Background. After the discovery that nitric oxide (NO) plays a major role in the regulation of vascular tone, this substance moved into the focus of interest with regard to vasospasm after subarachnoid haemorrhage (SAH). A multitude of interactions were discovered and some concepts of therapeutic intervention were developed.
Method. The present review is based on a Medline search with the terms “nitric oxide” and “subarachnoid haemorrhage”.
Findings. SAH and particularly liberated oxyhaemoglobin sequestrate the physiologically produced NO. Reactivity to NO appears to be principally preserved. As other types of injury, SAH leads to induction of inducible NO synthase (iNOS). The NO produced by this pathway cannot compensate for the lack of the physiological NO and may even lead to tissue damage by oxidative stress. Experimental therapeutic attempts use stimulation of NO production and delivery of NO donors. NO donors were also used in some small clinical trials. A final assessment of efficacy and safety is not yet possible.
Conclusion. NO physiology and pathophysiology are important in the genesis of vasospasm after subarachnoid haemorrhage. NO directed therapeutic strategies enlarge the spectrum of available instruments, but complete elimination of the problem of vasospasm cannot be expected.
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