littlelady774
running on empty
- Dec 20, 2018
- 708
I've written a small essay of what that happens in our body when we ingest sodium nitrite. I will do my best to describe the pathology and biochemistry of methemoglobinemia and nitrite poisoning. This is from my own research and I will post the sources from scientific articles and journals. Hopefully this information will shed some light for the community and those who are considering SN as their method. It is a rough estimate of what to expect from the time it reaches our mouths to the time of death. I'm mostly doing this because I learn and process things by writing . By the way, I'm no scientist or biology major, so if you want, please take this all with a grain of salt ( haha)
Upon mixing it with water and taking it orally, it reaches our stomach, where the stomach acid reduces some of the nitrite to nitric oxide, water, sodium chloride and nitrous acid. The nitric oxide acts as a vasodilator and reduces blood pressure, and it also has a protective effect on the gastrointestinal tract and other organs by protecting biomolecules from oxidative events. Nitric oxide reacts with oxygen to form nitrite and nitrate. Meanwhile, sodium nitrite is rapidly absorbed in the small intestine with a bioavailability of 92%. Nitrites react to oxygen to form oxygen-free radicals, which are powerful oxidizers of hemoglobin. It enters the bloodstream and is made available to other tissues. The oxygen free radicals oxidize the ferrous ion to a ferric ion, making it unable to carry oxygen. Furthermore, The methemoglobin results in a leftward shift of the oxygen dissociation curve, which causes hemoglobin to bind to oxygen more tightly and not release it to the peripheral tissues resulting in cellular hypoxia.This is where cyanosis and the beginning of lactic acidosis happens. At concentrations of 15%, patients may appear cyanotic and are typically asymptomatic.
Because of the leftward shift on the oxygen dissociation curve, and the body's ability to detect changes in the blood and tissue imbalance of O2 and CO2, shortness of breath may occur at methemoglobin levels of 30%. Arterial blood gas readings typically show normal oxygen levels due to the blood's increased oxygen affinity and failure of delivery to the tissues. The body's response to higher levels of lactate and low bicarbonate is to level out the pH of the blood and tissues by faster breathing. Signals are sent to the limbic system, which are sent to the lungs to breathe faster. It's similar to hyperventilating. Breathing can be described as fast and shallow. Methemoglobin is unable to carry oxygen nor carbon dioxide.
Therefore, cells need to rely on anaerobic respiration due to insufficient oxygen delivery. Anaerobic respiration relies on the breakdown of glucose and forms lactic acid in the process. Higher lactic acid and low bicarbonate leads to mild acidosis: weakness, fatigue, tachycardia, headache, nausea, loss of appetite, dizziness.
Likewise, heart rate increases from the changes of oxygenation and lactic acid amounts in the tissues. Lactate is fuel for the heart, the higher lactate levels, the higher heart rate. This is why propranolol is recommended. (Although not in new ppeh for some reason)
At 45%- 55% levels, lethargy and fainting generally occur due to insufficient oxygen delivery to the brain. However due to the nitric oxide produced in the stomach from the nitrite + stomach acid reaction, loss of consciousness might occur sooner from low blood pressure. Stomach acid is important for faster pass out time. This is why an acid reducer is no longer recommended.
Around 50% levels, cells can no longer run on anaerobic respiration as cellular glucose diminishes.
The ATP levels drop and the cell cannot perform its normal functions. At this point, the beginning of cell death occurs via apoptosis. Note this probably happens in the brain as well.
Around 70%, lactic acidosis has become very severe, Kussmaul breathing or rapid "deep and labored breathing" may occur. Furthermore, enough cell death has happened due to hypoxia where it is typical that overall death occurs.
