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At least 19 recordsLinked to original sources
PubMed1985

Quantitative EEG and neuropsychological effects of piracetam and of the association piracetam-lecithin in healthy volunteers.

The electroencephalographic (EEG) and neuropsychological effects of single, oral doses or piracetam (800-6,400 mg) and of its association with lecithin (4,800 mg and 25 g, respectively) were investigated in two groups of healthy volunteers in placebo-controlled studies. The EEG was quantified by power spectral analysis; both parametric and nonparametric procedures were applied to process the EEG and neuropsychological data statistically. The drug plasma concentration was assessed (gas chromatography) in concomitance with the EEG and neuropsychological measurements. Piracetam was found to elicit systematic EEG effects, namely a decrease in the low-frequency components and an increase in the power of the 8.5- to 12.0-Hz and of the fast-frequency components. The EEG modifications were restricted to the anterior scalp areas; its detection by means of parametric statistics was conditioned by the relevant individual variability and was inferred resting upon a number of criteria (indication at nonparametric tests, topography, consistency across subjects, replicability, etc). The correlation between EEG changes and drug plasma concentration was ambiguous, and the compound was not found to be effective on any of the neuropsychological variables considered. The study exemplifies some of the methodological problems in quantitative pharmaco-EEG and emphasizes the relevance of topography and replication.

Brain↗
PubMed1983

Compliance testing by measurement of piracetam in urine--a possible method of compliance control for piracetam intakers. An empirical investigation.

All teams of investigators concerned with compliance rate have come to the conclusion that one can seldom rely on patients to take their tablets as prescribed. In case of long-term medication the problem becomes even more acute. A method for checking on compliance is, therefore, of great help in controlling medical therapy as well as in judging the effectiveness of pharmaceuticals. The results of this study imply that diachronic determination of piracetam concentration in patients' urine is an especially simple way of testing compliance without undue strain on the patient.

Adult↗
PubMed1981

Profound effects of combining choline and piracetam on memory enhancement and cholinergic function in aged rats.

In an attempt to gain some insight into possible approaches to reducing age-related memory disturbances, aged Fischer 344 rats were administered either vehicle, choline, piracetam or a combination of choline or piracetam. Animals in each group were tested behaviorally for retention of a one trial passive avoidance task, and biochemically to determine changes in choline and acetylcholine levels in hippocampus, cortex and striatum. Previous research has shown that rats of this strain suffer severe age-related deficits on this passive avoidance task and that memory disturbances are at least partially responsible. Those subjects given only choline (100 mg/kg) did not differ on the behavioral task from control animals administered vehicle. Rats given piracetam (100 mg/kg) performed slightly better than control rats (p less than 0.05), but rats given the piracetam/choline combination (100 mg/kg of each) exhibited retention scores several times better than those given piracetam alone. In a second study, it was shown that twice the dose of piracetam (200 mg/kg) or choline (200 mg/kg) alone, still did not enhance retention nearly as well as when piracetam and choline (100 mg/kg of each) were administered together. Further, repeated administration (1 week) of the piracetam/choline combination was superior to acute injections. Regional determinations of choline and acetylcholine revealed interesting differences between treatments and brain area. Although choline administration raised choline content about 50% in striatum and cortex, changes in acetylcholine levels were much more subtle (only 6-10%). No significant changes following choline administration were observed in the hippocampus. However, piracetam alone markedly increased choline content in hippocampus (88%) and tended to decrease acetylcholine levels (19%). No measurable changes in striatum or cortex were observed following piracetam administration. The combination of choline and piracetam did not potentiate the effects seen with either drug alone, and in certain cases the effects were much less pronounced under the drug combination. These data are discussed as they relate to possible effects of choline and piracetam on cholinergic transmission and other neuronal function, and how these effects may reduce specific memory disturbances in aged subjects. The results of these studies demonstrate that the effects of combining choline and piracetam are quite different than those obtained with either drug alone and support the notion that in order to achieve substantial efficacy in aged subjects it may be necessary to reduce multiple, interactive neurochemical dysfunctions in the brain, or affect activity in more than one parameter of a deficient metabolic pathway.

