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Indlæg: 12 nov 2011 03:37 
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Hvis man som mig godt kan lide en drink eller to er det så noget der for ens tolerance til at stige i forhold til benzodiazepiner??? Det må vel påvirke ens tolerance lidt kunne jeg forestille mig?


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Indlæg: 12 nov 2011 03:49 
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tror det har en del at gøre med mængde, når du siger en drik eller 2 mener du så 2 drinks eller ? :)
benzoer trækker jo også på GABA receptoren som Ethanol gør .

fandt noget om det:

Cross toleranceBenzodiazepines share a similar mechanism of action with various sedative compounds that act by enhancing the GABAA receptor. Cross tolerance means that one drug will alleviate the withdrawal effects of another. It also means that tolerance of one drug will result in tolerance of another similarly-acting drug. Benzodiazepines are often used for this reason to detoxify alcohol-dependent patients and can have life-saving properties in preventing and/or treating severe life-threatening withdrawal syndromes from alcohol, such as delirium tremens. However, although benzodiazepines can be very useful in the acute detoxification of alcoholics, benzodiazepines in themselves act as positive reinforcers in alcoholics, by increasing the desire for alcohol. Low doses of benzodiazepines were found to significantly increase the level of alcohol consumed in alcoholics.[20] Alcoholics dependent on benzodiazepines should not be abruptly withdrawn but be very slowly withdrawn from benzodiazepines, as over-rapid withdrawal is likely to produce severe anxiety or panic, which is well known for being a relapse risk factor in recovering alcoholics.[21]

There is cross tolerance between alcohol, the benzodiazepines, the barbiturates, the nonbenzodiazepine drugs, and corticosteroids, which all act by enhancing the GABAA receptor's function via modulating the chloride ion channel function of the GABAA receptor.[22][23][24][25][26]

Neuroactive steroids, e.g., progesterone and its active metabolite allopregnanolone, are positive modulators of the GABAA receptor and are cross tolerant with benzodiazepines.[27] The active metabolite of progesterone has been found to enhance the binding of benzodiazepines to the benzodiazepine binding sites on the GABAA receptor.[28] The cross-tolerance between GABAA receptor positive modulators occurs because of the similar mechanism of action and the subunit changes that occur from chronic use from one or more of these compounds in expressed receptor isoforms. Abrupt withdrawal from any of these compounds, e.g., barbiturates, benzodiazepines, alcohol, corticosteroids, neuroactive steroids, and nonbenzodiazepines, precipitate similar withdrawal effects characterized by central nervous system hyper-excitability, resulting in symptoms such as increased seizure susceptibility and anxiety.[29] While many of the neuroactive steroids do not produce full tolerance to their therapeutic effects, cross-tolerance to benzodiazepines still occurs as had been demonstrated between the neuroactive steroid ganaxolone and diazepam. Alterations of levels of neuroactive steroids in the body during the menstrual cycle, menopause, pregnancy, and stressful circumstances can lead to a reduction in the effectiveness of benzodiazepines and a reduced therapeutic effect. During withdrawal of neuroactive steroids, benzodiazepines become less effective.[30]

Så ja det er der, hvis man har abstineser af den ene kan man dæmpe dem med den anden.
Har godt lagt mærke til at man kan drikke en god del mere end normalt når man lige er stoppet med benzoerne.
Så har vi også lært det hehe
.[/quote]


Senest rettet af Oblectamentum 12 nov 2011 03:55, rettet i alt 1 gang.

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Indlæg: 12 nov 2011 04:49 
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okay. mange tak. så vil jeg holde lidt igen med alkohol for at min tolerance ikker stiger:-) takker:-)


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Indlæg: 12 nov 2011 22:40 
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I lille grad måske. Benzoer virker positivt modulerende på GABA-A receptoren, hvilket vil sige, at den samme mængde frigivet GABA giver et kraftigere respons.

En sjov ting er at man stadig ikke er sikker på den basale mekanisme for ethanol's effekter. Det er muligt at måle effekten af ethanol ved den øgede transmittere-frigivelse in vivo og in vitro, men man er stadig ikke klar over, hvor effekten starter henne. Fx passer in vitro og in vivo data for GABA-frigivelse ikke sammen, hvilket er det samme som at ethanols effekt ikke bunder i en interaktion med GABA-neuroner. Mit bud er at ethanol for det første ændre membran potentiale af en bred vifte af receptorer i udstrakt grad. Og, at effekten muligvis i hovedsagen skyldes påvirkning af nogle undertyper af neurale nikotinerge receptorer - ligesom de fleste mindre alkoholer også har en kraftig effekt på disse receptorer.


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