Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

The effects of nitric oxide(NO) on the ischemic brain are thought to be dependent on the stage of the ischemic process. In the present study, we examined the time-course of NO production associated with transient cerebral ischemia. A microdialysis probe was inserted into the hippocampus. Levels of total NO metabolites(NOx-, NO2- plus NO3-) in dialysate were determined by the DAN(2,3-diaminoaphthalene) method and used as a marker of NO formation. Gerbils were subjected to various durations of bilateral carotid artery occlusion. Ischemia for 2 or 5 minutes did not induce a significant increase in NO production in the hippocampus, whereas the 10-min and 15-min ischemia produced significant and persistent increases in NO production. However, the magnitude of NO production following 20 min of ischemia was decreased. These findings suggest that NO production in the hippocampus after ischemia is dependent on the severity of ischemia. Since the production of NO in the hippocampus after 5 min of ischemia does not increase, it is unlikely that NO is involved in the vulnerability of the CA1 cells of the hippocampus after transient ischemia.

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Presentation Number SAlei0632
Keywords: Cerebral ischemia, Nitric oxide, Microdialysis, Hippocampus, Gerbils