摘要
目的探讨脑损伤后脑微循环障碍变化规律,为临床改善脑损伤后脑微循环障碍、治疗脑缺血、促进神经功能恢复提供理论依据。方法采用Feeney’s自由落体撞击法建立急性局灶性脑挫裂伤模型。每组6只行内源性过氧化物酶(EGPOX)组织化学染色、脑含水量测定,并进行图象分析。每组3只电镜观察微血管内皮细胞超微结构改变。结果①脑损伤后30min伤区可见出血灶,伤区内无血管染色,伤区周围存在“微无血管区”。“微无血管区”的存在持续至伤后72h。②脑损伤后30min微血管面密度明显下降,伤后48h达到高峰,直到伤后168h才有所恢复,但仍未达到正常水平。③脑损伤后30min微血管平均光密度明显下降,伤后24、48h回升,72h再次下降,至168h仍未恢复正常。④脑损伤后30min,微血管内皮细胞有轻度受损迹象,伤后2h毛细血管腔内有微绒毛形成,伤后6h微绒毛增多。伤后12-72h毛细血管腔明显狭窄。结论EGPOX组织化学染色方法能准确反应脑损伤后脑微循环的改变,脑损伤后即发生脑缺血改变,而脑缺血的发生源于脑损伤后脑微血管结构的破坏和微循环灌注不足。
Objective To explore the alteration law of cerebral microcireulation after brain injury and to furnish evidence to improve disturbance of cerebral microcirculation after brain injury and treat the cerebral ischemia. Methods Acute regional brain trauma was applied according to Feeney's apparatus. 81 rats were randomly divided into control group and traumatic group. Endogenous peroxidase(EGPOX) histochemieal staining was performed to 6 of each group, water content of the brain and the charts were analyzed by CMIAS system. Alteration of micrangium endotheliocyte ultrastructure was observed to 3 of each group. Results (1)The hemorrhage was observed at the traumatic area and the blood vessel did not stain, "non" or "less" microvessel area was shown and it continued 72h.(2)The density of microvasculature volume fraction declined at 30min. It reached peak at 48h and recovered at 168h. (3) MOD declined at 30min, raised again at 48h and 72h, declined again at 168h. (4)Microvessel endothelia were damaged at 30min, microvilli was formed at 2h and 6h, the cavity of capillary was narrow at 12 - 72h. Conclusion EGPOX histochemical staining could reflect correctly the changes of cerebral microcirculation. The brain ischemia appeared early after brain injury and which resulted from disruption of microvascular structure and hypoperfusion of microcirculation.
出处
《中国微循环》
北大核心
2007年第2期102-104,114,F0003,共5页
Journal of Chinese Microcirculation