
MB has very interesting quantum effects on mitochondria with stretched out respiratory proteins that lead to almost all illnesses. So, what does that mean? People who have poor mitochondrial function have enlarged mitochondria and a reduced efficiency with which to respirate (make energy, water, transfer oxygen/carbondyoxide and absorb light). As we know from the laws of thermodynamics, anything that is larger is less energy efficient. So, can MB improve sub-cellular thermodynamics? The modern world creates an environment that favours activation of the paraventricular nucleus (PVN) to cause a chronic stress response. MB can help someone who lives in a highly stressed environment. Your immediate environment must be considered when managing stressors in your life, it is often the key one (blue light, nnEMF, toxins, etc).
Focal activation of the sympathetic nervous system can lead to syndromes that lower vagal tone chronically. This can lead to any acute environmental stressor triggering a vasoplegic response.
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Acute vasoplegic syndrome is generally defined in medicine as an arterial pressure <50 mm Hg, cardiac index >2.5 L /min/m2, right atrial pressure <5 mm Hg, left atrial pressure <10 mm Hg and low systemic vascular resistance <800 dyne/sec/cm.
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Chronic vasoplegic syndrome is generally defined as an adrenal fatigue type syndrome.
Methylene Blue’s function in biology
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Mitochondria: It changes the oxidation state of iron from Fe+2 to Fe+3 which allows the body to regenerate melanin. When iron is at Fe+3, oxygen is delivered to mitochondria to accept the electrons. Oxygen is paramagnetic thus it’s drawn to things with a magnetic field. The ATPase is the result of the electron transport chain (faraday current) as electrons are reduced and oxidised (redoxed) and protons are pumped into the F0 head of the ATPase spinning it. The ATPase spins even faster when the mitochondria are exposed to full spectrum red/near infrared light. And again, even faster when the mitochondria sense the subtle strength earth’s magnetic field (or a transcranial magnet). Thus, MEG machines show that humans create a magnetic field. When a transcranial magnet and red/IR light are applied to a mitochondrion it is much more efficiently able to create water and melatonin. This melatonin can fix autophagy and apoptosis so that people can sleep better and heal. Add to this grounding whilst facing east watching sunrise, eating protein and fat with minimal carbs (like a great white shark), and add in UV light exposure so they can build back melanin on the outside to improve the amount of light we can make inside with our wide-band semiconductors like potassium. Methylene blue allows the body to delocalise electrons via melanin.
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MB delivers nitric oxide to the tissue that it is in resulting in increased oxygen absorption and thus a neuroprotective action. This is beneficial when the body is in a hypoxic state such as when exposed to excessive blue light and nnEMF. Nitric oxide production reduces with age and MB helps produce more Nitric Oxide. UVA sunlight also stimulates NO production, UVA + MB is a great recipe for oxygen delivery to the tissues.
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MB improves proton tunnelling (enzyme reactions, energy production in mitochondria). MB speeds up chemical reactions in the body such as energy production and enzyme reactions. MB allows the body to free up protons. MB works to deplete the TCA cycle of deuterium. Seed oils are loaded with deuterium.
Mechanisms of why MB works: Mitochondria as a role for neuroprotection – Methylene blue and Photobiomodulation (PBM)
The combined use of MB and PBM may provide a promising new avenue for the treatment of multiple brain diseases.
Primary Mechanisms Underlying Mitochondria Protection through PBM. PBM treatment causes NO to dissociate from Complex IV (cytochrome c oxidase, CCO), causing the complex’s activity to increase. This allows the flux of electrons, the pumping of protons, and the synthesis of ATP to increase, thereby boosting cellular energy levels. In addition, when PBM stimulates Complex IV activity in normal cells, mitochondrial membrane potential is increased above normal baseline levels, resulting in a brief and rather modest increase in ROS production. The short burst of ROS is able to activate cytoprotective signaling, which attenuate ROS induced oxidative damage and neuroinflammation.
Primary Mechanisms Underlying Mitochondria Protection through MB. MB reroutes the pathway of electron transfer by working as an alternative electron transporter. By bypassing the ETC between Complex I and Complex III, MB efficiently attenuates electron leakage and subsequent ROS generation.
