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Nitric oxide and cerebral blood flow: an update
1Gough-Cooper Department of Neurological Surgery, Institute of Neurology, London, England.
Cerebrovascular and Brain Metabolism Reviews
|January 1, 1995
Summary
A basal level of nitric oxide (NO) is essential for biological processes, but too much can be harmful. This review highlights the critical role of NO in conditions like vasospasm and atherosclerosis, contrasting with previous focus on its detrimental effects.
Area of Science:
- Biomedical Science
- Neuroscience
- Cardiovascular Science
Background:
- Nitric oxide (NO) plays a dual role in biological systems, with basal production being essential but excess levels proving cytotoxic.
- Previous research has primarily focused on the detrimental effects of excessive NO in conditions such as ischemia and neurodegeneration.
- Emerging evidence suggests that diminished NO or impaired NO signaling is significant in vasospasm post-subarachnoid hemorrhage, aging, and atherosclerosis.
Purpose of the Study:
- To contrast the established detrimental effects of excess nitric oxide (NO) with the emerging significance of diminished NO.
- To highlight the importance of NO's dual role in various physiological and pathological conditions.
- To explore the potential for targeted clinical interventions based on NO's specific actions.
Main Methods:
- Literature review focusing on studies of ischemia, neurodegeneration, vasospasm, subarachnoid hemorrhage, aging, and atherosclerosis.
- Analysis of the contrasting roles of nitric oxide (NO) in different pathological contexts.
- Exploration of therapeutic strategies targeting nitric oxide synthase (NOS) isoforms or NO redox states.
Main Results:
- Excess nitric oxide (NO) can be cytotoxic, a factor often emphasized in ischemia and neurodegeneration.
- Diminished NO or interference with its action is increasingly recognized as crucial in vasospasm following subarachnoid hemorrhage, aging, and atherosclerosis.
- The protective or detrimental effects of NO are highly dependent on its timing, source, and distribution.
Conclusions:
- Understanding the complex, context-dependent role of nitric oxide (NO) is vital for clinical applications.
- Future therapeutic interventions in cerebral ischemia require specificity, targeting distinct NO production pathways or redox forms.
- Modulating NO signaling offers potential for treating conditions like vasospasm, atherosclerosis, and neurodegenerative diseases.