blueclover_.
Better Never to Have Been: 2006, David Benatar
- Oct 11, 2021
- 668
Please beware that these are 100% my findings as a non-medical licensed person out of curiosity. Feel free to add or disprove any information on this thread.
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My hypothesis is that as Sodium Nitrite reacts with the blood causing hypoxia, at the same time by being converted into Nitric Oxide, It protects the brain from Hypoxic-Ischaemic (Brain tissue damage due to the lack of oxygen) brain injury up to the moment of death. Given that hypoxia is completely reversible as long as the brain tissue is not damaged, if a person is 'saved' before the Hypoxic-Ischaemic brain injury could occur, the protection from NO would leave the brain completely fine until it is supplied back with the normal amount of oxygen. As the protection wears off, your brain cells will start to die (Hypoxic-Ischaemic) and in this stage permanent brain damage is possible. In conclusion, your brain nerves won't start to die immediately after your oxygen level has dropped; it varies from minutes to hours until the effect of NO starts to wear off and leave your brain cells to die naturally due to the lack of oxygen.
So you can get brain damage if someone saves you at the tiny exact moment when the protection from Nitric Oxide wears off, but that is unlikely since most people get saved within the time the Nitric Oxide is still protecting your brain cells. We've never had any reported cases regarding brain damage due to SN poisoning separate from cardiac arrest. If you go into a cardiac arrest after ingesting SN, even after your blood is converted back to normal with Methylene Blue, the blood can no longer reach the brain since the heart has already stopped beating/not beating effectively to pump the normal blood back to the brain.
With similar methods such as Hanging or the Exit Bag method, there is no chemical that protects your brain cells and if someone finds you minutes later, you'll have a higher chance of getting permanent brain injury.
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Sodium Nitrite is converted into Nitric Oxide which helps to protect your brain's nerve cells:
Early Intravenous Infusion of Sodium Nitrite Protects Brain Against In Vivo Ischemia-Reperfusion Injury (ahajournals.org)
"The rate of nitric oxide (NO) generation from nitrite is linearly dependent on reductions in oxygen and pH levels. Recently, nitrite-derived NO has been reported to exert a profound protection against liver and heart ischemia-reperfusion injury. In this study, we hypothesized that nitrite would be reduced to NO in the ischemic brain and exert NO-dependent neuroprotective effects."
"Nitrite exerted profound neuroprotective effects with antioxidant properties in the ischemic brains. These results suggest that nitrite, as a biological storage reserve of NO, may be a novel therapeutic agent in the setting of acute stroke."
Beneficial Effect of Sodium Nitrite on EEG Ischaemic Markers in Patients with Subarachnoid Haemorrhage | SpringerLink
"Infused sodium nitrite is well suited to alter brain states after cerebral damage. It can safely be administered [23] and is converted to NO in hypoxic and acidic conditions [16, 17], which can be observed after SAH [6, 42]. It can support cerebral autoregulation after SAH [43] and, crucially, helps preserve and maintain cerebral microcirculation and protect nerve cells after cerebral insult [11, 44]."
"Our key finding in our main study group (patients that did not develop DCI) was that intravenous sodium nitrite led to an increase in ADR and alpha power above baseline and saline placebo. We suggest that these changes reflect the action of NO and relate to a generally less ischaemic brain pattern."
"As already discussed, nitrite is reduced to NO specifically well in hypoxic and acidic environments [16, 17]. Therefore, infused nitrite could preferentially be converted to NO in the injured brain, e.g. after SAH. In injured but residually functional tissue, NO could best exert its neuroprotective effects, including an increase in regional cerebral perfusion, which is reflected in EEG. In contrast, an increased level of nitrite in normoxic tissue of healthy brains would not have a large effect on brain perfusion and the EEG would not change accordingly."
Why is Nitric Oxide important?
Nitric oxide synthase in hypoxic or ischemic brain injury - PubMed (nih.gov)
"During brain hypoxia ischemia processes, nitric oxide (NO) may play either a neurotoxic or a neuroprotective role, depending upon factors such as the NO synthase (NOS) isoform, the cell type by which NO is produced, and the temporal stage after the onset of the hypoxic-ischemic brain injury."
"NO produced by endothelial NOS plays a neuroprotective role by maintaining cerebral blood flow and preventing neuronal injury, as well as inhibiting platelet and leukocyte adhesion."
The key role of nitric oxide in hypoxia: hypoxic vasodilation and energy supply-demand matching - PubMed (nih.gov)
"A mismatch between energy supply and demand induces tissue hypoxia with the potential to cause cell death and organ failure. Whenever arterial oxygen concentration is reduced, increases in blood flow--hypoxic vasodilation--occur in an attempt to restore oxygen supply. Nitric oxide (NO) is a major signaling and effector molecule mediating the body's response to hypoxia, given its unique characteristics of vasodilation (improving blood flow and oxygen supply) and modulation of energetic metabolism (reducing oxygen consumption and promoting utilization of alternative pathways)."
