1 / 2

Hydrogen sulfide and meningitis

Hydrogen sulfide and meningitis .

mercer
Download Presentation

Hydrogen sulfide and meningitis

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Hydrogen sulfide and meningitis Supplemental Digital Content 2. The subarachnoid space and adjacent brain is depicted. Bacteria (blue cocci) take up cysteine (Cys) from cerebrospinal or interstitial fluid, which is further enriched by phagocytes (polymorphonuclearneutrophils (PMN), monocytes, microglia) exporting Cys into their extracellular environment when activated. Bacteria metabolize Cys through one of 3 metabolic pathways (CBS, CSE, 3MST – see discussion) to elaborate H2S, a toxicant gas that diffuses freely. A gradient of H2S gas (green) is depicted permeating CSF, brain tissue and blood vessels. H2S inactivates the oxidative burst of polymorphonuclear (PMN) cells and kills all cells (phagocytes, glia, neurons) within a defined radius. Within neuronal mitochondria, the terminal cytochrome c oxidase complex (E) uses H2S as a poor substrate. H2S also binds the intermediate state (E*) to inhibit electron transport non-competitively and reversibly. Sites of action of other gases (HCN, CO, NO and O2) are also depicted, with kind permission from Springer Science+Business Media from reference 6, Figure 1. Within the radius of high concentrations of H2S, mitochondrial respiration ceases in all resident cells and necrosis ensues. Within vessels, H2S acts similarly to NO on vascular smooth muscle, causing dilatation. At high levels of H2S, refractory dilatation occurs. During treatment for H2S intoxication, hyperbaric oxygen directly oxidizes H2S and also boosts cytochrome c oxidase activity, restoring mitochondrial function and also consuming H2S as substrate. Dipyridamole potentiates production of nitric oxide (NO), which spontaneously, and through interaction with hemoglobin, decomposes to nitrite (NO2-) and nitrate. Nitrite, generated endogenously or administered, interacts with H2S to form NO, and also causes methemoglobin (metHb) formation. MetHb actively scavenges H2S to form sulfmethemoglobin.

  2. Activated monocyte Arachnoid mater Pia mater H2S HCN NO CO H2S Cys S H2S H2S producing bacteria Neuron: E E*ER H20 02 Cys H2S Activated PMN Cys Vascular smooth muscle Activated microglia NO Hyperbaric oxygen Dipyridamole, or Nitrite (NO2-) NO2- Endothelial cell metHb S-metHb

More Related