1997 Fiscal Year Final Research Report Summary
Nitric oxide in the development of vasospasm after subarachnoid hemorrhage
| Project/Area Number |
07671509
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Nagoya University |
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Principal Investigator |
SUZUKI Yoshio Nagoya University School of Medicine, Associate professor, 医学部, 助教授 (80171271)
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| Co-Investigator(Kenkyū-buntansha) |
NAGATANI Tetuya Nagoya University School of Medicine, Clinical accociate, 医学部, 医員
HARA Masato Nagoya University School of Medicine, Clinical associate, 医学部, 医員
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| Project Period (FY) |
1995 – 1997
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| Keywords | subarachnoid hemorrhage / vasospasm / nitric oxide / cytokine |
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| Research Abstract |
The nitric oxide (NO) metabolism in the brain is stimulated from the acute stage after subarachnoid hemorrhage (SAH), and continued until the chronic stage. The high concentration of NO metabolites in the CSF probably reflects elevated metabolism in the vascular as well as the nervous system, inasmuch as NO is a signal mediator in various vasacular and nervous functions. The amount of bleeding in the subarachnoid space may be an important factor that stimulates NO metabolism, although the patients' preoperative conditions, the presence of symptomatic vasospasm, or patients' prognosis are not correlated. The activity of NO synthase and NO synthase mRNA in the spastic vessels tended to decrease during the chronic stage. Recent evidence has demonstrated that the significant increase in endothelial and neuronal NO synthase mRNA in the brain tissue suppied by vessels in vasospasm occurs as a compensatory phenomenon in the chronic stage after SAH.This result may indicate that the activity of constitutive isoforms of NO synthase in brain parenchymal tissue and microvessels increases to compensate for the vasospasm-induced reduced regional cerebral blood flow. Nitrate is the dominant NO metabolite in CSF after SAH,probably indicating that hemoglobin can absorb NO with high affinity. The concentrations of inflammatrory cytokines, interleukin-1beta, interleukin-6 and interleukin-8, in CSF are also elevated from the acute stage after SAH.However, the involvement of inducible NO synthase in the pathophysiology of NO metabolism after SAH was not clearly suggested.
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