What do you think?
---
My hypothesis is that as Sodium Nitrite reacts with the blood causing hypoxia, at the same time by being converted into Nitric Oxide, It protects the brain from Hypoxic-Ischaemic (Brain tissue damage due to the lack of oxygen) brain injury up to the moment of death. Given that hypoxia is completely reversible as long as the brain tissue is not damaged, if a person is 'saved' before the Hypoxic-Ischaemic brain injury could occur, the protection from NO would leave the brain completely fine until it is supplied back with the normal amount of oxygen. As the protection wears off, your brain cells will start to die (Hypoxic-Ischaemic) and in this stage permanent brain damage is possible. In conclusion, your brain nerves won't start to die immediately after your oxygen level has dropped; it varies from minutes to hours until the effect of NO starts to wear off and leave your brain cells to die naturally due to the lack of oxygen.
So you can get brain damage if someone saves you at the tiny exact moment when the protection from Nitric Oxide wears off, but that is unlikely since most people get saved within the time the Nitric Oxide is still protecting your brain cells. We've never had any reported cases regarding brain damage due to SN poisoning separate from cardiac arrest. If you go into a cardiac arrest after ingesting SN, even after your blood is converted back to normal with Methylene Blue, the blood can no longer reach the brain since the heart has already stopped beating/not beating effectively to pump the normal blood back to the brain.
With similar methods such as Hanging or the Exit Bag method, there is no chemical that protects your brain cells and if someone finds you minutes later, you'll have a higher chance of getting permanent brain injury.
---
Sodium Nitrite is converted into Nitric Oxide which helps to protect your brain's nerve cells:
Early Intravenous Infusion of Sodium Nitrite Protects Brain Against In Vivo Ischemia-Reperfusion Injury (ahajournals.org)
"The rate of nitric oxide (NO) generation from nitrite is linearly dependent on reductions in oxygen and pH levels. Recently, nitrite-derived NO has been reported to exert a profound protection against liver and heart ischemia-reperfusion injury. In this study, we hypothesized that nitrite would be reduced to NO in the ischemic brain and exert NO-dependent neuroprotective effects."
"Nitrite exerted profound neuroprotective effects with antioxidant properties in the ischemic brains. These results suggest that nitrite, as a biological storage reserve of NO, may be a novel therapeutic agent in the setting of acute stroke."
Beneficial Effect of Sodium Nitrite on EEG Ischaemic Markers in Patients with Subarachnoid Haemorrhage | SpringerLink
"Infused sodium nitrite is well suited to alter brain states after cerebral damage. It can safely be administered [23] and is converted to NO in hypoxic and acidic conditions [16, 17], which can be observed after SAH [6, 42]. It can support cerebral autoregulation after SAH [43] and, crucially, helps preserve and maintain cerebral microcirculation and protect nerve cells after cerebral insult [11, 44]."
"Our key finding in our main study group (patients that did not develop DCI) was that intravenous sodium nitrite led to an increase in ADR and alpha power above baseline and saline placebo. We suggest that these changes reflect the action of NO and relate to a generally less ischaemic brain pattern."
"As already discussed, nitrite is reduced to NO specifically well in hypoxic and acidic environments [16, 17]. Therefore, infused nitrite could preferentially be converted to NO in the injured brain, e.g. after SAH. In injured but residually functional tissue, NO could best exert its neuroprotective effects, including an increase in regional cerebral perfusion, which is reflected in EEG. In contrast, an increased level of nitrite in normoxic tissue of healthy brains would not have a large effect on brain perfusion and the EEG would not change accordingly."
Why is Nitric Oxide important?
Nitric oxide synthase in hypoxic or ischemic brain injury - PubMed (nih.gov)
"During brain hypoxia ischemia processes, nitric oxide (NO) may play either a neurotoxic or a neuroprotective role, depending upon factors such as the NO synthase (NOS) isoform, the cell type by which NO is produced, and the temporal stage after the onset of the hypoxic-ischemic brain injury."
"NO produced by endothelial NOS plays a neuroprotective role by maintaining cerebral blood flow and preventing neuronal injury, as well as inhibiting platelet and leukocyte adhesion."
The key role of nitric oxide in hypoxia: hypoxic vasodilation and energy supply-demand matching - PubMed (nih.gov)
"A mismatch between energy supply and demand induces tissue hypoxia with the potential to cause cell death and organ failure. Whenever arterial oxygen concentration is reduced, increases in blood flow--hypoxic vasodilation--occur in an attempt to restore oxygen supply. Nitric oxide (NO) is a major signaling and effector molecule mediating the body's response to hypoxia, given its unique characteristics of vasodilation (improving blood flow and oxygen supply) and modulation of energetic metabolism (reducing oxygen consumption and promoting utilization of alternative pathways)."
What do you think?
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