Acetylcholine↗
PubMed1977

[Pharmacokinetic of piracetam during labour influence to acid-base-status in maternal and fetal blood (author's transl)].

PIRACETAM concentrations in fetal and maternal blood were measured during the first and second stage of labor and the elimination in maternal and fetal blood was studied. Fetal heart-rate, pH- and base-excess of the maternal and fetal blood were investigated to evaluate the influence of PIRACETAM on the acid-base-status of mother and child. PIRACETAM was administered intravenously to 43 patients in a dosage 2 g, 4 g and 6 g. The concentration in the maternal and fetal plasma was measured by gaschromatography. Before and after the injection of PIRACETAM and at delivery, blood was sampled from the mother's earlobe and the umbilical artery and vein, respectively. The results were compared with a control group. There was an exponential fall of PIRACETAM concentration in maternal and fetal blood. Maternal and fetal elimination half-life of PIRACETAM was about 112-98 minutes and 200 minutes, respectively. A fairly good correlation between the concentration of PIRACETAM in maternal and fetal blood was found. The fetal PIRACETAM concentration was about 50% below the maternal values. Fetal heart-rate, maternal and fetal pH- and base-excess-values were not significantly altered following PIRACETAM infusion. It may be concluded, that there exists a transfer of PIRACETAM across the placental barrier. However, the cytoprotective effect of PIRACETAM, as described in animal observations and by investigations in human, could not be verified by the methods and technology used in this study.

Acid-Base Equilibrium↗
PubMed1991

[The significance of quantified EEG in Alzheimer's disease. Changes induced by piracetam].

One study was performed in 12 patients with presenile Alzheimer's disease (group I), the other one in 16 patients with mild senile dementia of Alzheimer type (group II). In each study, patients were divided into two randomized parallel groups, one receiving placebo, the other piracetam (9 g daily in group I piracetam and 2.4 g daily in group II piracetam) during three months, piracetam induced a decrease in EEG power on the 2-6 Hz range (group I piracetam), 3-5 Hz and 7 Hz (group II piracetam) and an increase of EEG power in the 9-11 Hz range (group I piracetam) and in the 10 Hz and 13 Hz frequencies (group II piracetam). There was also a significant improvement in the Trail Making Test part A in group II piracetam. Correlations between decreased EEG low frequency components and improvement in some psychometric tests were found significant in the two groups. It seems that the main effect of piracetam was to induce increased alertness. The same results were found in both studies; the good reproducibility suggests that EEG spectral analysis is a reliable tool in the assessment of psychotropic drug effects.

Aged↗
PubMed1987

Facilitatory effects of piracetam on excitability of motor nerve terminals and neuromuscular transmission.

The possible in vivo facilitatory effects of the pyrrolidine acetamide no-otropic agent piracetam on neuromuscular transmission, were studied based upon reports of enhancement of central cholinergic function. Piracetam was shown to antagonize the lethal effects of the neuromuscular blocking agent hemicholinium-3 (HC-3), in female CF-1 mice when administered in a dose of 100 mg/kg (i.p.) simultaneously with HC-3. A 30 mg/kg (i.p.) dose of piracetam was ineffective by itself, although it potentiated the protective effects of choline (25 mg/kg i.p.). The analogs of piracetam, aniracetam, oxiracetam, pramiracetam and dupracetam also significantly antagonized the lethality of HC-3 at doses over a 30-300 mg/kg range. The acute facilitatory properties of piracetam on neuromuscular transmission were examined in more detail in vivo in the soleus nerve muscle preparation of the cat. A 100 mg/kg (i.v.) dose of piracetam, while having no effect on its own, significantly enhanced the ability of a 200 micrograms/kg (i.v.) dose of edrophonium to produce a potentiation of muscle contraction dependent on repetitive discharges in the soleus motor nerve terminals. In preparations in which the motor nerve terminals of the soleus were in a partially degenerated state as a result of section of the motor axons 48 hr earlier, piracetam acted to restore their sensitivity to edrophonium. Furthermore, in both normal and partially degenerated preparations, piracetam significantly decreased the neuromuscular blocking effects of a 150 micrograms/kg (i.v.) dose of d-tubocurarine. The mechanism of the neuromuscular facilitatory effects of piracetam on neuromuscular transmission is discussed in terms of an enhanced excitability of motor nerve terminals together with an action to increase the synthesis and/or release of acetylcholine.

