摘要
目的:研究大鼠短暂性全脑缺血-再灌流损伤后,海马齿状回门(DH)区、CA1区和大脑皮质纹状18a(Str18a)区生长抑素(SS)、SSmRNA表达及脑组织细胞内钙离子浓度[Ca2+]i的改变与尼莫地平对这些改变的影响。方法:大鼠麻醉后烧闭双侧椎动脉,右侧颈总动脉(CCA)注射尼莫地平(治疗组)或生理盐水(对照组),夹闭双侧CCA持续2min,5min或10min,松钳形成再灌流(持续2h)。脑组织石蜡切片免疫组化、原位杂交检测SS、SSmRNA的表达;Fura-2/AM检测脑组织[Ca2+]i。结果:治疗组与对照组短暂缺血(5min、10min)-再灌流损伤后DH区内SS、SSmRNA神经元显著减少,其它区域无明显变化,尽管治疗组[Ca2+]i显著低于对照组,但两组之间差异不明显。结论:①DH区SS神经元对于缺血性损伤的耐受能力最差;②尼莫地平虽可减轻缺血后细胞内钙超载。
Objective: To observe the changes of expression of somatostatin (SS) and somatostatin mRNA (SSmRNA) and intracellular [Ca 2+ ]i content and explore the effects of nimodipine on the changes after transient cerebral ischemia reperfusion in rats. Medthods: Nimodipine (group A) or normal saline (group B) was administered through the right common carotid artery (CCA) immediately before the global cerebral ischemia was induced in anesthetized Wistar rats. After ischemia/reperfusion, the expression of SS and SSmRNA was determined with in situ hybridization and intracellular [Ca 2+ ]i content with Fura 2/AM. Results: Though nimodipine obviously attenuated the increase of [Ca 2+ ]i, the expression of SS and SSmRNA was significantly down regulated following the injury of 5 or 10 min ischemia and 2h reperfusion in the area of hippocampal dentate hilus but not in CA1 or striate cortex 18a and there was no marked difference between the two groups. Conclusion: ①The tolerance of hilar SS neurons to ischemic injury is the poorest. ②Nimodipine can not exert protective effects on the loss of hilar SS neurons induced due to ischemia reperfusion injury.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
1998年第3期244-246,共3页
Journal of Third Military Medical University