Eriskat J, Schürer L, Kempski O, Baethmann A
Institute for Surgical Research, Ludwig-Maximilians-Universität, München, Federal Republic of Germany.
Acta Neurochir Suppl (Wien). 1994;60:425-7. doi: 10.1007/978-3-7091-9334-1_115.
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.
继发性脑损伤，如脑水肿或脑微循环障碍，可能由创伤或缺血引起的脑组织坏死演变而来。本实验室已提供了关于局灶性病变导致原发性脑组织坏死继发性增加的新信息。我们目前更深入地研究了创伤后24小时内这一过程的生长动力学。对大鼠进行标准化的局灶性脑冷冻损伤。在不同存活期（即创伤后5分钟、3、6、12、18和24小时）后，通过形态计量学定量评估所形成坏死灶的面积和体积。在创伤后观察期内，坏死灶的最大面积增加了45%（p<0.001）。创伤后坏死灶的生长并不局限于早期，而是在12至24小时之间持续，此时增加了29%（p<0.05）。基于组织学连续切片计算的坏死灶体积也观察到增加了45%。目前的研究结果证实，作为重度颅脑损伤中挫伤灶模型进行研究的标准低温损伤所诱导的原发性脑组织病变，在创伤后24小时内会发生继发性生长，尚未研究更长的存活期。损伤生长的量化不仅使研究潜在机制成为可能，而且使研究这一过程是否可以通过治疗得到抑制成为可能。
