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Related Experiment Videos

NOS inhibitors decrease hypoxia-induced ATP reductions in respiring cerebrocortical slices.

L Litt1, M T Espanol, K Hasegawa

  • 1Department of Anesthesia, Cardiovascular Research Institute, University of California, San Francisco 94143-0648, USA. llitt@post.harvard.edu

Anesthesiology
|May 13, 1999
PubMed
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Excessive neuronal nitric oxide (NO) production during brain hypoxia accelerates adenosine triphosphate (ATP) loss. Blocking NO synthase with L-NAME or 7-NI protected ATP levels and reduced cell damage in hypoxic brain slices.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Cellular Physiology

Background:

  • Excessive neuronal nitric oxide (NO) production is implicated in adenosine triphosphate (ATP) loss and cellular damage during brain hypoxia.
  • The role of NO in hypoxic brain injury was investigated in isolated cerebrocortical slices where NO scavenging is minimal.

Purpose of the Study:

  • To investigate the impact of nitric oxide synthase (NOS) blockade and augmentation on intracellular responses during hypoxia.
  • To determine the relationship between neuronal NO, ATP levels, and cellular damage in hypoxic brain tissue.

Main Methods:

  • 31P magnetic resonance spectroscopy was used to monitor ATP concentrations in respiring cerebrocortical slices under hypoxia (oxygen tension < 5 mmHg).
  • Slices were treated with NOS inhibitors (L-NAME, 7-NI, L-nitroarginine) or left untreated.

Related Experiment Videos

  • Nitrotyrosine:tyrosine ratios were measured by HPLC, and histological examination of Cresyl violet-stained sections was performed.

    • Main Results:

    • Hypoxia caused significant ATP reduction in untreated and L-nitroarginine-treated slices.
    • Pretreatment with L-NAME and 7-NI preserved ATP levels during hypoxia and facilitated recovery.
    • NOS inhibition reduced nitrotyrosine:tyrosine ratios and histological signs of cell swelling.

    Conclusions:

    • Neuronal NO contributes to rapid ATP depletion in acutely hypoxic brain slices.
    • Peroxynitrite formation, indicated by increased nitrotyrosine, is associated with NO during hypoxia.
    • Blocking NO synthase offers neuroprotection against hypoxic injury by preserving ATP and reducing cell damage.