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SODIUM NITRITE is a chemical compound with formula NaNO2 Our product is almost chemically pure, which makes it ideal for use in a analyses, photography, pharmacy, synthesis and crystal making. Product is dry, crystalline powder.
I don't know. Maybe I'm not typing the correct things but all I see is pink in the results.
The search results are definitely different using the uk site.
I'm gonna ask my question again as I would really like to have a clear explanation for this rather than simply doing the same as other people without understanding why.
I will be following the 48 hour antiemetic regimen and I was wondering : After taking the last dose of metoproclamide, how long do you wait before taking ranitidine ? Does it matter or can it be taken at the same time ? After the Ranitidine I will wait 50 minutes to take SN as the user jake3d explained : "Dosage for ranitidine would be 4x 75mg pills, 50 minutes before SN. Ranitidine is a bit slower in its onset than cimetidine is, according to the medicine leaflets. "
I'm asking that question because there's an issue with antacids hindering the absorption of Domperidone and I'm wondering if there's a similar problem with Metoproclamide, or if there's no problematic interaction between Metoproclamide and antacids.
I'm wondering about just taking Domperidone without any Famotidine because apparently they don't get along. People have died without antiemetics or acid regulators, so I feel pretty confident. Vomiting and being found seem to be the two biggest risks of failure, and if the Domperidone does its job, I'm safe from both.
I vaguely remember an 8chan post which instructed that you can take Domperidone with an acid regulator as long as you take the Domperidone first and have time between the intake of it and the acid regulator. Does anyone have it? I've seen a screenshot of the post on here but I don't remember where exactly.
I got meto coming up but I don't know how long it'll take to get here. I'm really not in any hurry but I'd also not prefer to just exist like I do now.
EDIT: Oh, and checking on this site daily has become a habit of mine. So if I suddenly stop logging in you know what happened to me and you can be sure that Domperidone works. I don't plan on making any goodbye post. I see those as silly theatrics.
<i>Case</i>. We report a case of severe methemoglobinemia due to sodium nitrite poisoning. A 28-year-old man was brought to our emergency department because of transient loss of consciousness and cyanosis. He was immediately intubated and ventilated with 100% oxygen. A blood test revealed a...
www.hindawi.com
"Cranial T2-weighted MRI findings 3 days after sodium nitrite ingestion were similar to those in carbon monoxide poisoning. It has been reported that the globus pallidus is most susceptible to hypoxia. Severe methemoglobinemia can cause severe tissue hypoxia similar to that in carbon monoxide poisoning; this may explain the involvement of the globus pallidus in our case."
He did not get permanent damage in the end, but had lesions in the bit of the brain that controls movement.
<i>Case</i>. We report a case of severe methemoglobinemia due to sodium nitrite poisoning. A 28-year-old man was brought to our emergency department because of transient loss of consciousness and cyanosis. He was immediately intubated and ventilated with 100% oxygen. A blood test revealed a...
www.hindawi.com
"Cranial T2-weighted MRI findings 3 days after sodium nitrite ingestion were similar to those in carbon monoxide poisoning. It has been reported that the globus pallidus is most susceptible to hypoxia. Severe methemoglobinemia can cause severe tissue hypoxia similar to that in carbon monoxide poisoning; this may explain the involvement of the globus pallidus in our case."
He did not get permanent damage in the end, but had lesions in the bit of the brain that controls movement.
<i>Case</i>. We report a case of severe methemoglobinemia due to sodium nitrite poisoning. A 28-year-old man was brought to our emergency department because of transient loss of consciousness and cyanosis. He was immediately intubated and ventilated with 100% oxygen. A blood test revealed a...
www.hindawi.com
"Cranial T2-weighted MRI findings 3 days after sodium nitrite ingestion were similar to those in carbon monoxide poisoning. It has been reported that the globus pallidus is most susceptible to hypoxia. Severe methemoglobinemia can cause severe tissue hypoxia similar to that in carbon monoxide poisoning; this may explain the involvement of the globus pallidus in our case."
He did not get permanent damage in the end, but had lesions in the bit of the brain that controls movement.
Yeah it's funny how it's the go-to bus ticket, but it's better if they do not publish that anyway. Really worries me that it may become unavailable like N.
Yeah it's funny how it's the go-to bus ticket, but it's better if they do not publish that anyway. Really worries me that it may become unavailable like N.
Yeah, I bet they will have to make the 98%+ grade a controlled substance similar to pure nitrogen gas or cyanide. You can still acquire those of course but its not as simple as a $10 Amazon transaction.