Diagram of electron leakage in brain disease. Electrons in the mitochondrial ETC are transferred along a series of four protein complexes (Complexes I-IV) with the aid of electron transporters NADH, FADH2, ubiquinone (Co-enzyme Q10, CoQ), and cytochrome c (Cyt c). As a result of this electron transfer, protons are pumped by Complexes I, III, and IV from the mitochondrial matrix into the intermembrane space, thereby generating an electrochemical gradient across the inner mitochondrial membrane. This gradient is used to propel ATP synthase (Complex V) to produce ATP. Although this process is highly efficient, electrons can escape from Complex I and Complex III and be transferred to O2, which is reduced to the radical O2•−. This ROS production is exacerbated under pathological conditions such as brain disease and activates inflammatory processes, thereby establishing a cycle of ROS production, inflammation, and neuronal damage.

Citation:
History of Methylene blue
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Methylene blue is a derivative of hydroxychloroquine.
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Albert Szent-Györgyi was working with Vitamin C [Hexuronic Acid] (C13H20O10, he also came across MB (C16H18N3SCl). When redox of electrons and proton tunnelling were interrupted for any reason, the biologic system became more linear instead of non-linear as its designed. Thus, the protons for NAD+/NADPH cannot be recycled well and NAD drops indicating a proton problem at cytochrome 1 of the mitochondria. Vitamin C re-established proton flow. Hence citric acid is critical in the TCA cycle. Methylene blue can also help fix this problem to re-establish cytochrome 1 NAD functioning.
Methylene blue In a clinical and medical setting
Methylene blue is used as a reducing agent to convert methemoglobin (an oxidized form of haemoglobin) back into functional haemoglobin. This helps haemoglobin to bind and release oxygen more effectively, allowing blood to work with oxygen better.
Methemoglobin is unable to transport oxygen effectively because it cannot release oxygen to the body's tissues. When methemoglobin levels are elevated, it can lead to a condition known as methemoglobinemia, which is characterized by reduced oxygen-carrying capacity in the blood.
Methylene blue, when administered under the appropriate medical supervision and in the right context, can help alleviate methemoglobinemia and improve the blood's ability to transport and deliver oxygen. It does this by facilitating the conversion of methemoglobin to haemoglobin, which is a critical process for maintaining adequate oxygen supply to the body's cells and tissues.
Benefits to MB
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MB provides a bigger benefit for people with low redox than those with well-functioning mitochondria.
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Improves mitochondrial ETC bioenergetics and combats hypoxia MB’s main effect is on proton spin in the TCA cycle within the mitochondria. MB acts as a proton acceptor in defective mitochondria to perform and augment substrate-level phosphorylation (SLP) by removing deuterium from the TCA intermediates, which results in the production of ATP independent from the ATP synthase (ATPase). Methylene blue oxidizes NADH into NAD+, to replenish falling NAD+ levels due to the mitochondrial damage and increases the NAD+/NADH ratio as a result. It is not the ratio that matters most, but the fact that the H in NADH comes from the TCA cycle intermediates and it must be in the H+ form and not come from any trapped deuterium in the matrix. So, MB is a proton acceptor (Oxidiser) and Depletes Deuterium from the mitochondrial matrix and can boost NAD+ improving bioenergetics.
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Improves pseudohypoxia by improving magnetic flux.
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Hypoxia is the lack of availability of molecular oxygen.
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Aromatase inhibitor: reduces the conversion of testosterone to estrogen, raising testosterone.
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Photosensitiser: Photosensitisers are taken up in greater quantities by more damaged cells and used to heal the cell more effectively. Eg: Methylene Blue, Vitamin C and Curcumin. This improves skin health because it’s able to absorb sunlight, particularly red/infrared as its 51% of the sun’s light.
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Anti-cancer: Can be used as an effective treatment for patients with cancer. It acts as an oxygenator when used in the human body. Taking it orally is not the most effective method. The best treatment with Methylene blue is IV. You must see a doctor to have this done. MB does the same as Vitamin C and depletes D+ (Deuterium) from the mitochondria, it also sensitises you to sunlight.