Animals↗
PubMed1990

The acute and chronic administrations of piracetam affect the movement-related brain macropotentials.

Neurophysiological and neurochemical studies have demonstrated that piracetam improves learning and memory both in animals and humans. In recent years it has been shown that when a subject is engaged in a motor perceptual task, some psychomotor functions are correlated with a consistent pattern of brain electrical activity. Given the relationship between the movement-related brain macropotentials (MRBMs) and the cognitive processes associated with them, we considered the MRBMs particularly suitable for the neurophysiological assessment of the efficacy of piracetam in man. The aim of this study was to test the acute and chronic effect of piracetam administration on the MRBMs in normal children during the performance of a motor perceptual task. The design was a triple-blind study, during which the subjects took either placebo or piracetam in random sequence, with a washout period of 3 weeks. The dose was 170 mg/kg for the acute treatment and 140 mg/kg/day for chronic treatment. No side-effects were reported by the children during or after acute or chronic treatment with piracetam. There was no statistically significant difference between placebo or piracetam treatment with regard to 'performance', which was already optimal at baseline, and to electromyographic activity. On the contrary, the MRBMs were significantly modified by treatment. In particular the Bereitschaftspotential was present as a positive shift during acute treatment with piracetam and increased after chronic treatment. Skilled performance positivity (SPP) amplitudes were significantly increased and SPP latency reduced by chronic treatment with piracetam. piracetam appears to act on the catecholaminergic and cholinergic systems via an increase of the inhibitory hyperpolarizing processes.

Adolescent↗
PubMed1982

The action of piracetam on the electrical activity of the hippocampal slice preparation: a field potential analysis.

The action of various doses of piracetam on the electrical responses of in vitro hippocampal slices from the rat was investigated. Piracetam increased dose dependently the amplitude of the population spike response of pyramidal neurons evoked by stimulation of the stratum radiatum. Piracetam began to affect the population spike at a dose of 100 microM and consistently increased it at a dose of 1 mM. The drug had a rapid onset of action and recovery was seen within a few minutes following its removal. The response of the pyramidal neurons to antidromic stimulation was not affected by piracetam at concentrations up to 50 mM. Also, neither the amplitude nor the slope of the dendritic response was changed by the drug.l Piracetam also did not affect either posttetanic or long-term potentiation of synaptic potentials. These findings suggest that the drug does not act through depolarization of the pyramidal cells or potentiation of the synaptic processes located on their dendrites. The action of piracetam on the feedforward- and feedback-mediated inhibition of pyramidal cells by basket cells was investigated in several series of experiments. At concentrations of 1 and 10 mM, piracetam did not change either of the two types of inhibitory mechanisms. Several hypothetical sites of action of piracetam are discussed.

Animals↗
PubMed1989

Effect of piracetam, a nootropic agent, on rat brain monoamines and prostaglandins.