SOURCES
I think that's all the sources, if you have a question on something, please comment below
Upon mixing it with water and taking it orally, it reaches our stomach, where the stomach acid reduces some of the nitrite to nitric oxide, water, sodium chloride and nitrous acid. The nitric oxide acts as a vasodilator and reduces blood pressure, and it also has a protective effect on the gastrointestinal tract and other organs by protecting biomolecules from oxidative events. Nitric oxide reacts with oxygen to form nitrite and nitrate. Meanwhile, sodium nitrite is rapidly absorbed in the small intestine with a bioavailability of 92%. Nitrites react to oxygen to form oxygen-free radicals, which are powerful oxidizers of hemoglobin. It enters the bloodstream and is made available to other tissues. The oxygen free radicals oxidize the ferrous ion to a ferric ion, making it unable to carry oxygen. Furthermore, The methemoglobin results in a leftward shift of the oxygen dissociation curve, which causes hemoglobin to bind to oxygen more tightly and not release it to the peripheral tissues resulting in cellular hypoxia.This is where cyanosis and the beginning of lactic acidosis happens. At concentrations of 15%, patients may appear cyanotic and are typically asymptomatic.
Because of the leftward shift on the oxygen dissociation curve, and the body's ability to detect changes in the blood and tissue imbalance of O2 and CO2, shortness of breath may occur at methemoglobin levels of 30%. Arterial blood gas readings typically show normal oxygen levels due to the blood's increased oxygen affinity and failure of delivery to the tissues. The body's response to higher levels of lactate and low bicarbonate is to level out the pH of the blood and tissues by faster breathing. Signals are sent to the limbic system, which are sent to the lungs to breathe faster. It's similar to hyperventilating. Breathing can be described as fast and shallow. Methemoglobin is unable to carry oxygen nor carbon dioxide.
Therefore, cells need to rely on anaerobic respiration due to insufficient oxygen delivery. Anaerobic respiration relies on the breakdown of glucose and forms lactic acid in the process. Higher lactic acid and low bicarbonate leads to mild acidosis: weakness, fatigue, tachycardia, headache, nausea, loss of appetite, dizziness.
Likewise, heart rate increases from the changes of oxygenation and lactic acid amounts in the tissues. Lactate is fuel for the heart, the higher lactate levels, the higher heart rate. This is why propranolol is recommended. (Although not in new ppeh for some reason)
At 45%- 55% levels, lethargy and fainting generally occur due to insufficient oxygen delivery to the brain. However due to the nitric oxide produced in the stomach from the nitrite + stomach acid reaction, loss of consciousness might occur sooner from low blood pressure. Stomach acid is important for faster pass out time. This is why an acid reducer is no longer recommended.
Around 50% levels, cells can no longer run on anaerobic respiration as cellular glucose diminishes.
The ATP levels drop and the cell cannot perform its normal functions. At this point, the beginning of cell death occurs via apoptosis. Note this probably happens in the brain as well.
Around 70%, lactic acidosis has become very severe, Kussmaul breathing or rapid "deep and labored breathing" may occur. Furthermore, enough cell death has happened due to hypoxia where it is typical that overall death occurs.
SOURCES
- https://courses.washington.edu/med610/abg/abg_primer2.html
- https://core.ac.uk/download/pdf/81131491.pdf
- https://my.clevelandclinic.org/health/diseases/24492-metabolic-acidosis
- https://flipper.diff.org/app/items/info/6026
- https://en.m.wikipedia.org/wiki/Kussmaul_breathing
- https://www.ncbi.nlm.nih.gov/books/NBK537317/
- https://www.chemicalaid.com/tools/equationbalancer.php?equation=NaNO2+%2B+HCl+%3D+NO+%2B+H2O+%2B+NaNO3+%2B+NaCl&hl=en
- https://biologydictionary.net/anaerobic-respiration/#definition
- http://toxicology.ucsd.edu/art 2 methemoglobin.pdf
- https://www.sciencedirect.com/science/article/pii/S089158491200336X
- https://link.springer.com/content/pdf/10.1007/s12245-009-0149-0.pdf
I think that's all the sources, if you have a question on something, please comment below
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