Yeah, I bet they will have to make the 98%+ grade a controlled substance similar to pure nitrogen gas or cyanide. You can still acquire those of course but its not as simple as a $10 Amazon transaction.
In UK it already is controlled by the 1972 Poisons Act as a "reportable" substance. That means that, whilst it is quite legal to acquire and possess without any form of licence, there is an obligation on suppliers to report any attempted purchase that they consider suspicious. This puts quite an onus on suppliers, of course, and many gold-plate the requirement. They will tell you that a licence is required, for example, or will ask you to complete a questionnaire before they will consider supplying.
The other category in the Poisons Act is "Regulated" and it is the substances in this category that require licensing. Any substance can be changed from one legal category to the other by a relatively simple legislative process.
Given the astonishing surge in knowledge of the lethal potential of SN over a short period, plus increased government efforts to prevent suicide, it may well be that we see further restrictions. I'd put money on this being limitations on the purity of SN. A similar process was followed several years ago with Ammonium Nitrate, which is widely used as an agricultural fertiliser, but is also (in a fairly pure form) the oxydising ingredient in the improvised substance which has come to be called ANFO (Ammonium Nitrate Fuel Oil), a potent explosive exploited by terrorist groups.
Here is an article on a poor guy 'saved', and an excerpt.
https://www.hindawi.com/journals/criem/2016/9013816/
"Cranial T2-weighted MRI findings 3 days after sodium nitrite ingestion were similar to those in carbon monoxide poisoning. It has been reported that the globus pallidus is most susceptible to hypoxia. Severe methemoglobinemia can cause severe tissue hypoxia similar to that in carbon monoxide poisoning; this may explain the involvement of the globus pallidus in our case."
He did not get permanent damage in the end, but had lesions in the bit of the brain that controls movement
Yeah, I did say there was no permanent damage. Did not mean it as a scare-story at all. Found it interesting that there was a particular bit of the brain most susceptible to hypoxia, that's all.
Where did the myth that SN causes blindness come from anyway?
Just to ensure I'm not spreading misinformation, I've seen a couple users talk about it but it doesn't appear to be true. I don't want to freak people out.
Hello all! I have been lurking on this thread for some time, and I have read all 160 pages, as well as the PPeH and everything else I could find on the topic. I am a safety inspector and hazmat coordinator by trade, so it is in my nature to be as informed and as thorough as possible. That being said, I have decided to share my regimen and plan, at the mercy of the general consensus.
I live in NorCal (in the US), and I have come to the conclusion that the safest course of action is to reserve a campground for the day I plan to CTB through 2 days past the day I plan to CTB. The time of year means that there should not be many people around my campsite, and no one should come looking for me until at least 2 days past my planned ingestion of SN. I have purchased and received 2 different brands of SN. My primary brand will the the popular LoudWolf brand available in the US. Should this fail, I have also purchased SN from Duda Energy and I will ingest an additional 15g of this product should the LoudWolf brand prove to be ineffective. I do not anticipate this happening but I thought it wise to have a backup source of SN on hand, just in case.
For the record, I am extremely thin, around 115lbs (52kg). For this reason, I believe that 15g of SN should be more than enough for me. If it proves to be too much, which I also considered as possible, I am relying on the relatively remote location of my campsite being enough to keep anyone from noticing any sounds I may cause from vomiting, seizing, or crying out in pain.
Please correct me if you see anything out of sorts:
11 October (Friday)
2300: start fast (no food, liquids (alcohol) ok)
13 October (Sunday)
0530: 10mg Primperan
1200: start total fast (only water)
1330: 10mg Primperan
2130: 30mg Primperan
14 October (Monday)
0530: 10mg Primperan
1330: 10mg Primperan
1430: head to campground
2130: 20-30mg Primperan
2145: 800mg Tagamet
2150: 1000mg Ibuprofen(?)
2230: 15-20g SN in 75-100mL water
I wish to fast for 72 hours for meditative reasons. I often fast in times of distress and so this is a personal choice for me, as it will be calming for me. I know that physiologically you do not need to fast for more than 8 hours, so do not read my schedule and feel pressured to fast for more than 8 hours.
My biggest question is regarding the use of ibuprofen or other OTC painkillers. I have seen a few posts about ibuprofen in particular increasing the chance of gastric distress. Can anyone confirm or deny? I would like to take some precaution against probable headache, and I do not wish to seek out benzos or other prescription painkillers/sedatives.
