全脑缺血/再灌注大鼠皮层PGI_2和TXA_2时程变化特征

Time course change of PGI_2 and TXA_2 levels in rat cortex following global cerebral ischemia reperfusion

目的观察PGI2、TXA2含量及PGI2/TXA2比值在全脑缺血/再灌注大鼠皮层中的时程变化特征。方法采用夹闭双侧颈总动脉,右侧颈总静脉抽血再回输建立大鼠全脑缺血/再灌注模型。多普勒激光脑血流仪监测大鼠在缺血/再灌注手术过程中的脑血流变化。Morris水迷宫检测大鼠空间学习记忆能力。HE染色观察大鼠皮层神经元形态结构变化。ELISA测定大鼠皮层中PGI2、TXA2含量。结果大鼠在全脑缺血过程中脑血流降低74.45%。与假手术组比较,全脑缺血/再灌注组大鼠寻台潜伏期明显增加,皮层神经元出现明显核固缩,细胞层次紊乱,神经细胞数目明显减少,并随再灌注时间延长而损伤加重。PGI2、TXA2、PGI2/TXA2比值在再灌注2 h内明显低于假手术组,再灌注6 h时明显升高,PGI2、TXA2峰值在48 h,PGI2/TXA2比值峰值在7 d。结论全脑缺血/再灌注损伤诱导大鼠皮层PGI2和PGI2/TXA2比值明显增加,并具有时间依赖性特征。

Aim To investigate the levels of PGI2, TXA2 and ratio of PGI2/TXA2 in the rat cortex at dif- ferent time points after global cerebral ischemia reper- fusion. Methods The rat model of global cerebral is- chemia reperfusion injury was established by bilateral common carotid artery occlusion and systemic hypoten- sion. MoorVMS-LDF laser Doppler blood flow monitor was conducted to record the cerebral blood flow during ischemia and repeffusion in rats. Morris water maze test was used to assess spatial learning and memory function of rats. Histological examination by HE stai- ning was employed to access the morphologic changes of cortex neuron after cerebral isehemia. Content of PGI2 and TXA2 in the rat cortex were detected by en- zyme-linked immunosorbent assay. Results CBF rap- idly decreased by 74.45% of the baseline during thecerebral ischemia phase. Compared with the sham group, the average escape latency was significantly lon- ger for all global cerebral ischemia rats. Cortex neuron in model group showed obviously disordered cell struc- ture and membrane shrinkage, and the injury aggrava- ted along with the repeffusion time when compared with that of sham group. The levels of PGI2, TXA2 and the ratio of PGI2/ TXA2 decreased within 2 hours after reperfusion, and begun to increase at 6 h after reperfu- sion. The TXA2 and PGI2 peaked at 48 h, and the rati- o of PGI2/TXA2 peaked at 7 d. Conclusion Global cerebral ischemia reperfusion insult significantly in- duced an increase of the PGI2 level and the ratio of PGI2/TXA2 in rat cortex in a time dependent manner.