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September2004 Vol.41 Issue:        3       (Supp.) Table of Contents
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Endothelin-1 and Nitric Oxide: Relation to Delayed Spasm and Neurological Deterioration in Subarachnoid Hemorrhage

Abdel Rahman A Hassan1, Adham M Ismael1, Magdi A Eidaros1, Khadiga E EI-Shahidy2

 

Departments of Neurology1, Clinical Pathology2, Zagazig University



ABSTRACT

Cerebral vasospasm and the resulting cerebral ischemia occurring after subarachnoid hemorrhage (SAH) are still responsible for the considerable morbidity and mortality in patients affected by cerebral aneurysm. Cerebral vasospasm caused by several mechanisms, of which is the interaction between vasoconstrictor and vasodilator substances. The aim of this work was to study endothelin-1(ET-1) as a potent vasoconstrictor and nitric oxide (NO) as a potent vasodilator in patients with SAH and study their relation to cerebral vasospasm and clinical neurological deterioration.Thirty patients suffering from SAH were included in the study and divided into two groups according to presence or absence of cerebral spasm in addition to 10 healthy subjects as control. The patients were subjected to neurological examination and Glasgow Coma Scale (GCS). MRA was done and plasma ET-1 and serum NO were assessed at 2 weeks of the onset of SAH.The results showed increase plasma ET-1 in SAH, and its level was highest in presence of vasospasm than in absence of vasospasm or in healthy controls (mean value ± SD was 5.17 ± 2.22, 3.18 ± 1.24 and 1.06 ± 0.46 pg ∕ ml respectively). NO was significantly lower in patients with vasospasm than those without vasospasm and both are lower than control (mean value ± SD 1.83 ± 0.66, 2.42 ± 0.79 and 3.36 ± 0.57 µM respectively). As regard correlation studies ET-1 was negatively correlated with GCS and NO level and positively correlated with vasospasm, while NO was negatively correlated with vasospasm and ET-1 and not correlated with GCS.We concluded that ET-1 and NO may play an important role in cerebral vasospasm and ET-1 may be responsible for neurological deterioration in patients with aneurysmal SAH.

(Egypt J. Neurol. Psychiat. Neurosurg., 2004, 41 (3) suppl.: 895-901).

 





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