Additionally, I would like to offer as support to those afraid of seizures: I used to have seizures as a teenager, and I can assure you that they are NOT painful. You will not know they are happening. When you become conscious after a seizure, you will remember nothing. You will wake up from the seizure merely confused. Please do not be afraid.
Please feel free to PM me regarding any questions, if you do not feel comfortable asking them in this thread. I am very glad to be part of this welcoming community.
Why are you taking 20-30mg of Meto on day 2? From my understanding you only need to take the 30mg dose an hour before you ingest the SN. Could you PM as well so your response does not get lost in the thread. Thank You, Umniak
I have domperidone and Tagamet+SN. I heard someone say Tagamet won't work with it. If so, what do I need instead? I need to CTB in the next few days and I'll do a live thread if it helps, but want to minimize discomfort. Don't want meto. Thanks!
I am uneasy about the frequently quoted claims that SN poisoning is totally reversible.
It seems true that the correct antidote acts very quickly when administered.
However, as we all know in the case of SN poisoning, death occurs due to the nitrite component chemically altering the blood so that it cannot carry and release the oxygen required by the brain.
So the brain cells start to die.
Surely, at some late point, before death, the patient can still be resuscitated after some cells have been damaged beyond recovery ?
Depending on the degree of damage this must mean that the attempt at death fails, but with the possibility of mental and/or physical impairment.
I am uneasy about the frequently quoted claims that SN poisoning is totally reversible.
It seems true that the correct antidote acts very quickly when administered.
However, as we all know in the case of SN poisoning, death occurs due to the nitrite component chemically altering the blood so that it cannot carry and release the oxygen required by the brain.
So the brain cells start to die.
Surely, at some late point, before death, the patient can still be resuscitated after some cells have been damaged beyond recovery ?
Depending on the degree of damage this must mean that the attempt at death fails, but with the possibility of mental and/or physical impairment.
I agree that according to that logic it is theoretically possible, but according to data we have 0 known cases of permanent impairment. The risk is very much worth taking given our current knowledge.
I mean I could have a stroke right now and have permanent mental impairment, it is probably about the same likelihood.
I agree that according to that logic it is theoretically possible, but according to data we have 0 known cases of permanent impairment. The risk is very much worth taking given our current knowledge.
I mean I could have a stroke right now and have permanent mental impairment, it is probably about the same likelihood.
Somewhere in all the reams of posts, attachments and the like I have seen an authoritative observation that stroke is a possible complication of the effects of SN poisoning.
IMHO anybody who is not serious should not make a demonstration based on the assumption that there will definitely not be any lasting damage.
And whilst I am at it:-
I had been waiting for an EI update on the SN method. Whilst there is absolutely no doubt of the fatal potential, I was keen to know details of any more observed cases.
Alas, there seem to be none, though a further drug has been added to the increasing pharmacopeia which is now recommended (propranolol, to minimise tachycardia.) How many more things are in the pipeline ?
But it's not this I want to address here; it's the steadily increasing dose of SN that is recommended with almost every PPH update. It's now 25gm, 35 if you weigh more than 100kg/224lb.
This indicates to me that previous recommendations for much smaller doses have been shown to be ineffective - why increase the dose if otherwise ?
"Ineffective" must mean failure, so where are the accounts of these failures ?
Somewhere in all the reams of posts, attachments and the like I have seen an authoritative observation that stroke is a possible complication of the effects of SN poisoning.
IMHO anybody who is not serious should not make a demonstration based on the assumption that there will definitely not be any lasting damage.
And whilst I am at it:-
I had been waiting for an EI update on the SN method. Whilst there is absolutely no doubt of the fatal potential, I was keen to know details of any more observed cases.
Alas, there seem to be none, though a further drug has been added to the increasing pharmacopeia which is now recommended (propranolol, to minimise tachycardia.) How many more things are in the pipeline ?
But it's not this I want to address here; it's the steadily increasing dose of SN that is recommended with almost every PPH update. It's now 25gm, 35 if you weigh more than 100kg/224lb.
This indicates to me that previous recommendations for much smaller doses have been shown to be ineffective - why increase the dose if otherwise ?
"Ineffective" must mean failure, so where are the accounts of these failures ?
Yeah that is a good question, can anyone get an answer from EI? Ineffective could be an extended time until passing out, discomfort while passing out, or an extended time until death. I also suspect the increased dosage is to guarantee comfort and fatality even if you vomit half of it up. If you inject 5g or whatever, it should be lethal, with 35 grams you can vomit half of it up, have some food in your stomach, have extra hemoglobin, and still have a successful exit.
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