Autor: |
Bitner BR; Interdepartmental Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, Houston, Texas, USA., Brink DC, Mathew LC, Pautler RG, Robertson CS |
Jazyk: |
angličtina |
Zdroj: |
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism [J Cereb Blood Flow Metab] 2010 Jun; Vol. 30 (6), pp. 1105-9. Date of Electronic Publication: 2010 Apr 07. |
DOI: |
10.1038/jcbfm.2010.47 |
Abstrakt: |
Traumatic brain injury (TBI) results in reduced cerebral blood flow (CBF) and low levels of the vasodilator nitric oxide (NO) may be involved. Arginase II negatively regulates NO production through competition for the substrate L-arginine. We determined whether arginase II-deficient (ArgII(-/-)) mice would show improved CBF after TBI through arterial spin-labeling magnetic resonance imaging (MRI). The ArgII(-/-) mice exhibit a significantly improved CBF recovery after trauma in the perilesional brain (P=0.0015) and in various other brain regions. In conclusion, arginase II deficiency leads to a better CBF recovery after TBI and implicates arginase II in hemodynamic processes. |
Databáze: |
MEDLINE |
Externí odkaz: |
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