Methylene blue or tolonium chloride antagonism of sodium nitrite induced methemoglobinemia

1979 ◽  
Vol 2 (1) ◽  
pp. 81-86 ◽  
Author(s):  
G.E. BURROWS
Keyword(s):  
Methylene Blue ◽  
Sodium Nitrite ◽  
Tolonium Chloride

Sodium nitrite, a potent relaxant of rat stomach fundus: in vitro evidence

1998 ◽  
Vol 76 (10-11) ◽  
pp. 989-999 ◽  
Author(s):  
Michal Ceregrzyn ◽  
Tsuyoshi Ozaki ◽  
Atsukazu Kuwahara ◽  
Maria Wiechetek
Keyword(s):  
Methylene Blue ◽  
Potassium Channels ◽  
Guanylate Cyclase ◽  
Sodium Nitrite ◽  
Longitudinal Muscle ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Rat Stomach ◽  
Longitudinal Muscle Layer ◽  
Stomach Fundus

The effects of sodium nitrite (0.1, 1, 10 mM) on mechanical activity of isolated rat stomach fundus muscle and the influence of guanylate cyclase activity inhibitor (methylene blue) and channel inhibitors (tetrodotoxin, charybdotoxin, apamin) were studied. Nitrite evoked dose-dependent relaxation in the longitudinal and circular muscle layers. The lowest effective concentration of sodium nitrite was 0.1 mM, which is comparable with the NOAEL (no observed adverse effect level). Tetrodotoxin (1 µM) markedly inhibited electrically induced contraction and rebound relaxation, but did not influence the nitrite-induced relaxation. Charybdotoxin (100 nM) decreased the relaxation evoked by 10 mM nitrite to 52.3 and 65.7% of control reaction in the circular and longitudinal muscle layer, respectively. Apamin (100 nM) did not influence the nitrite-induced relaxation. Methylene blue (10 µM) decreased relaxation induced by nitrite in the longitudinal and circular muscle layer, respectively, to 66.7 and 54.3% of the response to 1 mM nitrite alone. Relaxation induced by nitrite was decreased in the presence of L-cysteine (5 mM), and in the circular and longitudinal muscle layer reached 29.6 and 23.1%, respectively, of the response to 1 mM nitrite alone. We conclude that the relaxing effect of nitrite on gastric fundus results from its direct action on smooth muscle cells and probably the enteric nervous system is not involved in this action. The nitrite-elicited relaxation depends on activation of guanylate cyclase and high conductance Ca2+-activated potassium channels; however, activation of potassium channels might be a part of or might act in parallel with the mechanism involving the cyclic GMP system. Effects of nitrite observed in the presence of L-cysteine suggest that nitrosothiols are not responsible for nitrite-evoked activation of guanylate cyclase.Key words: nitrite, gastric motility, tetrodotoxin, methylene blue, charybdotoxin, L-cysteine.

Methylene blue and tolonium chloride impair cardiac performance in human atrial tissue

2013 ◽  
Vol 61 (S 01) ◽  
Author(s):  
H Weiler ◽  
O Moeller ◽  
M Wohlhöfer ◽  
C Bening ◽  
CF Vahl
Keyword(s):  
Methylene Blue ◽  
Cardiac Performance ◽  
Atrial Tissue ◽  
Tolonium Chloride

scholarly journals Severe Methemoglobinemia due to Sodium Nitrite Poisoning

2016 ◽  
Vol 2016 ◽  
pp. 1-3 ◽  
Author(s):  
Kenichi Katabami ◽  
Mineji Hayakawa ◽  
Satoshi Gando
Keyword(s):  
Intensive Care Unit ◽  
Methylene Blue ◽  
Sodium Nitrite ◽  
Blood Test ◽  
Gastric Lavage ◽  
Accurate Diagnosis ◽  
Loss Of Consciousness ◽  
Methemoglobin Level ◽  
Neurologic Impairment ◽  
Transient Loss

Case. 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 methemoglobin level of 92.5%.Outcome. We treated the patient with gastric lavage, activated charcoal, and methylene blue (2 mg/kg) administered intravenously. Soon after receiving methylene blue, his cyanosis resolved and the methemoglobin level began to decrease. After relocation to the intensive care unit, his consciousness improved and he could recall ingesting approximately 15 g sodium nitrite about 1 hour before he was brought to our hospital. The patient was discharged on day 7 without neurologic impairment.Conclusion. Severe methemoglobinemia may be fatal. Therefore, accurate diagnosis of methemoglobinemia is very important so that treatment can be started as soon as possible.

scholarly journals Comparative efficacy of ascorbic acid, adrenaline and oxytetracycline supplementation against nitrite poisoning in rats (Rattus norvegicus)

