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Mucolytic.
Pharmacology: Fluimucil/A has an intense fluidifying action, through its free sulfhydryl group, on mucoid or mucopurulent secretions by clearing the disulfide bonds in glycoprotein aggregates. Fluimucil/A makes it easy to cough the viscous secretion up. In this way, the respiratory airways in acute and chronic bronchitis, as well as bronchial asthma, quickly become free, and the patient can breathe more easily.
Mucokinetic Actions: Mucolytic: Breaks disulfide bridges of mucoprotein.
Emetic-Expectorant: Stimulates gastropulmonary vagal reflex.
Bronchorrheic: Stimulates mucosal secretion.
Mucoregulator: Biochemical normalizing effect on secretory cells.
Chelation: Disrupts ionic binding of calcium in mucoprotein.
Antioxidant: Prevents airway damage by scavenging effect.
Non-Mucokinetic Actions: In addition, Fluimucil/A can promote one of the body's own detoxification mechanisms, the glutathione system, and thus protect the lung tissue against harmful inhaled substances.
Antidote Acetaminophen Poisoning: Poisoning can be followed by hepatic necrosis that results from excess acetaminophen being converted into alkylating compounds that depletes glutathione or damage hepatic cell membranes. NAC is thought to serve as a precursor for glutathione synthesis but it may also form complexes with the toxic, reactive metabolites of acetaminophen, which bind to proteins and enzymes thus causing hepatic cell necrosis.
NAC has been employed to prevent the hemorrhagic cystitis that result from the administration of alkylating agents eg, isophosphamide and cyclophosphamide; this depends on the ability of NAC to scavenge free radicals that are liberated by the chemotherapy drugs.
Pharmacokinetics: Acetylcysteine is stable in stimulated gastric and intestinal fluid. It is rapidly absorbed after oral administration and distributed to body tissue, the lung. It is subsequently excreted by the tracheobronchial mucosa and it then has a mucolytic effect on the respiratory secretions.
