VelocideX
Bluelighter
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- May 26, 2003
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I've commented in several other threads (and perhaps here) that alcohol + piracetam + 5-HTP is LOTS of fun.
lostNfound: piracetam's primary mode of action is not through vasodilation. The exact mechanism is uncertain, but appears to relate to ion channels. Piracetam DOES have a mild vasodilatory effect after sustained use, but not anything like good vasodilators.
What makes you assume that it's alcohol that's killing your brain cells? Much of the hangover is probably from acetyldehyde + dehydration + trace products in your drink.
It's poor logic that piracetam will damage you more by exposing your brain to more alcohol. If your brain was exposed to more alcohol, then you'd simply be drunker. The equivalent effect is simply having more alcohol than you would have had otherwise....
Besides, studies show piracetam is neuroprotective with alcohol anyway:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9269855
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7639963
Here's some more reading material:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6677895
lostNfound: piracetam's primary mode of action is not through vasodilation. The exact mechanism is uncertain, but appears to relate to ion channels. Piracetam DOES have a mild vasodilatory effect after sustained use, but not anything like good vasodilators.
What makes you assume that it's alcohol that's killing your brain cells? Much of the hangover is probably from acetyldehyde + dehydration + trace products in your drink.
It's poor logic that piracetam will damage you more by exposing your brain to more alcohol. If your brain was exposed to more alcohol, then you'd simply be drunker. The equivalent effect is simply having more alcohol than you would have had otherwise....
Besides, studies show piracetam is neuroprotective with alcohol anyway:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9269855
Alcohol Alcohol. 1997 Jul-Aug;32(4):471-84. Related Articles,Links
The GABAergic system of the dentate gyrus after withdrawal from chronic alcohol consumption: effects of intracerebral grafting and putative neuroprotective agents.
Cadete-Leite A, Brandao F, Andrade JP, Ribeiro-da-Silva A, Paula-Barbosa MM.
Department of Anatomy, Porto Medical School, Portugal.
We have demonstrated that, in the rat hippocampal formation, withdrawal from chronic alcohol consumption aggravates the ethanol-induced loss of pyramidal neurons and dentate granule cells. We have also shown that intracerebral grafting and piracetam could have a protective effect in these conditions. In this study we utilized immunocytochemical methods to investigate whether gamma-aminobutyric acid (GABA)ergic dentate gyrus cells, which are known to be inhibitory, were also affected by withdrawal from alcohol and, if so, whether putative neuroprotective agents could ameliorate the alterations found. Rats were alcohol-fed for 6 months and further divided into several groups: (1) alcohol-fed for an extra 6 months; (2) withdrawn from alcohol for 6 months; (3) withdrawn and grafted with newborn rat hippocampal tissue; (4) withdrawn and orally treated with piracetam for 6 months; (5) withdrawn and treated systemically with monosialoganglioside GM1 for 6 months; (6) withdrawn and treated with the vehicle used to dissolve the GM1. Control animals were pair-fed. All animals were killed 12 months after the beginning of the experiment and processed for GABA immunocytochemistry. GABA-immunoreactive (IR) neurons in the dentate gyrus were quantified and we found that alcohol-fed animals had a significant reduction in the numerical profile density of GABA-IR neurons in the dentate gyrus as a whole and in the hilus and in the granular layer of the suprapyramidal limb. Withdrawal from alcohol aggravated the GABAergic neuronal loss. Of the treatments used, only piracetam had a striking beneficial effect. Data gathered from the present work and from our previous studies indicate that the neuronal loss following chronic alcohol consumption and withdrawal affects both excitatory and inhibitory neurons in the dentate gyrus and that piracetam may have a useful protective role in this condition.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7639963
Alcohol. 1995 May-Jun;12(3):279-88. Related Articles,Links
Piracetam impedes hippocampal neuronal loss during withdrawal after chronic alcohol intake.
Brandao F, Paula-Barbosa MM, Cadete-Leite A.
Department of Anatomy, Porto Medical School, Portugal.
In previous studies we have demonstrated that prolonged ethanol consumption induced hippocampal neuronal loss. In addition, we have shown that withdrawal after chronic alcohol intake augmented such degenerative activity leading to increased neuronal death in all subregions of the hippocampal formation but in the CA3 field. In an attempt to reverse this situation, we tested, during the withdrawal period, the effects of piracetam (2-oxo-1-pyrrolidine acetamide), a cyclic derivative of gamma-aminobutyric acid, as there is previous evidence that it might act as a neuronoprotective agent. The total number of dentate granule, hilar, and CA3 and CA1 pyramidal cells of the hippocampal formation were estimated using unbiased stereological methods. We found out that in animals treated with piracetam the numbers of dentate granule, hilar, and CA1 pyramidal cells were significantly higher than in pure withdrawn animals, and did not differ from those of alcohol-treated rats that did not undergo withdrawal. These data suggest that piracetam treatment impedes, during withdrawal, the pursuing of neuronal degeneration.
Here's some more reading material:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6677895
Pol J Pharmacol Pharm. 1983 Nov-Dec;35(6):451-65. Related Articles,Links
The effect of piracetam on the central action of ethanol in mice and rabbits.
Czarnecka E, Stanislawska E.
The effect of combined single administration of ethanol and piracetam on the rabbit EEG and on locomotor activity and ethanol sleep in mice was investigated. In addition, the effect of prolonged administration of piracetam together with ethanol on rabbit EEG and after-discharges evoked by electrical stimulation of the hippocampus was studied. The blood ethanol concentrations were also monitored. Single administration of piracetam did not change the effects of ethanol, while when given prolongly with ethanol piracetam attenuated the effects of ethanol. Piracetam did not affect the ethanol blood level.