Abstract—Lymph heart of frog are hollow pulsating organs 1–2 mm in diameter that pump lymph into the venous system. They were used in this work as an experimental model to study the processes of initiation and development of aseptic inflammation in damaged tissues and necrosis-like death of mast cells (MCs). The ultrastructure of damaged and dying MCs was studied in striated muscle tissue of the posterior lymph heart of the adult frog in conditions of temporary ischemia (hypoxia) caused by autotransplantation of this organ into its own bed. It was found that damaged MCs die via oncotic necrosis after autotransplantation of the lymph heart within the period of time from 3 days to 6 weeks. Swelling of the cells and their membrane organelles (except for cytoplasmic secretory granules), dilatation of perinuclear space, budding of vesicles strewn with ribosomes from the outer nuclear membrane, and enrichment of nuclei of some MCs with heterochromatin occur at the early stages of oncosis. For late stages of oncotic necrosis, disintegration of the plasma membrane, release of intact and structurally little modified secretory granules into extracellular space, and karyolysis are typical. The presence of presumably nuclear material was found in extended perinuclear spaces of some damaged and dying MCs. The release of vesicles of rough endoplasmic reticulum (RER) into extracellular space was detected in places of local violation of the plasma membrane integrity of still undestroyed MCs. Immunocytochemical labeling of MCs using antibodies to histamine, substance P (SP), and atrial natriuretic peptide (ANP) (conducted at the ultrastructural level) detected the localization of aurum particles both over secretory granules located in the cytoplasm of damaged and dying cells and over the granules released into extracellular space after disintegration of MCs. Data obtained in the present study suggest that MCs dying via oncotic necrosis may be involved in the initiation and development of aseptic inflammatory process in autotransplanted lymph heart of frog and be a source of alarmins that contribute to the development of inflammation.

中文翻译：

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成年蛙蛙颞叶自体淋巴心肥大细胞死亡的超微结构特征

摘要—青蛙的淋巴中心是直径为1-2 mm的空心搏动器官，可将淋巴泵入静脉系统。他们在这项工作中用作实验模型，以研究受损组织中无菌性炎症的发生和发展以及肥大细胞（MC）坏死样死亡的过程。研究了成年青蛙在由于自身器官自身移植而导致的局部缺血（缺氧）情况下，成年蛙后淋巴心脏横纹肌组织中受损和垂死的MCs的超微结构。发现受损的MC在3天至6周的时间内自体转移淋巴心脏后，由于肿瘤坏死而死亡。细胞及其膜细胞器肿胀（胞浆分泌颗粒除外），核周间隙扩张，从核外膜散布着核糖体的囊泡发芽，并且在肿瘤的早期阶段发生了异染色质富集某些MC的细胞核。对于晚期肿瘤坏死，质膜解体，完整的和结构上几乎没有修饰的分泌性颗粒释放到细胞外空间，以及核溶解是典型的。在某些受损和垂死的MC的扩展核周空间中发现了可能存在的核材料。在仍未破坏的MC的质膜完整性受到局部侵犯的地方，检测到粗面内质网（RER）的囊泡释放到细胞外空间。使用针对组胺，P物质（SP）的抗体对MC进行免疫细胞化学标记 心房利钠肽（ANP）（在超微结构水平传导）检测了受损和垂死细胞的细胞质中分泌颗粒上的金质颗粒的定位，以及MCs分解后释放到细胞外空间的颗粒上的金黄色颗粒的定位。在本研究中获得的数据表明，通过渗透性坏死死亡的MCs可能参与了青蛙自身移植的淋巴心脏无菌性炎症过程的发生和发展，并且是促发炎症反应的警报蛋白的来源。