http://www.springerlink.com/content/y000866m06750526/
Abstract
It
was recently discovered that while under normal conditions inhaled
nitric oxide (iNO) does not affect cerebral blood flow,
it selectively dilates arterioles in the ischemic penumbra
during experimental cerebral ischemia, thereby increasing collateral
blood flow and reducing ischemic brain damage. The mechanism
was verified in multiple models, but only in male animals. Our
aim was to evaluate the effects of iNO on brain injury in
neonatal males and females. Nine-day-old mice were subjected to
unilateral hypoxia–ischemia (HI), using 10 % oxygen balanced
with nitrogen, with or without 50 ppm NO. Brain injury 72 h after
HI was reduced by iNO as judged by percentage of injury
(−21.7 %), atrophy (−23.7 %), and total pathological score (−29 %).
The injury was significantly reduced in males (−32.4 %, p
< 0.05) but not in females (−7.1 %, n.s.). Neither the numbers nor
the proliferation rates of neural stem cells in the dentate
gyrus were affected by iNO. In summary, intraischemic iNO
reduced neonatal HI brain injury in a gender-related manner.
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