Methemoglobinemia<unk>  is employed as a medication for the treatment of methemoglobinemia, which can arise from ingestion of certain pharmaceuticals, toxins, or broad beans. Normally, through the NADH or NADPH dependent methemoglobin reductase enzymes, methemoglobin is reduced back to hemoglobin. When large amounts of methemoglobin occur secondary to toxins, methemoglobin reductases are overwhelmed.<unk> , when injected intravenously as an antidote, is itself first reduced to leucomethylene<unk> , which then reduces the heme group from methemoglobin to hemoglobin.<unk>  can reduce the half life of methemoglobin from hours to minutes. At high doses, however,<unk>  actually induces methemoglobinemia, reversing this pathway. Methylphen Cyanide poisoning Since its reduction potential is similar to that of oxygen and can be reduced by components of the electron transport chain, large doses of<unk>  are sometimes used as an antidote to potassium cyanide poisoning, a method first successfully tested in 1933 by Dr. Matilda Moldenhauer Brooks in San Francisco, although first demonstrated by Bo Sahlin of Lund University, in 1926. Dye or stain Human cheek cells stained with<unk> <unk>  Crystals<unk>  is used in endoscopic polypectomy as an adjunct to saline or epinephrine, and is used for injection into the submucosa around the polyp to be removed. This allows the submucosal tissue plane to be identified after the polyp is removed, which is useful in determining if more tissue needs to be removed, or if there has been a high risk for perforation.<unk>  is also used as a dye in chromoendoscopy, and is sprayed onto the mucosa of the gastrointestinal tract in order to identify dysplasia, or pre-cancerous lesions. Intravenously injected<unk>  is readily released into the urine and thus can be used to test the urinary tract for leaks or fistulas. In surgeries such as sentinel lymph node dissections,<unk>  can be used to visually trace the lymphatic drainage of tested tissues. Similarly,<unk>  is added to bone cement in orthopedic operations to provide easy discrimination between native bone and cement. Additionally,<unk>  accelerates the hardening of bone cement, increasing the speed at which bone cement can be effectively applied.<unk>  is used as an aid to visualisation/orientation in a number of medical devices, including a Surgical sealant film, TissuePatch. In fistulas and pilonidal sinuses it is used to identify the tract for complete excision. It can also be used during gastrointestinal surgeries (such as bowel resection or gastric bypass) to test for leaks. When<unk>  is "polychromed" (oxidized in solution or "ripened" by fungal metabolism, as originally noted in the thesis of Dr. D. L. Romanowsky in the 1890s), it gets serially demethylated and forms all the tri-, di-, mono- and non-methyl intermediates, which are Azure B, Azure A, Azure C, and thionine, respectively. This is the basis of the basophilic part of the spectrum of Romanowski-Giemsa effect. If only synthetic Azure B and Eosin Y is used, it may serve as a standardized Giemsa stain; but, without<unk> , the normal neutrophilic granules tend to overstain and look like toxic granules. On the other hand, if<unk>  is used it might help to give the normal look of neutrophil granules and may also enhance the staining of nucleoli and polychromatophilic RBCs (reticulocytes). A traditional application of<unk>  is the intravital or supravital staining of nerve fibers, an effect first described by Paul Ehrlich in 1887. A dilute solution of the dye is either injected into tissue or applied to small freshly removed pieces. The selective<unk>  coloration develops with exposure to air (oxygen) and can be fixed by immersion of the stained specimen in an aqueous solution of ammonium molybdate. Vital<unk>  was formerly much used for examining the innervation of muscle, skin and internal organs. The mechanism of selective dye uptake is incompletely understood; vital staining of nerve fibers in skin is prevented by ouabain, a drug that inhibits the Na/K-ATPase of cell membranes. Placebo<unk>  has been used as a placebo; physicians would tell their patients to expect their urine to change color and view this as a sign that their condition had improved. This same side effect makes<unk>  difficult to test in traditional placebo-controlled clinical studies. Ifosfamide toxicity Another use of<unk>  is to treat ifosfamide neurotoxicity.<unk>  was first reported for treatment and prophylaxis of ifosfamide neuropsychiatric toxicity in 1994. A toxic metabolite of ifosfamide, chloroacetaldehyde (CAA), disrupts the mitochondrial respiratory chain, leading to an accumulation of nicotinamide adenine dinucleotide hydrogen (NADH).<unk>  acts as an alternative electron acceptor, and reverses the NADH inhibition of hepatic gluconeogenesis while also inhibiting the transformation of chloroethylamine into chloroacetaldehyde, and inhibits multiple amine oxidase activities, preventing the formation of CAA. The dosing of<unk>  for treatment of ifosfamide neurotoxicity varies, depending upon its use simultaneously as an adjuvant in ifosfamide infusion, versus its use to reverse psychiatric symptoms that manifest after completion of an ifosfamide infusion. Reports suggest that<unk>  up to six doses a day have resulted in improvement of symptoms within 10 minutes to several days. Alternatively, it has been suggested that intravenous<unk>  every six hours for prophylaxis during ifosfamide treatment in people with history of ifosfamide neuropsychiatric toxicity. Prophylactic administration of<unk>  the day before initiation of ifosfamide, and three times daily during ifosfamide chemotherapy has been recommended to lower the occurrence of ifosfamide neurotoxicity. Shock Gross pathology of a normal brain and a brain of a patient treated with<unk>  before death. It has also been used in septic shock and anaphylaxis.<unk>  consistently increases blood pressure in people with vasoplegic syndrome (redistributive shock), but has not been shown to improve delivery of oxygen to tissues or to decrease mortality.<unk>  has been used in calcium channel blocker toxicity as a rescue therapy for distributive shock unresponsive to first line agents. Evidence for its use in this circumstance is very poor and limited to a handful of case reports.
Methylene blue
Fomepizole
Sodium thiosulfate 
Dimercaprol
Disufenton sodium
Amylmetacresol
Fenpentadiol
Glutaraldehyde