Piracetam is the prototype of a new class of psychotropic drugs, the nootropic agents, which are claimed to selectively improve the higher telencephalic integrative activities. The effect of piracetam on rat brain monoamines and prostaglandins (PGs) was assessed so as to garner information on its mode of action. Two doses of the drug were used, a lower dose (20 mg/kg ip) and a higher dose (100 mg/kg, ip), the latter being known to exert a facilitatory effect on learning and memory. Piracetam produced a dose-related effect on rat brain serotonin (5HT) and noradrenaline (NA), with the lower dose inducing a decrease in 5HT levels and an increase in NA concentrations. The higher dose of piracetam produced the opposite effect. Dopamine (DA) levels were not significantly affected. The lower dose of the drug attenuated 5HT turnover and augmented that of NA, whereas the higher dose of piracetam produced the reverse effects, in clorgyline treated rats. The lower dose of piracetam produced a slight and statistically insignificant increase in rat brain PGE2 and PGF2 alpha. However, the higher dose of the drug produced marked increase in the levels of both the PGs. The observed biochemical effects may provide a basis for the nootropic effect of piracetam. However, they may also be due to the GA-BA-mimetic action of the drug, particularly those observed with the lower dose of piracetam.

Animals↗
PubMed1976

Piracetam-induced facilitation of interhemispheric transfer of visual information in rats.

The effect of Piracetam (UCB 6215, 2-pyrrolidoneacetamide) on learning mediated by transcommissural information flow was studied in hooded rats. Acquisition of monocular pattern discrimination was faster in drug-treated rats (100 mg/kg, 30 min before training) than in untreated controls. Subsequent relearning with one hemisphere functionally eliminated by cortical spreading depression showed that the strength of the primary engram formed under Piracetam in the hemisphere contralateral to the trained eye remained unaffected but that the secondary trace (in the ipsilateral hemisphere) was considerably improved and almost equalled the primary one (savings increased from 20-30% to 50-60%). Learning with uncrossed optic fibers was unaffected by the drug. Interhemispheric transfer of lateralized visual engrams acquired during functional hemidecortication was facilitated by Piracetam administration preceding the five transfer trials performed with the untrained eye open (imperative transfer). Piracetam was ineffective when the trained eye was open during transfer trials (facultative transfer). After a visual engram had been lateralized by 5 days of monocular overtraining, Piracetam facilitated formation of the secondary engram induced by 3 interocular transfer trials. It is concluded that Piracetam enhances transcommissural encoding mechanisms activated in the initial stage of monocular learning and in some forms of interhemispheric transfer, but does not affect the transcommissural readout. This effect is interpreted as a special case of the Piracetam-induced facilitation of the phylogenetically old mechanisms of redundant information storage which improve liminal or subnormal learning.

Animals↗
PubMed1984

Physiological disposition of oral piracetam in Sprague-Dawley rats.

The distribution and fate of piracetam (2-oxo-1-pyrrolidine acetamide, Nootropil), the prototype 'nootropic drug', was examined in rats given 100-1000 mg kg-1 by gavage, with or without [3H]piracetam as a tracer. Peak serum concentrations were attained after 60 min. Its half-life of disappearance from serum was about 2 h during the initial 8 h after administration and then about 6.4 h for the next 16 h. Brain piracetam concentrations equilibrated with those of serum at about 4 h, after which they fell exponentially but remained about twice those of serum; piracetam concentrations in the brainstem were lower (by 30-40%) than those in the cortex, olfactory bulb, and colliculi. No evidence could be obtained for significant piracetam metabolism, either in-vivo or when incubated with liver homogenates. No specific binding of [3H]piracetam to any of various subcellular fractions was observed after its administration along with unlabelled carrier. Repeated daily doses of piracetam (7 days, 100 mg kg-1) failed to elevate serum or brain concentrations beyond those observed after a single dose.

Animals↗
PubMed1991

Piracetam. An overview of its pharmacological properties and a review of its therapeutic use in senile cognitive disorders.

