Methemoglobin

Methemoglobin (also Hemiglobin or ferric hemoglobin) is a derivative of hemoglobin, the red blood pigment in erythrocytes ( red blood cells).

Is the divalent iron in the hemoglobin ( Hb), oxidized to the trivalent ( Fe 2 → Fe 3 ), is produced methemoglobin ( MetHb ). This can not bind oxygen, and changes the hemoglobin in its environment so that this only absorb oxygen, but can no longer give. Methemoglobin is produced in the erythrocytes under physiological conditions by the addition of oxygen in terms of auto-oxidation.

Methemoglobin is formed in cases of poisoning by oxidizing agents such as nitrites and hydrogen peroxide or by aromatic amino and nitro compounds such as aniline and nitrobenzene. Also include a number of drugs to the potential Methämoglobinbildnern: dapsone, prilocaine, sulfonamides, nitroglycerin, nitroprusside, nitric oxide (NO).

The enzyme methemoglobin reductase reduces methemoglobin to hemoglobin again, hence the Methämoglobinanteil generally does not exceed 1.5%. A particular sensitivity to Methämoglobinbildnern consists in infants, since up to the middle of the first year of life the activity of methemoglobin reductase is not yet fully developed.

From a Methämoglobinanteil of 15% cyanosis is observed from 30 to 40 %, the signs of oxygen deficiency show in tissues, particularly in the brain (confusion, dizziness, disturbance of consciousness ). Values ​​between 60 and 80% are fatal. Note that the measured pulse oximetry oxygen saturation is not lower than even at very high methemoglobin 80 to 85%.

The treatment is carried out by intravenous administration of methylene blue. This substance is itself a methemoglobin, however, the enzymatic regression high methemoglobin concentrations accelerate, with an equilibrium at around 10% Methämoglobinanteil. The exchange transfusion is a treatment option in very severe cases.

Another antidote is toluidine blue, which is also known as tolonium chloride.

In a cyanide poisoning in addition to sodium thiosulfate and hydroxocobalamin and methaemoglobin (4- dimethylamino phenol, abbreviated as DMAP ) were added. Cyanide has a high affinity for ferric ions. These ions are in the cytochrome oxidase ( enzyme of the respiratory chain of cells localized in the mitochondria ) is present. If it comes to complexation of the ferric ion by cyanide, this is reversibly inhibited, so that no metabolic energy (ATP) is provided more. By the formation of methemoglobin, the cyanide is maintained by forming a complex with the iron ( III) ions in the blood, so that the transfer to the tissues and thus the inhibition of cytochrome oxidase is prevented. The actual detoxifying of the rhodanese extends to thiocyanate which is accelerated by the therapeutic administration of compounds of sulfur ( sodium thiosulfate ).

Bedside test

In bedside test methemoglobinemia a drop and a drop of normal striking blood is placed on a filter paper, compared after one minute. The methemoglobin blood retains a brown color.

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