Shneĭvaĭs V B, Levin G S
Patol Fiziol Eksp Ter. 1996 Apr-Jun(2):39-43.
The mechanisms responsible for necrotic damage to liver cells at the stages of experimental visceral-ischemic shock were studied by computerized morphometric techniques for interphasic nuclei of hepatocytes. A number of geometric, optical, and textural parameters of the structure of chromatin have been defined, which characterize the extent of its damage as shock progresses. The increment of degenerative signs of the nuclear structures occurred concurrently with the enhancement of free radical processes, which may be indicative of the fact that there is their pathophysiological relationship. The findings were comparable with those of a multiparametric analysis of chromatin in the isolated hepatocytes exposed to free radical oxidation. The coincidence of temporal and structural parameters of hepatocytic nuclear alteration in shock and in the model system makes the authors conclude that in visceral-ischemic shock a great role in the genesis of cytolysis is played by the generation of active oxygen forms and their direct or lipid peroxidation-mediated action on the nuclear structures.
利用计算机形态测量技术研究实验性内脏缺血性休克阶段肝细胞坏死损伤的机制,该技术用于检测肝细胞间期细胞核。已经确定了染色质结构的一些几何、光学和纹理参数,这些参数表征了随着休克进展染色质损伤的程度。核结构退化迹象的增加与自由基过程的增强同时发生,这可能表明它们之间存在病理生理关系。这些发现与对暴露于自由基氧化的分离肝细胞中染色质的多参数分析结果相当。休克和模型系统中肝细胞核改变的时间和结构参数的一致性使作者得出结论,在内脏缺血性休克中,活性氧形式的产生及其对核结构的直接作用或脂质过氧化介导的作用在细胞溶解的发生中起重要作用。