Jamshidi J, Yoshimine T, Ushio Y, Hayakawa T
Department of Neurosurgery, Osaka University Medical School, Japan.
J Neurooncol. 1992 Mar;12(3):197-204. doi: 10.1007/BF00172707.
To study the effects of glucocorticoids and chemotherapeutic agents on the pathophysiology of the tumor-induced brain edema, the site of Evans blue-albumin extravasation, the distribution of extravasated serum albumin, and the extent of local astrocytic reaction were examined in a rat model of implanted brain tumor. Experimental brain tumors were produced by implanting small pellets of Walker 256 carcinosarcoma into the cerebral cortex of Wistar rats. In the steroid group, rats were administered with intraperitoneal methylprednisolone succinate (15 mg/kg) daily on and after the 6th day postimplantation, and sacrificed on the 14th day. In the chemotherapy group, rats were given an intravenous injection of cyclophosphamide (30 mg/kg) on the 14th day, and sacrificed on the 21st day. Rats in the untreated group were sacrificed on the 14th day without any therapy. Each animal was sacrificed by the transcardiac perfusion with paraformaldehyde 30 min after intravenous injection of Evans blue. Firstly, coronal blocks of the brain were examined for Evans blue staining macroscopically. Paraffin embedded sections were studied for the Evans blue fluorescence and for the immunohistochemical reaction to serum albumin and GFAP. The examination of Evans blue demonstrated that the origin of extravasation of serum albumin was the tumor and the adjacent brain with dense tumor cell infiltration in any group of rats. The extravasated serum albumin distributed widely and the astrocytic reaction was prominent in the brain of the untreated group. A positive correlation was observed between the intensity of albumin immunoreaction and the degree of astrocytic proliferation. Chemotherapy effectively decreased the size of tumor and reduced the extravasation of serum albumin. The astrocytic reaction was however, not reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
为研究糖皮质激素和化疗药物对肿瘤诱导的脑水肿病理生理学的影响,在植入性脑肿瘤大鼠模型中,检测了伊文思蓝-白蛋白外渗部位、外渗血清白蛋白的分布以及局部星形细胞反应程度。通过将Walker 256癌肉瘤小丸植入Wistar大鼠大脑皮层来制备实验性脑肿瘤。在类固醇组中,大鼠在植入后第6天及之后每天腹腔注射琥珀酸甲泼尼龙(15 mg/kg),并在第14天处死。在化疗组中,大鼠在第14天静脉注射环磷酰胺(30 mg/kg),并在第21天处死。未治疗组的大鼠在第14天未经任何治疗即处死。每只动物在静脉注射伊文思蓝30分钟后经心脏灌注多聚甲醛处死。首先,宏观检查脑的冠状块的伊文思蓝染色。对石蜡包埋切片进行伊文思蓝荧光以及血清白蛋白和胶质纤维酸性蛋白的免疫组化反应研究。伊文思蓝检查表明,在任何一组大鼠中,血清白蛋白外渗的起源都是肿瘤及肿瘤细胞密集浸润的相邻脑区。外渗的血清白蛋白广泛分布,未治疗组大鼠脑内星形细胞反应明显。观察到白蛋白免疫反应强度与星形细胞增殖程度之间呈正相关。化疗有效减小了肿瘤大小并减少了血清白蛋白外渗。然而,星形细胞反应并未减轻。(摘要截短至250字)