1970 ◽  
Vol 25 (1) ◽  
pp. 25-31
Author(s):  
F Yasmin ◽  
MA Awal ◽  
A Ghosh ◽  
MB Rashed ◽  
M Mostofa
Keyword(s):  
Methylene Blue ◽  
Vitamin C ◽  
Sodium Nitrite ◽  
Rattus Norvegicus ◽  
Leukocyte Count ◽  
Total Leukocyte Count ◽  
Comparative Efficacy ◽  
Haemoglobin Content ◽  
Group D ◽  
Nitrite Intoxication

The effects of methylene blue, vitamin C, adrenaline and oxytetracycline against sodium nitrite intoxication was studied in Long Evan's (Rattus norvegicus) rats (n=128) in eight groups (A - H). Except control, intoxication was produced by administering sodium nitrite. Rats were treated with methylene blue (group C), vitamin C (group D), adrenaline (group E) and oxytetracycline (group F), and with vitamin C, adrenaline and oxytetracycline (group G); methylene blue, vitamin C, adrenaline and oxytetracycline (Group H). Rats of group C and group H recovered within 24-72 and 13-40 hours, respectively. Other groups showed severe toxic signs including excitement, restlessness, muscle tremor, anoxia, and coma, followed by death within 60 hours. Total erythrocyte count, total leukocyte count, haemoglobin content and packed cell volume were significantly (p<0.01) reduced, and returned to normal at day 14 after methylene blue treatment. The activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were elevated significantly (p<0.01) in all intoxicated groups and within 14 days ALT values reached normal level after methylene blue administration. DOI: 10.3329/bvet.v25i1.4615 Bangl. vet. 2008. Vol. 25, No. 1, 25-31

Methaemoglobin Production and Reduction by Methylene Blue and the Interaction of Methylene Blue with Sodium Nitrite in vivo

1989 ◽  
Vol 8 (5) ◽  
pp. 359-364 ◽  
Author(s):  
T.C. Marrs ◽  
J.E. Bright ◽  
R.H. Inns
Keyword(s):  
Methylene Blue ◽  
Sodium Nitrite ◽  
High Concentrations

Methylene blue, at high concentrations, interferes with the estimation of methaemoglobin using the IL 282 CO-oximeter: the dye does not interfere with the method of Evelyn & Malloy for determination of methaemoglobin. In beagle bitches methylene blue causes both methaemoglobinogenesis and methaemoglobin reduction, the effect of the former being to delay the decline of methaemoglobin levels, when methylene blue is used to reverse the methaemoglobinaemia produced by sodium nitrite.

scholarly journals Fatal Methaemoglobinaemia Due To Intentional Sodium Nitrite Poisoning

2021 ◽  
Vol 20 (2) ◽  
pp. 148-150
Author(s):  
GR Huntington ◽  
◽  
JM Pennington ◽  
Keyword(s):  
Emergency Department ◽  
Methylene Blue ◽  
Sodium Nitrite ◽  
Venous Blood ◽  
Blood Gas ◽  
Hypoxic Brain Injury ◽  
Improved Outcomes ◽  
Hypoxic Brain ◽  
Ct Head ◽  
Venous Blood Gas

We report a case of fatal methaemoglobinaema resulting from sodium nitrite poisoning. A 28 year old woman arrested in the emergency department following collapse. During resuscitation a venous blood gas revealed a methaemoglobin percentage of 81%. Following treatment with methylene blue, sodium bicarbonate and adrenaline, the methaemoglobin decreased. Prior to transfer to intensive care, a CT head revealed extensive hypoxic brain injury. Two days later brain death was confirmed on brainstem testing. Severe methaemoglobinaemia is rapidly fatal, with fast diagnosis and treatment associated with improved outcomes.

scholarly journals Glucose-6-phosphate dehydrogenase and glutathione reductase activity in methemoglobin reduction by methylene blue and cyst amine: study on glucose-6-phosphate dehydrogenase-deficient individuals, on normal subjects and on riboflavin-treated subjects

1988 ◽  
Vol 30 (5) ◽  
pp. 370-378 ◽  
Author(s):  
Benedito Barraviera ◽  
Paulo Eduardo de Abreu Machado ◽  
Domingos Alves Meira ◽  
Paulo Roberto Curi ◽  
Jair Natal Pires Martins ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Glutathione Reductase ◽  
Sodium Nitrite ◽  
Reductase Activity ◽  
Red Cells ◽  
Residual Amount ◽  
Before And After ◽  
Glutathione Reductase Activity ◽  
Males And Females ◽  
Glucose 6 Phosphate Dehydrogenase