Piracetam is the first of the so-called 'nootropic' drugs, a unique class of drugs which affect mental function. In animal models and in healthy volunteers, the drug improves the efficiency of the higher telencephalic functions of the brain involved in cognitive processes such as learning and memory. The pharmacology of piracetam is unusual because it protects against various physical and chemical insults applied to the brain. It facilitates learning and memory in healthy animals and in animals whose brain function has been compromised, and it enhances interhemispheric transfer of information via callosal transmission. At the same time, even in relatively high dosages it is devoid of any sedative, analeptic or autonomic activities. How piracetam exerts its effects on memory disorders is still under investigation, although among other proposed mechanisms of action it is thought to facilitate central nervous system efficiency of cholinergic neurotransmission. Results from trials involving elderly patients with senile cognitive disorders have been equivocal, as have the results obtained when piracetam has been combined with acetylcholine precursors. Piracetam seems to be almost completely devoid of adverse effects, and is extremely well tolerated. In conclusion, opinion is divided as to the benefits of piracetam in the treatment of senile cognitive decline. Although double-blind studies in the elderly have produced mixed results, some such trials (particularly those involving larger numbers of patients) have reported favourable findings, thus offering some reason for cautious optimism in a notoriously difficult area of therapeutics. However, further investigations of piracetam alone and in combination therapy are required before any absolute conclusions can be drawn.

Aged↗
PubMedDate not supplied

[Influence of piracetam on the effects of narcotic analgesics and opioid peptides].

Piracetam possesses some properties not related to the nootropic activity. The purpose of the work was to study piracetam influence on effects of narcotic analgesics and opioid peptides at intracerebroventricular administration. In experiments on cats it was found that piracetam in a dose-dependent way prevented the emetic effect of morphine and leu-enkephalin. In experiments on rats (tail-flick test) piracetam was shown to be able of blocking the analgesic effect of fentanyl. Experiments on the study of the anticataleptogenic effect of piracetam also showed antagonism between piracetam and agonists of opioid receptors. Thus, it was shown on a number of models that piracetam exhibits antagonistic properties with respect of opioid peptides and narcotic analgesics.

Analgesics, Opioid↗
PubMed1985

Interaction of piracetam with several neurotransmitter receptors in the central nervous system. Relative specificity for 3H-glutamate sites.

The influence of the nootropic drug piracetam (Normabrain) on specific ligand binding to several neurotransmitter and drug receptors was investigated using established receptor binding procedures. Even at concentrations of 20 mmol/l of piracetam no or only marginal inhibition was observed for the dopamine- and muscarinic cholinergic receptors and for the peripheral benzodiazepine binding site, while for the benzodiazepine receptor, the GABA receptor, the opiate receptor, and the serotonin receptor half-maximal inhibitory concentrations between 20 and 50 mmol/l could be determined. In contrast to these effects seen only at relatively high piracetam concentrations, piracetam is considerably more active at the L-glutamate receptor with a half-maximal inhibitory concentration of about 1 mmol/l. This relatively specific effect of piracetam at the L-glutamate receptor could also take place under therapeutic conditions in vivo, since brain levels of piracetam in man may range between 0.1 and 1 mmol/l. It is concluded that effects within the glutaminergic system of the brain could contribute to the therapeutical effects of piracetam in man.

Animals↗
PubMedDate not supplied

Effect of piracetam, a cyclic GABA analogue, on haloperidol-induced catalepsy in the rat.

Piracetam, 2-oxo-1-pyrrolidine acetamide (Nootropil), is a cyclic GABA analogue. As GABA-mimetic compounds have been reported to potentiate haloperidol-induced catalepsy it was decided to study the effect of piracetam on haloperidol-induced catalepsy in rats. Piracetam, in high doses, was found to induce catalepsy while sub-cataleptic doses of piracetam were found to potentiate haloperidol-induced catalepsy. Piracetam, however, failed to antagonise apomorphine stereotypy in rats thereby ruling out the possibility of its possessing dopamine receptor blocking activity. The possible mechanism involved in the induction of catalepsy by piracetam and in the potentiation of haloperidol-induced catalepsy by sub-cataleptic doses of piracetam is discussed on the basis of its chemical relationship to GABA.

