Growth kinetics of a primary brain tissue necrosis from a focal lesion.

J Eriskat, L Schürer, O Kempski, A Baethmann
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引用次数: 35

Abstract

Secondary brain damage, such as brain edema or impairment of the cerebral microcirculation may evolve from tissue necrosis of the brain induced by trauma or ischemia. This laboratory has provided novel information on the secondary increase of a primary brain tissue necrosis resulting from a focal lesion. We have presently investigated more closely the growth kinetics of this process during 24 h after trauma. Rats were subjected to a standardized focal freezing injury of the brain. Area and volume of the resulting necrosis were quantitatively assessed by morphometry after different periods of survival (i.e., 5 min, 3, 6, 12, 18 and 24 h after trauma). The maximal area of necrosis increased by 45% (p < 0.001) during the posttraumatic observation period. Growth of necrosis after trauma was not limited to the early period, but continued between 12 and 24 h, amounting then to 29% (p < 0.05). The volume of necrosis calculated on the basis of histological serial sections was also observed to increase by 45%. The current findings confirm that a primary brain tissue lesion induced by a standard cryogenic injury, studied as model of a contusion focus in severe head injury, is subjected to secondary growth within a period of 24 h after trauma, longer periods of survival were not investigated yet. Quantification of lesion growth makes possible not only to study underlying mechanisms, but also of whether this process can be therapeutically inhibited.

局灶性脑组织坏死的生长动力学。
继发性脑损伤,如脑水肿或脑微循环损伤,可由外伤或缺血引起的脑组织坏死演变而来。本实验室为局灶性病变引起的原发性脑组织坏死继发性增加提供了新的信息。目前,我们对创伤后24小时内这一过程的生长动力学进行了更密切的研究。对大鼠进行标准化脑局灶性冻伤。不同生存期(即创伤后5分钟、3小时、6小时、12小时、18小时和24小时),通过形态测定法定量评估坏死面积和体积。创伤后观察期间最大坏死面积增加了45% (p < 0.001)。创伤后坏死的生长不局限于早期,在12 ~ 24 h仍在继续,占29% (p < 0.05)。根据组织学序列切片计算的坏死体积也增加了45%。目前的研究结果证实,作为重型颅脑损伤挫伤灶模型的标准低温损伤引起的原发性脑组织病变在创伤后24小时内发生继发性生长,目前尚未研究更长的生存期。病变生长的量化不仅可以研究潜在的机制,还可以研究这一过程是否可以被治疗性地抑制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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