Assessment of brain oxygenation imbalance following soman exposure in rats

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Authors
  1. Lee, K.
  2. Bohnert, S.
  3. Wu, Y.
  4. Vair, C.
  5. Mikler, J.
  6. Campbell Teskey, G.
  7. Dunn, J.F.
Corporate Authors
Defence Research and Development Canada, Suffield Research Centre, Ralston AB (CAN);Calgary Univ, Calgary ALTA (CAN)
Abstract
Nerve agents (NAs) are potent organophosphorus (OP) compounds with applications in chemical warfare. OP compounds act by inhibiting acetylcholinesterase (AChE). Soman (O-pinacolyl methyl- phosphonofluoridate) is one of the most potent NAs. It is well known that small doses of NAs can be lethal, and that even non-lethal exposure leads to long-term mental debilitation/neurological damage. However, the neuropathology following exposure to sub-lethal nerve agents is not well understood. In this study, we examined changes in tissue oxygenation (pO2) in the cortex and hippocampus after a sub-lethal dose of soman [80–90 mg/kg; subcutaneous]. pO2 changes can provide information regarding oxygen delivery and utilization and may be indicative of a disruption in cerebral blood flow and/or metabolism. Changes in oxygenation were measured with chronically implanted oxygen sensors in awake and freely moving rats. Measurements were taken before, during, and after soman-induced convulsive seizures. Soman exposure resulted in an immediate increase in pO2 in the cortex, followed by an even greater increase that precedes the onset of soman-induced convulsive seizures. The rise in hippocampus pO2 was delayed relative to the cortex, although the general pattern of brain oxygenation between these two regions was similar. After convulsive seizures began, pO2 levels declined but usually remained hyperoxygenated. Following the decline in pO
Keywords
Soman;Nerve Agents;Seizures;Oxygenation;Metabolism;Cerebral Blood Flow;Organophosphates;Organophosphours Compounds
Report Number
DRDC-RDDC-2018-P018 — External Literature
Date of publication
01 Feb 2018
Number of Pages
14
Reprinted from
Elsevier NeuroToxicology 65 (2018) 28 37
DSTKIM No
CA045874
CANDIS No
806328
Format(s):
Electronic Document(PDF)

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