The authors have standardized methods for evaluation of the activity of the glucose-6-phosphate dehydrogenase and of glutathione reductase. The general principle of the first method was based on methemoglobin formation by sodium nitrite followed by stimulation of the glucose-6-phosphate dehydrogenase with methylene blue. Forty six adults (23 males and 23 females) were studied. Subjects were not G6PD deficient and were aged 20 to 30 years. The results showed that methemoglobin reduction by methylene blue was 154.40 and 139.90 mg/min (p<0.05) for males and females, respectively, in whole blood, and 221.10 and 207.85 mg/min (n.s.), respectively, in washed red cells. These data showed that using washed red cells and 0.7g% sodium nitrite concentration produced no differences between sexes and also shortened reading time for the residual amount of methemoglobin to 90 minutes. Glutathione reductase activity was evaluated on the basis of the fact that cystamine (a thiol agent) binds to the SH groups of hemoglobin, forming complexes. These complexes are reversed by the action of glutathione reductase, with methemoglobin reduction occurring simultaneously with this reaction. Thirty two adults (16 males and 16 females) were studied. Subjects were not G6PD deficient and were aged 20 to 30 years. Methemoglobin reduction by cystamine was 81.27 and 91.13 mg/min (p<0.01) for males and females, respectively. These data showed that using washed red cells and 0.1 M cystamine concentration permits a reading of the residual amount of methemoglobin at 180 minutes of incubation. Glutathione reductase activity was evaluated by methemoglobin reduction by cystamine in 14 females before and after treatment with 10 mg riboflavin per day for 8 days. The results were 73.69 and 94.26 jug/min (p<0.01) before and after treatment, showing that riboflavin treatment increase glutathione reductase activity even in normal individuals. Three Black G6PD-deficient individuals (2 males and 1 female) were also studied. The G6PD and glutathione reductase were partially activated, the change being more intense in males. On the basis of race and of the laboratory characteristics observed, it is possible to suggest that the G6PD deficiency of these individuals is of the African type and that the female is heterozygous for this deficiency. Analysis of the results as a whole permitted us to conclude that the methods proposed here were efficient for evaluating the activity of the glucose-6-phosphate dehydrogenase and of glutathione reductase. The latter is dependent on the pentose pathway, which generates NADPH, and on riboflavin, a FAD precursor vitamin.

A Case of Severe Methemoglobinemia with Shock and High Saturation Gap Following Suicidal Ingestion of Sodium Nitrite-Saved by Oral Methylene Blue

2015 ◽  
Vol 22 (3) ◽  
pp. 147 ◽  
Author(s):  
Pahadiya Hans Raj ◽  
Choudhary Akanksha ◽  
Lakhotia Manoj ◽  
Gandhi Ronak ◽  
Mohamed Sadik
Keyword(s):  
Methylene Blue ◽  
Sodium Nitrite ◽  
High Saturation

Methylene blue inhibits coronary arterial relaxation and guanylate cyclase activation by nitroglycerin, sodium nitrite, and amyl nitrite

1981 ◽  
Vol 59 (2) ◽  
pp. 150-156 ◽  
Author(s):  
Carl A. Gruetter ◽  
Philip J. Kadowitz ◽  
Louis J. Ignarro
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Smooth Muscle ◽  
Guanylate Cyclase ◽  
Sodium Nitrite ◽  
Soluble Guanylate Cyclase ◽  
Enzyme Activation ◽  
Amyl Nitrite ◽  
Cyclase Activation ◽  
Guanylate Cyclase Activation

Relaxation by nitroglycerin, sodium nitrite, and amyl nitrite of bovine coronary arterial smooth muscle was inhibited by the oxidant methylene blue. Methylene blue also inhibited activation of bovine coronary arterial soluble guanylate cyclase by nitroglycerin, which required addition of cysteine. At concentrations less than 10 mM, sodium nitrite required the addition of one of several thiols or ascorbate to activate guanylate cyclase from bovine coronary artery. Guanylate cyclase activation by large amounts (50 μL) of saturated amyl nitrite gas did not require, but was enhanced by, the addition of thiols or ascorbate. However, similar to sodium nitrite, guanylate cyclase activation by smaller amounts (5 μL) of saturated amyl nitrite gas did require the addition of one of various thiols or ascorbate. Methylene blue markedly inhibited guanylate cyclase activation by sodium nitrite in the presence of cysteine or ascorbate and similarly inhibited enzyme activation by amyl nitrite either in the absence or presence of cysteine or ascorbate. These data support the hypothesis that nitrates and nitrites relax vascular smooth muscle by stimulating cyclic GMP formation. The results further suggest that, similar to relaxation and guanylate cyclase activation by nitroso-containing compounds, relaxation and enzyme activation by nitrates and nitrites may involve the formation of nitric oxide or complexes of nitric oxide as active intermediates.

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