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A lack of UV and IR light with excessive chronic blue light exposure bends light in the brain to make aquaporin 4 water gates stay open and causes more seizures and poor thinking because this lowers dopamine levels. The longer an AQA 4 gate stays open the more AMPK pathways are up regulated and the more glucose a cell uses and the more ELF-UV light it releases and the more calcium will efflux. Nora Volkow and Allan Frey have published on this. The more ELF-UV light emitted the lower your vitamin D levels will be measured in your blood plasma. This is the basis of the Warburg effect. It is a chronic light stress response and not a cancer pathway as most believe today. Blue light elicits the Warburg metabolism. Hack it with MB.
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Methylene blue might work to mitigate this effect. Biohack with methylene blue. Methylene blue has massive effects on mitochondria. Remember water can be blue shifted when it has less light energy within its molecular networks. By absorbing blue light and appearing blue, it can circulate easily through the bodies’ fluids; it reflects blue light inside of us while acting as another electron donor would in a mitochondria, oxygenating cells and reversing the very damages caused by an excess of blue light at our surfaces.
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Methylene blue combined with sun light has been used to treat resistant plaque psoriasis, AIDS-related Kaposi’s sarcoma, West Nile virus, and to inactivate staphylococcus aureus, [used it in a biohack] HIV-1, Duck hepatitis B, adenovirus vectors, and hepatitis C. It is now being used in autoimmune conditions, neurodegeneration, TBI, and diabetes. Phenothiazine dyes and light have been known to have virucidal properties for over 70 years. This is why methylene blue works in combating many viral diseases. I have a sense this is why MB is on the ISS in space. It is also why I think endosymbiosis might have been between a virus and a bacterium and not an archaea and bacteria. Eukaryotes still benefit from MB treatments, so it means our viral marketing is a deep evolutionary link to our nucleic acid design and function.
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Methylene blue also blocks accumulation of cyclic guanosine monophosphate (cGMP) by inhibiting the enzyme guanylate cyclase: this action results in reduced responsiveness of vessels to cGMP-dependent vasodilators like nitric oxide (NO) and carbon monoxide (CO). These work critically in the RPE of the retina where the melanopsin receptors are in our ganglion cells. NO and CO both work with incident UV light to increase O2 in tissues. Most diseases are associated with low venous oxygen saturation. This is why David Sinclair’s work showed most neolithic diseases were always linked to pseudohypoxia and low NAD+. Methylene blue increases O2 by helping haemoglobin’s heme protein offload more O2. Methylene blue can also serve as a non-selective inhibitor of NO synthase based upon the amount of UV light and oxygen present in a stimulus. This is very important in the vascular bed. It also makes every tissue have its own quantum signals. This is why RCT are close to worthless when you understand mitochondria function well. It also points out why the first four thoracic sympathetic rami link directly to the carotid system in humans. This pathway can be used to modulate the central retinal pathways in the eyes of man when his environment is made alien by an altered light frequency or by nnEMF.
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Methylene blue can act as an alternative electron acceptor and reverses the NADH inhibition in mitochondria. This means it raises NAD+. This is why cardiac and neurosurgeons and orthopaedic muscular surgeons like to use it in their sick patients. Methylene blue can be an adjunct in the management of patients experiencing vagoplegic syndrome after cardiac surgery and also in neurogenic vasospasm in subarachnoid aneurysmal bleeds. It has been used in compartment syndrome by orthopaedic surgeons for these reasons.
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Methylene blue is a monoamine oxidase inhibitor. MAOI’s act by inhibiting the activity of monoamine oxidase, thus preventing the breakdown of monoamine neurotransmitters and thereby increasing their availability. Thusly, methylene blue increases dopamine, melatonin, serotonin, and melanin levels on our surfaces to increase our ability to deal with sunlight properly. This makes MB a classic silent vagal stimulant. It means that vagal tone and UV light assimilation are fundamentally linked in the autonomic nervous system. It will also increase epinephrine and nor-epinephrine levels to increase BP and muscle power on a short-term basis. This explains why cold thermogenesis increases beta three sympathetic receptors to liberate protons in brown fat for beta oxidation on mitochondria.
