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The key role of the Cerebrospinal Fluid (CSF) in solute transport and clearance through the brain makes it an interesting way to deliver new therapeutic agents, by avoiding the complicated passage of the Blood Brain Barrier (BBB). Organophosphorus intoxication may lead to BBB breakdown, neuroinflammation and cellular damage within the brain, initially as a consequence of Cholinesterase Inhibition (ChE). In this pilot study, a swine model of paraoxon intoxication has been used to prove the existence of ChE activity within the CSF and early brain inflammation. This CSF ChE activity is strongly inhibited following exposure to paraoxon. We also provide evidence that despite the lack of brain immune cells activation 6 hours after poisoning, vascular cells adhesion molecule is expressed by endothelial cells. This is the first time that CSF ChE activity is described in a large animal model. The role and origin of ChE in the CSF remains unclear and has to be explored. This finding can be useful to develop new therapeutic strategies to offset post intoxication brain cholinesterase inhibition. Vascular inflammation should be considered and cured to avoid related post intoxication brain disorder.

hsoa journal of toxicology

Organophosphorus Compound Poisoning: Initial Data Providing Evidence Of The Presence Of Cholinesterase Within The Cerebrospinal Fluid And Early Neurovascular Inflammation