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The Effect of Hydrogen Sulphide on Experimental Cerebral Vasospasm
AIM: Cerebral vasospasm is the primary cause of morbidity and mortality
after subarachnoid hemorrhage (SAH). Hydrogen Sulfide (H2S), a gaseous
neurotransmitter, is produced in many tissues including the central
nervous system (CNS). The vasodilatatory effect of H2S has been shown in
the CNS; however, its role in cerebral vasospasm has not been
investigated before.
MATERIAL and METHODS: The rats were divided into 8 groups: control, SAH,
sodium hydrosulphide (NaHS), propargylglycine (PPG), aminooxy acetic
acid (AOAA), SAH+NaHS, SAH+PPG, and SAH+AOAA. After establishing
experimental SAH, the basilar artery and brain stem were harvested at
24th hours. The diameter and wall thickness of basilar artery were
measured. Production of H2S was assessed by showing the activity of
cystathionine beta-synthase (CBS) and cystathionine gamma-lyase enzymes
(CSE).
RESULTS: NaHS treatment significantly reduced vasospasm at 24 hours
following SAH. This vasodilatatory effect was correlated with the CSE
expression in basilar artery. CSE and CBS enzyme expressions were
significantly lower in brain stem and basilar artery in PPG and
AOAA-treated groups. PPG and AOAA treatments exerted a vasoconstrictive
effect in the basilar artery. There were statistically significant
differences between NaHS, PPG and AOAA groups, in terms of basilar
artery lumina! diameter.
CONCLUSION: H2S may have a therapeutic potential in the treatment of
vasospasm with its vasodilatator activity