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Direct binding of eNOS to the scaffolding domain of Cav-1 is a well-accepted mechanism to repress eNOS activity that is associated with endothelial dysfunction and cardiovascular disease 39,40

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Top panels illustrate mechanisms of action: atropine (2.1 mg) competitively antagonizes acetylcholine at muscarinic receptors to reverse cholinergic effects (e.g., bronchorrhea, bronchospasm, bradycardia), while pralidoxime (2PAM, 600 mg) reactivates acetylcholinesterase by cleaving the nerve agentenzyme bond prior to irreversible aging. Middle panels depict the dualchamber autoinjector design, which contains atropine and pralidoxime in separate compartments and delivers both drugs sequentially via a springloaded intramuscular mechanism from a single needle