Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.99.1 (NADPH-diaphorase)
 3,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methemoglobin (MHb) is the oxidized form of Hemoglobin (Hb) containing iron in its ferric (Fe3+) rather than ferrous (Fe2+) state. Under physiologic conditions, diaphorase II accounts for only a small percentage of the red blood cell reducing capacity but can be pharmacologically activated by exogenous cofactors. Methemoglobinemia is an abnormal elevation of MHb levels resulting in impaired oxygen delivery to tissues as well as a left shift of the oxygen-Hb dissociation curve. We present the case of a 56-year-old female patient who underwent transesophageal echocardiography (TEE) prior to elective cardioversion. Prep for TEE included use of Hurricane spray. Twenty min after receipt, the patient's O2 saturation by pulse oximetry dropped from 100% to 86%; heart rate and blood pressure were unchanged. Physical exam revealed pallor, perioralcyanosis and acrocyanosis without tachypnea, respiratory distress, or jugular venous distension. A 100% non-rebreather mask provided no improvement. MHb was suspected and arterial blood gasses were drawn which was dark chocolate in appearance. Methylene Blue at 1 mg/kg over 5 minutes was administered empirically. ABG results were: pH 7.44/ CO2 40/ O2 315/ HCO2 26/ O2 sat 69%; MHb levels were 30.1% confirming the diagnosis of methemoglobinemia. This condition resolved within minutes. Though uncommon, MHb is the most Sported adverse event associated with topical benzocaine use. Untreated, it can lead to significant cardiopulmonary compromise, neurologic sequelae, and even death. Prompt recognition of this potentially life-threatening side-effect is essential in order to provide opportune treatment.
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PMID:Methemoglobinemia and transesophageal echo. 1860 50

Excitotoxicity is the major component in neuropathological conditions, related to harmful action of imbalanced concentrations of glutamate and its agonists in the nervous tissue, ultimately resulting in cell death. In the present study, we evaluated the effects of an acute striatal lesion induced by a focal N-methyl-D-aspartate (NMDA) microinjection on the morphometry of NADPH diaphorase-reactive neurons (NADPH-d+ ), a subset of cells which release nitric oxide (NO) in the brain and are known by its resistance in pathological conditions. Two hundred and forty NADPH-d neurons from NMDA-lesioned striatum and contralateral counterpart were tridimensionally reconstructed at 1, 3 and 7 post-lesion days (PLDs). Cell body and dendritic field areas, length of dendrites by order and fractal dimension were analyzed. There were no significant morphometric differences when NADPH-d+ neurons from lesioned and control striatal regions were compared among PLDs evaluated. Conversely, a conspicuous pallor in striatal neuropil reactivity was evidenced, especially in latter survival time. In addition, we observed a noticeable inflammatory response induced by NMDA. Our results suggest that NADPH-d+ neurons were spared from deleterious effects of acute NMDA excitotoxic damage in the striatum, reinforcing the notion that this cell group is selectively resistant to injury in the nervous system.
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PMID:Morphometric analysis of NADPH diaphorase reactive neurons in a rat model of focal excitotoxic striatal injury. 2723 70