The protective role of nitric oxide in the brain ischemia

A role of nitric oxide in ischemia/reperfusion (I/R) injury of brain in nor motensive (Sprague-Dawley rats, SD) and stroke-prone spontaneously hyperten sive rats (SHR-SP) was studied. Cerebral ischemia was produced in rats by o cclusion of the middle cerebral artery (MCA). NO and O-2(-) releases in the brain in response to MCA occlusion followed by reperfusion were simultaneo usly monitored (2h) using electrochemical microsensors. The size of infarct was evaluated in the course of I/R from images of brain slices stained wit h 2,3,5-triphenyltetrazolium chloride. Similar patterns of NO and O-2(-) re leases were exhibited for SD and SHR-SP rats in the entire course of the ex periments. However, the concentration of NO release was significantly lower during I/R in SHR-SP than in SD rats (the maximal NO concentration was 2.6 1 +/- 0.22 mu mol/L for SD and 1.51 +/- 0.16 mu mol/L for SHR-SP rats; *P < 0.01). In contrast, the concentration of O-2(-) release during cerebral is chemia was significantly higher in SHR-SP than SD rats (the maximal increas e was 122 +/- 24 nmol/L for SD and 220 +/- 44 nmol/L for SHR-SP rats; *P < 0.01). The infarct sizes revealed in the course of I/R were larger in SHR-S P than SD rats (1.8 +/- 0.4% vs. 1.1 +/- 0.4% at 30 min., 2.84 +/- 0.8% vs. 2.21 +/- 0.6% at 100 min. and 9.20 +/- 1.1% vs. 5.8 +/- 0.6% at 180 min. o f the brain weights, respectively; *P < 0.01 for each time-point). These st udies indicate that nitric oxide plays a protective role during I/R and def iciency of NO in SHR-SP rats is due to excess of O-2(-) production. The def iciency in NO concentration correlates positively with the increase of cere bral I/R injury.