Abe H, Sugino N, Matsuda T, Ueda Y, Mori H, Aono M
Department of Anesthesiology, Kanazawa Medical University, Ishikawa.
Masui. 1996 Oct;45(10):1216-22.
The effects of prostaglandin E1 (PGE1) on transient forebrain ischemia were studied in the gerbil. The animals were randomly divided into six groups of 6 each according to the method of administration as follows: group 1, no administration; group 2, subcutaneous administration with 5 ml.kg-1 of physiological saline, 30 min prior to ischemia; group 3, the same method with 3 mg.kg-1 of PGE1; group 4, 3 mg.kg-1 of PGE1, during 24 hours (12 hours prior to ischemia, and 12 hours following ischemia); group 5, 3 mg.kg-1 of PGE1, during 96 hours (12 hours prior to ischemia and 84 hours following ischemia); and group 6, sham operation. They were anesthetized with isoflurane and transient forebrain ischemia was induced by occluding bilateral common carotid arteries for 5 min. The extracranial electroencephalogram (EEG) was recorded from the electrodes placed at the vertex. During the experimental procedures, temperatures at tympanic membrane and rectum were maintained at 37.0 +/- 0.2 degrees C by means of a heating mat and control of the air temperature in all groups. After 6 days of survival, they were sacrificed, and the brain tissues were fixed for the immunohistochemical and histopathological analyses. The hippocampal CA 1 regions were stained for monoclonal anti microtubule-associated protein 2 (MAP 2), and hematoxylin and eosin. In the 4th group, EEG recovery was recognized earlier than the other groups. Immunoreactivities for MAP 2 and the number of surviving pyramidal cells after ischemia in the CA 1 regions were also well maintained. These results suggest the PGE1, has protective effects against degradation of cytoskeletal proteins and delayed neuronal death in the gerbil, and it might be due to direct protective action of cell membrane in addition to its microcirculatory improvement.
在沙鼠身上研究了前列腺素E1(PGE1)对短暂性前脑缺血的影响。根据给药方法将动物随机分为6组,每组6只,具体如下:第1组,不给药;第2组,在缺血前30分钟皮下注射5 ml.kg-1生理盐水;第3组,采用相同方法注射3 mg.kg-1 PGE1;第4组,在24小时内(缺血前12小时和缺血后12小时)注射3 mg.kg-1 PGE1;第5组,在96小时内(缺血前12小时和缺血后84小时)注射3 mg.kg-1 PGE1;第6组,假手术。用异氟烷麻醉动物,通过阻断双侧颈总动脉5分钟诱导短暂性前脑缺血。从置于头顶的电极记录颅外脑电图(EEG)。在实验过程中,通过加热垫和控制所有组的气温,将鼓膜和直肠温度维持在37.0±0.2℃。存活6天后,将它们处死,固定脑组织用于免疫组织化学和组织病理学分析。对海马CA1区进行单克隆抗微管相关蛋白2(MAP 2)、苏木精和伊红染色。在第4组中,EEG恢复比其他组更早。CA1区缺血后MAP 2的免疫反应性和存活锥体细胞数量也得到良好维持。这些结果表明,PGE1对沙鼠细胞骨架蛋白降解和延迟神经元死亡具有保护作用,这可能是由于其除改善微循环外对细胞膜的直接保护作用。