Role of nitric oxide in the cerebrospinal fluid by subarachnoid hemorrhage and vasospasm
Keywords:
nitric oxide, nitrite, subarachnoid hemorrhage, cerebral vasospasm, cerebral spinal fluid, delayed cerebral ischemiaAbstract
The role of nitric oxide (NO) in the pathogenesis of delayed cerebral vasospasm (VS) and cerebral ischemia after subarachnoid hemorrhage (SAH) was investigated by analyzing the stable metabolites of NO — nitrite by Griess method in the cerebrospinal fluid (CSF) 45 patients with SAH compared with patients of nonruptured aneurysms. The levels of nitrite in CSF before surgery treatment and in CSF obtained daily from the cisternai drainage after surgery significantly increased with time and were higher than those of control patients, but in the patients with severe VS the levels nitrite transiently decreased on 4–9 days. Decreased levels nitrite in the CSF may be an indicator of the presence of VS and delayed ischemic complication due to SAH.References
Зозуля Ю.А., Сенько Л.Н. Церебральный вазоспазм после субарахноидальной геморрагии. Молекулярные аспекты эндотелиальной дисфункции // Укр. нейрохірург. журн. — 2001. — №1. — С.4–16.
Карпюк В.Б., Черняк Ю.С., Шубич М.Г. Лабораторный мониторинг состояния нитроксидергической вазорелаксации при субарахноидальном кровоизлиянии // Клин. лаб. диагностика. — 2000. — №5. — С.16–17.
Alabadi J., Torregrosa G., Miranda F. et al. Impairment of Modulatory Role of Nitric oxide on the Endothelin-1- elicited contraction of Cerebral Arteries: A Pathogenetic Factor in Cerebral Vasospasm after subarachnoid Hemorrhage // Neurosurgery. — 1997. — V.41, №1. — P.245–253.
Chang C-Z., Winardi D.,Lin C-L. et al. Attenuation of Hemolysate-Induced cerebrovascular Endothelial Cell Injury and of Production of Endothelin-1 and Big Endothelin-1 by an Endothelin-Converting Enzyme Inhibitor //Surg.Neurol. — 2002. —V.58, №3–4. — P.181–188.
Chehrazi B.B., Giri S., Joy R.M. Prostaglandins and vasoactive amines in cerebral vasospasm after aneurysmal subarachnoid hemorrhage // Stroke. — 1989. — V.20. — P. 217–224.
Dawson D.A. Nitric oxide and focal cerebral ischemia: Multiplicity of actions and diverse outcome // Cerebrovas. Brain Metab. Rev. — 1994. —№6. — P. 299–324.
Dawson T.M., Snyder S.H. Gases as biological messengers: nitric oxide and carbon monoxide in the brain // J.Neurosci. — 1994. — V.14. — P. 5147–5159.
Edvinsson L., Delgado-Zygmunt T., Ekman R. et al. Involvement of perivascular sensory fibers in the pathophysiology of cerebral vasospasm following subarachnoid hemorrhage // J. Cereb. Blood Flow Metab. — 1990. — V.10. — P.602–607.
Edwards D.H., Byrne J.V., Griffith S. The effect of chronic subarachnoid hemorrhage on basal endothelium — derived relaxing factor activity in intrathecal cerebral arteries // J.Neurosug. — 1992. — V.76. — P.830–837.
Faraci F.M., Brian J.E. Nitric oxide and cerebral circulation // Stroke. — 1994. — V.25. — P.692–703.
Faraci F.M., Brian J.F. 7-Nitroindozole inhibits brain nitric oxide synthase and cerebral vasodilatation in response to N–methyl–D–aspartate // Stroke. — 1995. — V.26. — P.2172–2175.
Faraci F.M., Heistad D.D. Regulation of the cerebral circulation: role of endothelium and potassium channels // Physiol. Rev. — 1998. — V.78, №1. — P.53–97.
Fisher C.M., Kistler J.P., Davis J.M. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computed tomographic scanning // Neurosurgery. — 1980. — V.6. — P.1–9.
Folley P.L., Takenaka K., Kassell N.F., Lee K.S. Cytotoxic effects of bloody cerebrospinal fluid on cerebral endothelial cells in culture // J.Neurosurg. — 1994. — V.81. — P. 87–92.
Green L.G., Wagner D.A., Glogowski J. et al. Analysis of Nitrate, Nitrite and [N15] Nitrate in Biological Fluids // Ann. Biochem. — 1982. — V.126. — P. 131–138.
Hatake K., Wakabayashi J., Kakishita E., Hishida S. Impairment of endothelium — dependent relaxition in human basilar artery after subarachnoid hemorrhage // Stroke. — 1992. — V.23. — P. 1111–1117.