Animals↗
PubMed1995

Double-blind, placebo-controlled, pharmacokinetic and -dynamic studies with 2 new formulations of piracetam (infusion and sirup) under hypoxia in man.

In a double-blind, placebo-controlled study, pharmacokinetics and pharmacodynamics of 12 g piracetam in 2 different formulations were investigated utilizing blood gas analysis, EEG mapping and psychometry under a transient, reversible, hypoxic hypoxidosis. The latter was induced by a fixed gas combination of 9.8% oxygen (O2) and 90.2% nitrogen (N2, found in 6,000 m altitude), which was inhaled for 23 minutes under normobraic conditions by 18 healthy volunteers. They received after an adaptation session randomized at weekly intervals 12 g piracetam i.v. (250 ml infusion over 30 minutes), 12 g piracetam p.o. (60 ml sirup) and placebo. Blood levels were determined by means of an HPLC at the hours 0, 1, 2, 4, 6, 8 and 24. The 2 formulations showed a very similar time-course, with slightly higher blood levels in the 1st hour after the intravenous than oral administration, and vice versa thereafter. The elimination half-life was 4.3 hours for both formulations, the area under the curve and the clearance value were also almost identical. Evaluation of blood gases, EEG mapping and psychometry were carried out at 0, 2, 4, 6 and 8 hours post-drug. Blood gas analysis demonstrated a drop in SaO2 from 99 to 73 and 70%, in PO2 from 100 to 35 and 33 mmHg, in PCO2 from 36 to 31 and 31 mmHg in the 14th and 23rd minute of inhalation, respectively. pH increased from 7.43 to 7.48 in the respective minutes, while base excess and standard bicarbonate remained stable. EEG mapping exhibited under hypoxia a marked increase of total power, mostly due to an augmentation of delta/theta, and a decrease of alpha activity, which reflects deterioration of vigilance. Both piracetam preparations significantly attenuated this vigilance decrement, with 12 g piracetam i.v. showing its encephalotropic peak effects in the earlier hours, 12 g piracetam sirup in the later hours. At the behavioral level, hypoxic hypoxidosis induced a deterioration of the noo- and thymopsyche, which was mitigated by both piracetam preparations, mostly in the 6th hour. Both formulations were well tolerated.

Administration, Oral↗
PubMed1981

Effect of piracetam on sickle erythrocytes and sickle hemoglobin.

Piracetam, 2-oxo-1-pyrrolidine acetamide, inhibits sickling of red cells containing sickle hemoglobin (Hb S). The concentration required for 50% inhibition is about 300 mM. Addition of piracetam into the supersaturated Hb S solution in concentrated phosphate buffer prolongs the delay time prior to gelation. Piracetam shifts the oxygen equilibrium curves of blood toward the right, with a stronger effect at higher piracetam concentrations. Piracetam increases the viscosity of oxygenated cells but reduces the relative viscosity of deoxygenated sickle cells. The mechanism for the antisickling effect of piracetam will be discussed.

Anemia, Sickle Cell↗
PubMed1984

Habituation of exploratory activity in mice: effects of combinations of piracetam and choline on memory processes.

The effects of various piracetam + choline combinations on an experimental model of memory were investigated. Mice were given two sessions in a simple photo-cell activity cage and the decrease in activity at the second session (habituation) served as an index of retention. Retention was facilitated by post-session administration of 2000 mg/kg piracetam IP and 50 mg/kg piracetam + 50 mg/kg choline IP. Similar injections of choline alone (10 to 200 mg/kg IP), piracetam alone (10 to 1000 mg/kg IP) or other combinations of piracetam and choline were without effect. These results, consistent with those reported elsewhere, suggest that piracetam can interact with choline to facilitate memory processes in mice.

Animals↗