Góngora Castillo C, Gómez de Segura I A, López Bravo A, de Miguel del Campo E
Servicio de Cirugía Experimental, Hospital La Paz, Madrid, España.
Angiologia. 1993 Mar-Apr;45(2):59-63.
On this study, parenchymal changes during a cerebral edema caused by thermic injury (cool) on the rabbit, are analyzed. The work was based on the ultrastructural findings obtained by transmission electronic microscopy and on the effects produced by a benzopironic derived (F-117 Hydrosmina). The injury was produced with solid CO2, previous a craniectomy, on the dura mater of the left hemisphere. Forty rabbits were included into the study, the animals were distributed into five groups (n = 8): a control group and 4 treatment groups. One of the groups received treatment without previous cerebral injury. The group of rabbits with doses of 50 mg/Kg of weight showed focal and diffuse areas of edema alternating with less damaged areas, the edema was evident on the white substance. This group also showed a dissociation of the myelinic fibers and an intracytoplasmatic tumefaction into the glial cells. These findings contrast with the histopathological findings obtained from the rabbits (V), the extracellular edema was poor, the myelinic fiber disorganization was minimal with no vacuolar degeneration and no structural mitochondrial changes had been showed. The discontinuance of the hematoencephalic barrier caused by the cool could be a possible mechanism that causes the opening of the endothelial unions from the capillary vessels, changing their membranes and resulting in a free penetration of the molecule into the cerebral parenchyma.(ABSTRACT TRUNCATED AT 250 WORDS)
在本研究中,分析了热损伤(冷却)引起的家兔脑水肿期间的实质变化。该研究基于透射电子显微镜获得的超微结构结果以及一种苯并吡喃衍生物(F - 117 Hydrosmina)产生的效应。损伤是在左半球硬脑膜上进行颅骨切除术后,用固态二氧化碳造成的。40只家兔纳入研究,动物被分为五组(n = 8):一个对照组和4个治疗组。其中一组在没有先前脑损伤的情况下接受治疗。体重剂量为50 mg/Kg的家兔组显示出局灶性和弥漫性水肿区域与损伤较轻区域交替出现,水肿在白质中明显。该组还显示出髓鞘纤维解离和胶质细胞内的胞质肿胀。这些发现与从家兔(V)获得的组织病理学结果形成对比,细胞外水肿较轻,髓鞘纤维紊乱最小,无空泡变性,且未显示线粒体结构变化。冷却导致的血脑屏障中断可能是导致毛细血管内皮连接开放、改变其膜并使分子自由渗透到脑实质的一种可能机制。(摘要截于250字)