Nootropic.
Pharmacology: Pharmacodynamics: Piracetam acts on the CNS and has been described as a "nootropic", it is said to protect the cerebral cortex against hypoxia. It is also reported to inhibit platelet aggregation and reduce blood viscosity at high doses.
Piracetam binds physically in a dose-dependent manner to the polar head of phospholipids membrane models, inducing the restoration of the membrane lamellar structure characterized by the formation of mobile drug-phospholipid complexes. This accounts for an improved membrane stability, allowing the membrane and transmembrane proteins to maintain or recover the three-dimensional structure or folding essential to exert their function.
Piracetam has neuronal and vascular effects.
Neuronal effect: Piracetam protects and restores cognitive abilities in animals and man after various cerebral insults such as hypoxia, intoxications and electroconvulsive therapy. It protects against hypoxia-induced changes in brain function and performance assessed by electroencephalograph (EEG) and psychometric evaluations.
Vascular effect: Piracetam applies its hemorrhagic effect to thrombocytes, erythrocytes and the walls of the blood vessels by increasing the deformability of erythrocytes, reducing the aggregability of thrombocytes, reduces the adhesion of erythrocytes to the walls of vessels and reduces capillary vasospasm.
Pharmacokinetics: Absorption: Piracetam is rapidly and extensively absorbed from the gastrointestinal tract; peak plasma concentrations are reached within 1.5 hours after oral doses. The absolute bioavailability of piracetam is close to 100%. Food does not affect the extent of absorption of piracetam but it decreases Cmax by 17% and increases Tmax from 1 to 1.5 hours.
Distribution: Piracetam is not plasma protein bound and volume distribution is 0.61/kg. Piracetam crosses the blood brain barrier (BBB) and it has been measured in cerebrospinal fluid (if administered intravenously); Piracetam diffuses to all tissues except adipose tissues, crosses placental barrier and penetrates the membranes of isolated red blood cells.
Metabolism: Piracetam is not known to be metabolized in the human body. The lack of metabolism explains the lengthy plasma half-life in anuric patients and high recovery of parent compound in urine.
Elimination: The major route of excretion is via urine, accounting for 80% to 100% of the dose. Piracetam is excreted by glomerular filtration.
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