用缺乏硫胺素的日粮来诱导食物性维生素B1缺乏症。通过每12小时皮下注射剂量为10mg/kg的维生素B1抗代谢物——氧硫胺素，持续10天来模拟氧硫胺素缺乏症。两种类型的维生素缺乏症均诱导细胞成分产生相似反应。巨噬细胞胞质中溶酶体和吞噬体的体积分数降低，线粒体的体积密度增加，成纤维细胞的分化延迟。嗜中性粒细胞、嗜酸性粒细胞和淋巴细胞的超微结构未检测到明显变化。巨噬细胞吞噬活性降低是坏死物质吸收延迟和修复过程后续发展受到抑制机制中的主要因素之一。
