McIntosh T K, Ferriero D
Department of Surgery, University of Connecticut Health Center, Farmington.
J Cereb Blood Flow Metab. 1992 Jul;12(4):697-702. doi: 10.1038/jcbfm.1992.95.
We utilized a model of fluid percussion (FP) brain injury in the rat to examine the hypothesis that alterations in brain neuropeptide Y (NPY) concentrations occur following brain injury. Male rats (n = 44) were subjected to FP traumatic brain injury. One group of animals (n = 38) was killed at 1 min, 15 min, 1 h, or 24 h after brain injury, and regional brain homogenates were analyzed for NPY concentrations using radioimmunoassay. A second group of animals (n = 6) was killed for NPY immunocytochemistry. Concentrations of NPY in the injured left parietal cortex were significantly elevated at 15 min post injury (p less than 0.05). No changes were observed in other brain regions. NPY-immunoreactive fibers were seen at 15 min post injury predominantly in the injured cortex and adjacent hippocampus. These temporal changes in NPY immunoreactivity, together with previous observations concerning posttraumatic changes in regional CBF in these same areas, suggest that an increase in region NPY concentrations after brain injury may be involved in part in the pathogenesis of posttraumatic hypoperfusion.
我们利用大鼠液压颅脑损伤模型来检验脑损伤后脑海马神经肽 Y(NPY)浓度会发生改变这一假说。雄性大鼠(n = 44)接受液压创伤性脑损伤。一组动物(n = 38)在脑损伤后 1 分钟、15 分钟、1 小时或 24 小时处死,使用放射免疫分析法分析脑匀浆中 NPY 的浓度。另一组动物(n = 6)处死用于 NPY 免疫细胞化学分析。损伤后 15 分钟,损伤的左侧顶叶皮质中 NPY 的浓度显著升高(p < 0.05)。在其他脑区未观察到变化。损伤后 15 分钟,NPY 免疫反应性纤维主要出现在损伤皮质和相邻海马区。NPY 免疫反应性的这些时间变化,连同之前关于这些相同区域创伤后局部脑血流量变化的观察结果,表明脑损伤后局部 NPY 浓度的增加可能部分参与了创伤后低灌注的发病机制。