Beneficial effects of a ketamine/atropine combination in soman-poisoned rats under a neutral thermal environment

Cholinesterase reactivators and bioscavengers for pre‐ and post‐exposure treatments of organophosphorus poisoning

“…The purpose of delayed treatment is to inactivate remaining OP molecules present in the bloodstream, to reactivate inhibited AChEs, to stop seizures with specific drugs like ketamine (Barbier et al . ) and prevent brain damage and other neurologic damage. Delayed post‐exposure therapy implies administration of oximes and anti‐muscarinic drugs for several hours (Ben Abraham et al .…”

Naloxone Antagonizes Soman‐induced Central Respiratory Depression in Rats

“…Urethane was chosen due to a lack of known specific receptor interactions in the central nervous system (CNS) of the anaesthetized rodents, although it was proven to block both clinical and electroencephalographic seizures induced by the electrical stimulation of the amygdala and by pentylenetetrazol . Other anaesthetic agents, such as pentobarbital and ketamine, were avoided to eliminate the negative cardiovascular effects of the former and the interference with the glutamate receptors of the latter one , as both the N‐methyl‐D‐aspartate (NMDA) and non‐NMDA receptor were shown to stimulate phrenic motoneurons in rats . Although it was previously said that organophosphate‐induced seizures and central respiratory depression coincide, it is obvious that in the present experiments, soman induces central respiratory depression also in urethane‐anaesthetized rats.…”

“…It is well known that the toxic doses of cholinesterase inhibitors affect the respiratory function in a complex manner and that respiratory failure precedes cardiovascular collapse . The mounting level of acetylcholine in the cholinergic synapses that follows the acetylcholinesterase (AChE) inhibition produces overstimulation of muscarinic and nicotinic cholinoceptors in the central nervous system and elsewhere . Peripheral muscarinic receptor overstimulation results in bronchoconstriction and bronchorrhea , while the excessive stimulation of the nicotinic receptors at the neuromuscular junction induces the fasciculations and Wedensky‐type depolarization blockade .…”

Ketamine for the treatment of (super) refractory status epilepticus? Not quite yet

“…Interestingly, ketamine, in combination with atropine and a benzodiazepine, appears a good candidate for the outof-hospital treatment of severe nerve agent-induced SE [10]. The ketamine/atropine combination also exhibited beneficial therapeutic effects in intoxicated rats such as a limitation of convulsion-induced hyperthermia [11]. At the time the 2013 review was published [5], it was clear that more and more clinicians were advocating that ketamine should be considered earlier in the management of RSE.…”