Hino A., Tokuyama Y., Weir B. et al. Changes in endothelial nitric oxide synthase mRNA during vasospasm after subarachnoid hemorrhage in monkeys // Neurosurgery. — 1996. — 39. — P. 562–568.
Hunt W., Hess R.M. Surgical risk as related to time of intervention in the repair of intracranial aneurysm //J.Neurosurg. — 1968. — V.28. — P. 14–21.
Iadecola C. Bright and dark sides of nitric oxide in ischemic brain injury // Trends Neurosci. — 1997. — V.20, №1. — P. 132–139.
Ignarro L.J., Buga G.M., Wood K.S., Byrns R.E. Endothelium — derived relaxing factor produced and reeased from artery and vein is nitric oxide // Proc. Natl. Acad. Sci. USA. — 1987. — V.84. — P. 9265–9269.
Kajita Y., Takayasu M., Dietrich H., Dacey R. Possible Role of Nitric Oxide in Autoregulatory. Response in Rat Intracerebral Arterioles // Neurosurgery. — 1998. — V. 42, №4, — P. 834–842.
Koedel U., Bernatowicz A. Experimental pneumococcal meningitis: cerebrovascular alterations, brain — edema and meningeal inflammation are linked to the production of nitric oxide // Ann. Neurol. — 1995. — V.37. — P. 186–189.
Lin G., Macdonald R.L., Marton L.S. et al. Hemoglobin increases endothelin —1 inendothelial cells by decreasing nitric oxide // Biochem.Biophys. Res. Commun. — 2000. — V.280. — P.824–830.
Macdonald L.L., Weir R.K. A review of hemoglobin and the pathogenesis of cerebral vasospasm // Stroke. — 1991. — V.22. — P. 971–982.
Mathiesen T., Anderson B., Loftenius A.,van Holst H. Increased interleukin 6 levels in cerebrospinal fluid following subarachnoid hemorrage // J.Neurosurg. —1993. — V.78. — P.562–567.
Merrill J.E., Benveniste E.N. Cytokines in inflammatory brain lesions: Helpful and harmful // Trends Neurosci. — 1996. — V.19. — P. 331–338.
Nozaki K., Moskowitz M., Maynard K.J. et al. Possible origins and distribution of immunoreactive nitric oxide synthase — containing nerve fibers in cerebral arteries // J. Cereb. Blood Flow Met. — 1993. — V.13. — P. 70–79.
Ono S., Komuro T., Macdonald R.L. Heme oxygenase — 1 therapy for prevention of vasospasm in rats // J.Neurosurg. — 2002. — V.96. — P. 1094–1102.
Onoue H., Kaito N., Akiyama M. et al. Altered reactivity of human cerebral arteries after subarachnoid hemorrhage // J. Neurosurg. — 1995. — V.85. — P. 510–515.
Pluta R.M., Thompson B.G., Dawson T.M. et al. Loss of nitric oxide synthase immunoreactivity in cerebral vasospasm // J. Neurosurg. — 1996. — V.84. — P. 648–654.
Ratsep T., Asser T. Cerebral hemodynamic impairment after aneurysmal subarachnoid hemorrhage as evaluated using transcranial Doppler ultrasonography: relationship to delayed cerebral ischemia and clinical outcome // J. Neurosurg. — 2001. — V.95. — P. 393–401.
Suzuki M., Asahara H., Endo S. et al. Inereased levels of nitrite/nitrate in the cerebrospinal fluid of patients with subarachnoid hemorrhage // Neurosurg. Rev. — 1999. — V.22, №2–3. — P. 96–98.
Suzuki S., Kassell N.F., Lee K.S. Hemin activation of an inducible isoform of nitric oxide synthase in vascular smooth — muscle cells // J. Neurosurg. — 1995. — V.83. — P. 862–866.
Suzuki Y., Osuka K., Noda A. et al. Nitric Oxide Metabolites in the Cisternal Cerebral Spinal Fluid of Patients with Subarachnoid Hemorrhage // Neurosurgery. — 1997. — V.41, №4. — P. 807–812.
Toda N., Ayajika K., Okamura T. Cerebroarterial relaxations mediated by nitric oxide derived from endothelium and vasodilator nerve // J. Vasc. Res. — 1993. — V.30. — P. 61–67.
Zuccarello M., Romano A., Passalacqua M., Rapoport R.M. Decreased endothelium — dependent relaxation in subarachnoid hemorhage-induced vasospasm. Role of ET–1 // Amer. J. Physiol. — 1995. — V.269. — P. 1009–1015.
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