Endothelial Nitric Oxide Synthase (eNOS) Mediates the Cerebrovascular Effects of Erythropoietin in Traumatic Brain Injury

Frontiers in Immunology

Jerry Clay Goodman¹  Claudia S. Robertson¹  Jovany eCruz Navarro¹  Lucido I Ponce¹  Shibu ePillai¹  Mai eVan¹ 

[1] Baylor College of Medicine;

关键词: Erythropoietin;    Nitric Oxide;    Nitric Oxide Synthase;    Neuroprotection;    Traumatic Brain Injury;    cerebral blood flow (CBF);   

DOI  :  10.3389/fimmu.2014.00494

来源: DOAJ

【 摘 要 】

Background: Erythropoietin (Epo) improves post-traumatic cerebral blood flow (CBF), pressure auto-regulation, and vascular reactivity to L-arginine. This study examines the dependence of these cerebral hemodynamic effects of Epo on nitric oxide (NO) generated by endothelial nitric oxide synthase (eNOS). Methods: Using laser Doppler flow imaging, CBF was monitored in wild-type (WT) and eNOS-deficient mice undergoing controlled cortical impact (CCI) followed by administration of Epo (5000 U/kg) or normal saline. Results: CBF decreased in all groups post-injury with the greatest reductions occurring at the impact site. Epo administration resulted in significantly higher CBF in the peri-contusional sites in the WT mice (70.2 ± 3.35 % in Epo-treated compared to 53 ± 3.3 % of baseline in saline-treated mice (p< .0001), but no effect was seen in the eNOS-deficient mice.No CBF differences were found at the core impact site where CBF dropped to 20-25% of baseline in all groups. Conclusion: These differences between eNOS-deficient and WT mice indicate that the EPO mediated improvement in CBF in TBI is eNOS dependent.

【 授权许可】

Unknown