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The parasympathetic nervous system uses chiefly acetylcholine (ACh) as its neurotransmitter, although peptides (such as cholecystokinin) can be used. The ACh acts on two types of receptors, the muscarinic and nicotinic cholinergic receptors. Most transmissions occur in two stages: When stimulated, the preganglionic neuron releases ACh at the ganglion, which acts on nicotinic receptors of postganglionic neurons. The postganglionic neuron then releases ACh to stimulate the muscarinic receptors of the target organ. These changes occur by monitoring how much UV light is being added back into the atomic lattice of our tissues at night. Nicotine is a fluorophore protein.
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Nicotinic channels mediate the majority of fast excitation in autonomic ganglia. Nicotine is made from aromatic amino acids that absorb UV light. Nicotine is a nightshade plant. People whose cells lack a decent quantity of ELF- UV light have trouble tolerating nightshade plants. Nicotine increases dopamine levels naturally. Anything that increases dopamine levels has huge effects on silent vagal stimulation. Not everyone can use this because not everyone can assimilate UV light well photoelectrically.
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Methylene blue is also a photosensitiser that generates peroxides and has a huge effect on catalase in RBC’s. MB can used to create singlet oxygen when exposed to both oxygen and light. Singlet oxygen is needed at cytochrome one in small bursts to lower mitochondrial heteroplasmy. This is why diabetics and obese people have no superoxide burst at cytochrome 1. Diabetics and the obese are people who came into the world with loose mito-nuclear coupling that got worse by blue light and nnEMF to lead to their other diseases. Diabetics and the obese need an ideal superoxide burst to clear our badly functioning mitochondria to increase their coupling to better match the environment they choose to live in. Fasting can help, but those who are leptin resistant have low ELF-UV light, so the effect is lowered. Hence why it’s wise to do the Leptin reset before using intermittent fasting as a way to shrink their respiratory proteins. MB can be used in this regard to make organic peroxides by a Diels-Alder reaction, which is “electron spin forbidden” with normal atmospheric triplet oxygen.
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Anti-nnEMF (i.e. RF and Blue Light)
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MB + Red/IR Light (sun) + DDW + Ketosis
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The main biologic defect of nnEMF is dehydration, or a loss of H+ recycling in TCA intermediates or a change in proton spin fractionation. MB can lighten this load in environments with nnEMF. Red light from the sun helps extend the effect and water from glaciers can be another adjunct. It turns out ketosis can also extend the effect too, but all need to be present together to get the mitochondrial effect of removing a Warburg shift (glucose metabolism). MB does this through nitric oxide regulation, regulating iron from Fe2+ -> Fe3+ (to regenerate melanin) and speeding up proton tunnelling (ETC and enzyme reactions)
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MB is capable of lowering nitric oxide when something in the environment is stimulating calcium efflux that releases too much nitric oxide to lead to diseases.
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Nitric oxide synthases are a family of enzymes catalyzing the production of nitric oxide (NO) from L-arginine. Nitric oxide is an important cellular signaling molecule that has sensitive and specific functions that have to be controlled on a dose response basis but more importantly on a time scale basis. When both are affected, cell signaling is unyoked and can lead to autoimmune, metabolic, and cell growth disorders that all have elevated ubiquitin marking associated with them. Nitric Oxide helps modulate vascular tone, insulin secretion, airway tone, and peristalsis, and is involved in angiogenesis and neural development.
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Combats Septic Shock
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Nitric oxide (NO) is a free radical with an unpaired electron with a specific spin state that is affected by electric and magnetic fields. It is the proximate cause of septic shock and functions in autoimmune disease generation. This is because nitric oxide is mediated in mammals by the calcium-calmodulin controlled isoenzymes like eNOS (endothelial), nNOS (neuronal NOS), and iNOS (immune). This is how calcium efflux and calcium flows in mitochondria can be affected by nnEMF and blue light link to diseases like Hashimoto’s, MS, all types of diabetes, and brain degeneration.
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Calcium efflux destroys Nitric Oxide which destroys the blood.
