Ogawa H, Sasaki T, Kassell N F, Nakagomi T, Lehman R M, Hongo K
Department of Neurological Surgery, University of Virginia School of Medicine, Charlottesville 22908.
Acta Neuropathol. 1987;75(1):62-8. doi: 10.1007/BF00686794.
Immunohistochemical localization of prostaglandin F2 alpha (PG F2 alpha) was studied in 24 rats. In 21 rats, global brain ischemia was produced for 5 min by Pulsinelli's method. Prior to decapitation, 13 were recirculated for 5 min, while the remaining eight were not. Three recirculated rats were pretreated with indomethacin before the occlusion. Hypotension was induced during the occlusion to 40-50 mm Hg of mean arterial blood pressure in 11 rats including those unrecirculated, recirculated and pretreated with indomethacin. Three normal rats without occlusion of arteries served as control. The brains were snap frozen and 10-microns cryostat sections were incubated in rabbit anti-PG F2 alpha serum and stained by the indirect immunofluorescence method after fixation in carbodiimide and in Zamboni's solution. Positive staining for PG F2 alpha was noted mainly in pial vessels in normal and ischemic rats both with and without hypotension. The rats recirculated without hypotensive ischemia revealed a positive reaction in the walls of pial and parenchymal vessels. All rats recirculated after the hypotensive occlusion showed positive staining in blood vessels, in the cytoplasm of neurons (especially in hippocampi) and in the interfascicular oligodendrocytes. The above results indicate that recirculation after ischemia results in an increase in PG F2 alpha in parenchymal vessels, neurons and oligodendrocytes.
对24只大鼠进行了前列腺素F2α(PG F2α)的免疫组织化学定位研究。21只大鼠采用普尔西内利法造成全脑缺血5分钟。断头前,13只大鼠再灌注5分钟,其余8只未进行再灌注。3只再灌注大鼠在闭塞前用吲哚美辛预处理。11只大鼠(包括未再灌注、再灌注和用吲哚美辛预处理的大鼠)在闭塞期间诱导低血压至平均动脉血压40 - 50毫米汞柱。3只未闭塞动脉的正常大鼠作为对照。将大脑速冻,切成10微米厚的低温恒温器切片,用兔抗PG F2α血清孵育,在碳二亚胺和赞博尼溶液中固定后,采用间接免疫荧光法染色。在正常和缺血大鼠(无论有无低血压)中,PG F2α的阳性染色主要见于软脑膜血管。未发生低血压性缺血的再灌注大鼠在软脑膜和实质血管壁显示阳性反应。所有低血压性闭塞后再灌注的大鼠在血管、神经元细胞质(尤其是海马体)和束间少突胶质细胞中均显示阳性染色。上述结果表明,缺血后再灌注导致实质血管、神经元和少突胶质细胞中PG F2α增加。