Anticonvulsants post-exposure

GA GB GD GF VX Anticholinesterase agents. Pre-treatment with pyridostigmine. Post-exposure therapy Cholinergic blockage - atropine. Enzyme reactivation - oximes. Anticonvulsant - diazepam. Assisted ventilation. e. Suction for respiratory secretions. Occasional early transient tachycardia and/or hypotension followed by bradycardia and hypotension. 

Post-Exposure Therapy. The main principles of therapy for nerve agent poisoning are early treatment, assisted ventilation, bronchial suction, muscarinic cholinergic blockade (atropine), enzyme reactivation (2 Pam Chloride) and anticonvulsants (Diazepam). GD permanently binds to receptors in two minutes after that 2 PAM Cl is not useful. 

Traumatic brain injury, simulated by a model of closed head injury to mice, had also been shown to result in disruption of the BBB. The temporal resolution of this disruption was monitored by MRI in rats subjected to closed head injury. Blood-brain barrier disruption appeared immediately after the impact, and declined gradually, until full reversal to control levels 30 min post-injury. Opening of the BBB was similarly demonstrated in response to acute anticholinesterase exposure, however, low-level exposure has not yet been tested. BBB disruption under anticholinesterase exposure was proven to be seizure-dependent, as it could be blocked by the use of anticonvulsant agents. The anticholinesterase effect on BBB ultrastructure did not impair endothelial tight junctions. Yet, an increased number of endothelial vesicles were observed, suggesting increased transcytosis as the mechanism involved. ... 

---