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Calcium is the concrete of the lipid bilayer in all eukaryotic cell membranes, sticking them together tighter. The tighter they are the less they move. When UVB sunlight or light liberated from the microbiome hits the atoms on your biologic surfaces and nitric oxide (NO) and Vitamin D3 are present and working together, they lower molecular vibrations of cell membrane atoms. This low vibration state allows calcium to function optimally and energy to be transduced more effectively from nature to the biologic system. The more nnEMF or blue light you face, the larger the amplitude of the vibrations and this causes the cell membranes to lose electrons. A loss of electrons from the pi-electron cloud on cell membranes lower lipids and proteins hydrophilic potential. This also reduces the size of the coherent domains (EZ) in cell water. These signals cannot properly link our surfaces to the waveforms that are truly presented in our mitochondria and humans get diseases. Our mitochondria move further from our nucleus and the subsequent illness causes more heteroplasmy in mitochondria. This results in more severe diseases with different phenotypes. This is how obesity can turn into Hashimoto’s and Hashimoto’s into MS, and MS into psoriasis, and psoriasis into a cancer.
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What does this mean if you live at sea level at a latitude away from the equator? It means you have a lower threshold to handle electromagnetic nonnative energies and you are more likely to suffer from more diseases like MS, cancer, or diabetes. This is what we see in Scandinavians. This is why autoimmune conditions like Multiple Sclerosis, cancer, and diabetes cases are explosive in incidence and prevalence as we travel away from the equator.
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Wi-Fi, Microwaves, Blue light and other nnEMF both liberate calcium by causing it to efflux. This causes mitochondria to swell, the respiratory proteins get further apart, changing their geometry, causing the tunnelling of electrons to slow dramatically. Every increase of one Angstrom between respiratory proteins slows tunnelling of electrons by a factor of ten. This size and shape change also slows proton tunnelling; and since proton tunnelling is how enzymes work this slows biochemical flux and leads to even more circadian disruption. Anytime electron and proton tunnelling are disrupted timing in life is altered, diseases manifest.
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The more microwaves and mobile technology you use or allow in your life the less NO and Vitamin D3 you can make on your skin, retina, gut, and lung to quiet the atoms in your cell membrane to make the energy or decipher environmental signals from the Schumann resonance or from the sun. As life loses this ability to organise, neolithic diseases become expressed. As heteroplasmy increases neolithic disease incidence increase due to clonal amplification of badly functioning mitochondria. The quantitative amount of heteroplasmy is as important as the qualitative changes. The amount of heteroplasmy has been shown to alter the phenotype of the disease humans get without any changes ever occurring to the nuclear genome. This is the work that Doug Wallace has worked on for 4 decades.
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Combats Dehydration
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Combats Calcium Efflux
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How Methylene Blue Antioxidants can slow cognitive decline.

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Methylene Blue can be a hydrogen proton donor and acceptor and it can be an electron donor and acceptor.
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Methylene Blue can help regenerate melanin because it reverses hypoxia and oxygenates tissues. It keeps the oxidation state of iron to Fe+3 which delivers more nitric oxide and oxygen to the melanin sheaths. High levels of oxygen renovate melanin and hypoxia degrades melanin.
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MB donates and accepts electrons, combine with hyperbaric oxygen or infrared light. MB provides a hermetic on the mitochondria via generating H2O2 which can also be induced by exercise.
Contraindications for MB
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Mutated or blocked methylation pathways: If too many +/+ MTHFR SNP’s then this may result in MB oxidising where it shouldn’t.
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G6PD deficiency the use of MB may have serious complications and is contraindicated in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. Methylene blue can actually cause methemoglobinemia in high doses by its oxidant effect and induce haemolysis in cases of G6PD deficiency. Vitamin C, ascorbic acid, has been used successfully to treat methemoglobinemia instead of methylene blue. Case studies have shown the ability of ascorbic acid to normalize oxygen saturation within one hour of administration.
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Be careful with MB if you have kidney or liver issues or low Serotonin. Serotonin syndrome is the issue with MB, but it is only really a concern when MB is delivered in IV. Oral MB
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If you are taking SSRI’s or MAO Inhibitors Methylene blue may be problematic. Check with your doctor first.
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MB inhibits MAO A and B. hence MB doesn’t allow the body to break down MAO’s so Serotonin can rise in this case. Extreme Serotonin syndrome is hypopyrexia or tachycardia.
