Marinov M, Wassmann H
Department of Neurosurgery, Medical Academy, Sofia, Bulgaria.
Stroke. 1991 Aug;22(8):1064-7. doi: 10.1161/01.str.22.8.1064.
We evaluated the influence of a continuous intravenous infusion of 0.24 mg/kg PN 200-110 started 20 minutes before the induction of ischemia and continued for 2 hours on infarct size, histopathology, and neurological outcome in middle cerebral artery-occluded rats treated with PN 200-110 (n = 8), placebo (n = 7), or saline (n = 8). Neurological examination was performed 24 hours after occlusion. We quantified infarct size by 2,3,5-triphenyl-tetrazolium chloride, hematoxylin and eosin, and Nissl staining and by computerized analysis of tracings of the infarcted areas and evaluated neuronal injury at the infarct periphery. The different types of ischemic cell damage were quantified by direct visual counting. We found no differences among saline-, placebo-, and PN 200-110-treated rats regarding infarct size, amount of neuronal alteration, and neurological outcome. Our results indicate the lack of a significant protective effect of this drug in experimental focal ischemia.
我们评估了在大脑中动脉闭塞大鼠中，于缺血诱导前20分钟开始持续静脉输注0.24mg/kg PN 200 - 110并持续2小时，对梗死面积、组织病理学及神经功能转归的影响。将大鼠分为三组，分别给予PN 200 - 110（n = 8）、安慰剂（n = 7）或生理盐水（n = 8）。在闭塞24小时后进行神经功能检查。我们通过氯化三苯基四氮唑、苏木精和伊红以及尼氏染色，并通过对梗死区域图像的计算机分析来量化梗死面积，同时评估梗死周边的神经元损伤。通过直接视觉计数对不同类型的缺血性细胞损伤进行量化。我们发现，在梗死面积、神经元改变程度及神经功能转归方面，生理盐水组、安慰剂组和PN 200 - 110治疗组大鼠之间没有差异。我们的结果表明，该药物在实验性局灶性缺血中缺乏显著的保护作用。
