The Study Of Isosorbide Mononitrate Remission Cerebral Vasospasm After Subarachnoid Hemorrhage In Rat

Background and Purpose—: A reduction in the local availability of nitric oxide (NO) may play a role in the etiology of chronic cerebral after subarachnoid hemorrhage (SAH). We tested the ability of the long-acting, water-soluble, NO donor_isosorbide mononitrate and observed it influence on vasospasm and cerebral ischemia after SAH.Methods—: SAH was induced in rats via blood injection into the cisterna magna (300 μl).36 rats were randomly divided into four groups: normal group (group A); SAH group (group B); SAH+nimodipin group (group C); SAH+ isosorbide mononitrate group (group D). Doppler ultrasonography has used for monitoring rats' cerebral blood flow velocities every group after SAH. Levels of NO\NOS and cyclic guanosine monophosphate (cGMP) were measured in cerebral arteries on DAY 6.And to observe the expression of Bax/Bcl₂ protein and the ultrastructure of hippocampus.Results: Isosorbide mononitrate, as nimodipin can increase cerebral blood flow velocities after SAH; Level of NOS demonstrated with no significant difference in all four groups (P > 0.05, analysis of variance); Level of NO in D group was higher than other groups(P<0.05).The level of cGMP in D group was higher than B C groups and no statistic difference compared with A group. The expression of Bax was increased according to following order: A group>D group>C group>B group(P<0.05).Conclusion: Isosorbide mononitrate is able to improve chronic posthemorrhagic vasospasm after SAH via NO-cGMP mediated relaxation pathways. Isosorbide mononitrate plays a neuroprotective role in experimental cerebral ischemia after SAH.