Role of nitric oxide in cerebral ischemia reperfusion injury in rats

Objective To explore the role of nitric oxide (NO) in the brain injury in the rat model of reperfusion 20 min after cerebral ischemia. Methods Eighty four male Wistar rats (weight 220±20 g) were randomized into control group ( n =12) and ischemia group ( n =72). The rats of ischemia group were established with Pulsinelli's method and killed at the time points of 8, 24, 48, 72, 96, 168 h after reperfusion. The neuron specific enolase (NSE) level in serum, the NO content and the pyramidal neuron (PN) density of CA1 area in the hippocampus were determined respectively. Results ①The NO content in the hippocampus increased significantly at the 48th h ( P 0.01), reached a peak at the 72nd h ( P 0.01), decreased gradually from the 96th h ( P 0.05) and fell to the level of control group at the 168th h after reperfusion. ②The NSE level in serum was significantly higher in ischemia group at every time points than in control group ( P 0.01). ③The PN density in CA1 area of the hippocampus decreased in ischemia group and was significantly lower in this group than in the control ( P 0.01). It was only 22.8% of that of the control at the 168th h after reperfusion. ④In ischemia group, the NO content in the hippocampus had linear correlation with the change of the serum NSE level ( r =0.9022, P 0.01). Conclusion NO plays an important role in cerebral ischemia reperfusion and is an important factor which contributing to delayed neuronal death in CA1 area of the hippocampus.