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Genes to be aware of affected by Methylene Blue
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SNPs slows down MAO-A and MAO-B thus accumulate Serotonin
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SNP’s which slow down COMT which then means the body will accumulate adrenaline, noradrenaline and dopamine.
MB Interesting Points
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Methylene blue (MB) is an inhibitor of nitric oxide synthase and guanylate cyclase.
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MB has been found to improve:
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The hypotension associated with various clinical states.
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Hyper dynamic circulation in cirrhosis of liver and severe hepatopulmonary syndrome.
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Transient and reproducible improvement in blood pressure and cardiac function in septic shock.
Cites:
1. Bosoy, Dimitry , Axelband , et al. Utilization of methylene blue in the setting of hypotension associated with concurrent renal and hepatic failure: a concise review. OPUS 12 Scientist. 2008;2:21–9.
2. Peter schenk, Christian Madl, Shahrzad Rezaie-Majd, Stephen Lehr, Christian Muller. Methylene blue improves the hepatopulmonary syndrome. Ann Intern Med. 2000;133:701–6.
3. Preiser, Jean-Charles, Lejeune, et al. Methylene blue administration in septic shock: A Clinical Trial. Critical Care Medicine. 1995;23:259–64.
4. Ertugrul Ozal, Erkan Kuralay, Vedat Yildirim, et al. Preoperative methylene blue administration in patients at high risk for vasoplegic syndrome during cardiac surgery. Ann Thorac Surg. 2005;79:1615–9.
5. Armand Mekontso-Dessap, Remi Houel, Celine Soustelle, Matthias Kirsch, Dominique Thebert, Daniel Y. Loisance.Risk factors for post-cardiopulmonary bypass vasoplegia in patients with preserved left ventricular function. Ann Thorac Surg. 2001;71:1428–32.
6. Tuman KJ, McCarthy RJ, O’Connor CJ, Holm WE, Ivankovich AD. Angiotensin-converting enzyme inhibitors increase vasoconstrictor requirements after cardiopulmonary bypass. Anesth Analg. 1995;80:473–9.
7. Leyh Reiner G, Kofidis Theo, Struber Martin, et al. Methylene Blue: The drug of choice for catecholamine-refractory vasoplegia after cardiopulmonary bypass? J Thorac Cardiovasc Surg. 2003;125:1426–31.
8. Levin Ricardo L, Degrange Marcela A, Bruno Gustavo F, et al. Methylene blue reduces mortality and morbidity in vasoplegic patients after cardiac surgery. Ann Thorac Surg. 2004;77:496–9.
9. Gachot B, Bedos J.P, Veber B, Wolff M, Regnier B. Short-term effects of methylene blue on hemodynamics and gas exchange in humans with septic shock. Intensive Care Medicine. 1995;21:1027–31.
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13. Moritoki Egi, Rinaldo Bellomo, Christoph Langenberg, et al. selecting a vasopressor drug for vasoplegic shock after adult cardiac surgery: A systematic literature review. Ann Thorac Surg. 2007;83:715–23.
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16. Schirmer R.H, Coulibaly B, Stich A, et al. Methylene blue as an antimalarial agent. Redox rep. 2003;8:272–5.
17. Marianne Boylston, Deborah Beer. Methemoglobinemia: A Case Study. Critical Care Nurse. 2002;22:50–5.
18. Clifton, Jack II, Leikin, Jerrold Methylene blue. American Journal of Therapeutics. 2003;10:289–91.
19. Wondrak GT. NQO1-activated phenothiazinium redox cyclers for the targeted bioreductive induction of cancer cell apoptosis. Free Radic Biol Med. 2007;43:178–90.
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21. Pelgrims J, De Vos F, Van den Brande J, Schrijvers D, Prové, Vermorken JB. Methylene blue in the treatment and prevention of ifosfamide-induced encephalopathy: report of 12 cases and a review of the literature. British Journal of Cancer. 2000;82:291–4.
22. Gordan Donald L, Airan Mohan C, Thomas William, Seidman Leon H. Parathyroid identification by methylene blue infusion. British Journal of Surgery. 2005;62:747–9.
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37. www.ncbi.nlm.nih.gov/pmc/articles/PMC3949155/
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