Abstract TP103: Brain Protection Effect By Exposure To Hydrogen Sulphide In Cerebral Infarct In Rat

Abstract

Introduction: Hydrogen sulphide (H2S) can regulate oxygen consumption by competing with O2 in binding to cytochrome C oxydase. At micro molar concentrations H2S interferes with antinecrotic and antiapoptotic mechanisms, including up regulation of cytoprotective genes. We studied the effect of H2S exposure on lesion and functional recovery after permanent middle cerebral artery occlusion (pMCAO) in rats. Methods: Young adult male and female Sprague- Dawley rats distributed into three groups: 1- Sham (control for craniotomy); 2-Control: Surgery + permanent MCAO; 3- Treated: Surgery + permanent MCAO + inhalation of 40 ppM hydrogen sulphide. We analyzed functional outcome (Rogers modified scale), lesion volume by MRI at 24h and 14 day and by hematoxyline-eosin, cell death by TUNEL, repair markers implicated in brain plasticity (cellular proliferation by BrdU, GFAP (glial fibrillar acis protein), VEGF (vascular endothelial growth factor), Synaptophysine) by western-blot and immunofluorescence at 14 days. Rats were sacrificed at day 14th. Results: Treated animals showed a benefit in functional outcome both at 24h (p = 0,004445) and sacrifice day (p = 0,000942). We observed a decrease in infarct size at day 14th on MRI (p= 0,0383 ) and in Hematoxyline Eosine infarct areas (p= 0.026672 ). At 24 hours there was no statistical difference on MRI (p= 0,380644). TUNEL analysis showed a decrease in the expression of marked cells in the perinfarct zone of treated animals (p= 0,048877). We did not observe significant differences in cellular proliferation (BrdU), GFAP, VEGF and synapthophysin levels between control and treated groups. Conclusions: Exposure to hydrogen sulphide in rats with cerebral infarct was effective in functional recovery associated to brain protection mechanisms with reduction in size volume and cell death and may be associated with reperfusion increased but not in repair effects.