It is suggested that the mechanism involved in physostigmine management of early alcohol withdrawal may lie in physostigmine induced beta-endorphin release.

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http://dx.doi.org/10.1016/0306-9877(89)90067-4DOI Listing

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  • The study investigates how intramuscular injections of two drugs, physostigmine and neostigmine, affect Na,K-ATPase activity in rat red blood cells after intense exercise.
  • Both drugs help reduce stress responses by lowering indicators such as adrenal ascorbic acid, stress-related red blood cell increases, and lipid peroxidation (LPO) markers.
  • The drugs appear to restore Na,K-ATPase activity affected by stress and can correct the functions of cholinergic systems in the body’s stress response mechanisms.
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Despite the advent of new treatment strategies, cholinesterase inhibitors (ChEIs) are still the go-to treatment for dementia disorders. ChEIs act by inhibiting the main acetylcholine-degrading enzyme, acetylcholinesterase (AChE). Nonetheless, accumulating evidence indicates that the impact of inhibition of the sister enzyme, butyrylcholinesterase (BChE), could be even broader in older adults due to the multifaceted role of BChE in several biological functional pathways.

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Introduction: Physostigmine is an effective antidote for antimuscarinic delirium. There is little evidence for its use to reverse delirium following second generation antipsychotic exposure. The purpose of this study is to describe the safety and effectiveness of physostigmine in reversing delirium from second generation antipsychotic exposure.

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Background: Flumazenil is a competitive benzodiazepine (BZD) antagonist most used for treating delirium in BZD overdoses. Since its introduction, many have expressed concerns about its safety secondary to the risk of inducing BZD withdrawal and refractory seizures.

Study Question: What is the incidence of adverse drug events after the administration of flumazenil in patients with suspected iatrogenic BZD delirium?

Study Design: This is a retrospective cross-sectional study of patients from a single center from 2010 to 2013.

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Prevailing hypotheses on the mechanisms of antidepressant action posit that antidepressants directly counteract deficiencies in major neurotransmitter signaling systems that underlie depression. The rapidly acting antidepressant ketamine has been postulated to correct excess glutamatergic signaling via glutamatergic antagonism leading to the rescue of neuronal structural deficits and reversal of behavioral symptoms. We studied this premise using systemic administration of the acetylcholinesterase inhibitor physostigmine, which has been shown to rapidly elicit a shorter-term period of depressed mood in humans via cholinergic mechanisms.

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