CAJ | 학술논문

目的观察一过性缺血后脑组织中嗜酸性神经元、反应性星形胶质细胞和梗死区域的分布,探明脑缺血病理形态学改变的时序性变化.方法通过2次10 min、间隔5h的单侧颈总动脉夹闭制造蒙古沙鼠脑缺血模型,激光多普勒血流仪检测前部脑皮质血流；于24 h,4d,2、4、16周观察脑组织病理形态学改变.结果颈总动脉夹闭后激光多普勒血流仪显示前部至后部脑血流量明显降低:分别为22.1％±9.5％,26.3％±4.9％,37.5％±3.5％,F =67.219,P＜0.01；位于前脑部的脑血流量的降低明显高于后脑部.缺血24h后,嗜酸性神经元出现于脑前部皮质中层和深层、4d后遍及整个皮质各层,4d至4周大范围的高密度嗜酸性神经元区域(≥80个/mm2)进展为梗死.脑后部皮质中层和深层进展为低嗜酸性神经元区(＜ 80个/mm2),未进一步进展为梗死.反应性星形胶质细胞分布区域与嗜酸性神经元一致；反应性星形胶质细胞伴随高密度嗜酸性神经元区域在缺血后4d至4周大部分转化为梗死.迟发性星形胶质细胞死亡发生于反应性星形胶质细胞伴随高密度嗜酸性神经元区域.结论嗜酸性神经元密度是缺血脑组织梗死及迟发性星形胶质细胞死亡的重要标志.
목적 관찰일과성결혈후뇌조직중기산성신경원、반응성성형효질세포화경사구역적분포,탐명뇌결혈병리형태학개변적시서성변화.방법 통과2차10 min、간격5h적단측경총동맥협폐제조몽고사서뇌결혈모형,격광다보륵혈류의검측전부뇌피질혈류；우24 h,4d,2、4、16주관찰뇌조직병리형태학개변.결과 경총동맥협폐후격광다보륵혈류의현시전부지후부뇌혈류량명현강저:분별위22.1％±9.5％,26.3％±4.9％,37.5％±3.5％,F =67.219,P＜0.01；위우전뇌부적뇌혈류량적강저명현고우후뇌부.결혈24h후,기산성신경원출현우뇌전부피질중층화심층、4d후편급정개피질각층,4d지4주대범위적고밀도기산성신경원구역(≥80개/mm2)진전위경사.뇌후부피질중층화심층진전위저기산성신경원구(＜ 80개/mm2),미진일보진전위경사.반응성성형효질세포분포구역여기산성신경원일치；반응성성형효질세포반수고밀도기산성신경원구역재결혈후4d지4주대부분전화위경사.지발성성형효질세포사망발생우반응성성형효질세포반수고밀도기산성신경원구역.결론 기산성신경원밀도시결혈뇌조직경사급지발성성형효질세포사망적중요표지.
Objective To investigate the distribution of eosinphililic neurons ( ENs),reactive astrocytes ( RAs),and infarction after transient cerebal ischemia,and the time profile of pathomorphological changes.Methods Unilateral forebrain ischemia was induced in Mongolian gerbils by two 10 minutes unilateral common carotid artery occlusions with a 5 hours interval.Laser Doppler flowmetry was used to detect intra-ischemic anterior cortex blood flow.Animals were sacrificed at 24 hours,4 days,2 weeks,4 weeks,16 weeks and the brain were prepared for pathomorphological assay.Results Intra-ischemic laser Doppler flowmetry show significant ischemia during carotid artery occlusion:22.1％ ± 9.5％,26.3％ ± 4.9％,37.5％ ± 3.5％,F =67.219,P ＜ 0.01 ; the decrease was significantly greater in the anterior cortex.ENs appeared in middle and deep layers at 24 hours postischemia,and ENs area extend to all layers of cortex by 4 days.Large areas of high EN density ( ≥80/mm2) evolved to infarcts between 4 days and 4 weeks.Posterior cortex evolved to low EN area ( ＜ 80/mm2) without transformation into infarcts.RAs were consistently distributed in areas with ENs,and RA areas with high EN density were largely transformed into infarcts between 4 days and 4 weeks. Delayed astrocytic death took place in the RA areas with high EN density.Conclusion Density of ENs is an important indicator of delayed astrocytic death and infarction in postischemic tissue.