Disease relevance of nitrous oxide

• Nitrous oxide in myocardial infarction [1].
• Nitrous oxide analgesia for refractory pain in the terminally ill [2].
• Nitrous oxide reductase, which catalyzes the reduction of N2O to N2, was purified in a largely oxidized form from Pseudomonas aeruginosa strain P2 by a simple anaerobic procedure to yield an enzyme with a peptide purity of 95-98% [3].
• Nitrous oxide reductase from the denitrifying bacterium Paracoccus denitrificans has been purified very nearly to homogeneity by an anaerobic procedure that results in a product with high specific activity [4].
• Nitrous oxide reductase from Wolinella succinogenes was purified very nearly to homogeneity [5].

Psychiatry related information on nitrous oxide

• Nitrous oxide and treatment of withdrawal symptoms [6].
• Nitrous oxide, xenon, and memantine may be of therapeutic interest for treating drug dependence [7].
• Nitrous oxide stimulation of locomotor activity: evidence for an opiate-like behavioral effect [8].
• RATIONALE: Nitrous oxide (N(2)O) inhalation, at subanaesthetic concentrations, impairs choice reaction time (RT) [9].
• Nitrous oxide potentiated psychomotor impairment that was induced by sevoflurane [10].

High impact information on nitrous oxide

• Nitrous oxide and oxygen in coronary artery disease [11].
• Nitrous oxide and megaloblastic bone marrow change [12].
• Nitrous oxide and vitamin B12 [13].
• Nitrous oxide (N20) is a greenhouse gas, the third most significant contributor to global warming [14].
• Myocardial cGMP was measured by radioimmunoassay, and serum nitrogen oxide levels (NOx = NO2 + NO3) were measured by chemiluminescence. iNOS mRNA was detected in allograft myocardium at some point in each patient and in 59 of 123 biopsies (48%) overall [15].

Chemical compound and disease context of nitrous oxide

• Insight into Catalysis of Nitrous Oxide Reductase from High-resolution Structures of Resting and Inhibitor-bound Enzyme from Achromobacter cycloclastes [16].
• An Early Example of Evidence-based Medicine: Hypoxemia due to Nitrous Oxide [17].

Biological context of nitrous oxide

• Nitrous oxide/oxygen inhalation produced significant CBV increase, which showed nonsignificant decrease of no clinical significance during standing up [18].
• Nitrous oxide also increases pulmonary vascular resistance, possibly via alpha-adrenergic stimulation [19].
• Nitrous oxide withdrawal reduces intracranial pressure in the presence of pneumocephalus [20].
• Nitrous oxide increases intraocular pressure after intravitreal sulfur hexafluoride injection [21].
• Nitrous oxide effects on cerebral evoked potential to pain: partial reversal with a narcotic antagonist [22].

Anatomical context of nitrous oxide

• Nitrous oxide impairs the neutrophil oxidative response [23].
• Nitrous oxide, in an incubator concentration of 70%, failed to inhibit nuclear enlargement of lymphocytes stimulated to transform by phytohemagglutinin (PHA) [24].
• Nitrous oxide activates GABAergic neurons in the spinal cord in Fischer rats [25].
• Nitrous oxide does not alter infarct volume in rats undergoing reversible middle cerebral artery occlusion [26].
• Nitrous oxide enhances Na+/Ca++ exchange in the neuroblastoma cell line SK-N-SH [27].

Associations of nitrous oxide with other chemical compounds

• Protein Crystallography under Xenon and Nitrous Oxide Pressure: Comparison with In Vivo Pharmacology Studies and Implications for the Mechanism of Inhaled Anesthetic Action [28].
• Re: Nitrous oxide (Entonox) inhalation and tolerance of transrectal ultrasound guided prostate biopsy: a double-blind randomized controlled study [29].
• CONCLUSIONS: Nitrous oxide, an N-methyl-D-aspartate receptor antagonist, prevented the enhancement of pain sensitivity induced by both nociceptive inputs and fentanyl and opposed acute morphine tolerance [30].
• RESULTS: Nitrous oxide (N2O) and sevoflurane (SEV) concentrations for five surgeries in four different operating rooms were determined [31].
• Nitrous oxide can enhance the hypnotic effect, but not the suppression of spinal motor neuron excitability by propofol in humans [32].

Gene context of nitrous oxide

• Nitrous oxide produces antinociceptive response via alpha2B and/or alpha2C adrenoceptor subtypes in mice [33].
• Nitrous oxide reductase (nosZ) gene-specific PCR primers for detection of denitrifiers and three nosZ genes from marine sediments [34].
• Nitrous oxide reductase from Wolinella succinogenes, an enzyme containing one heme c and four Cu atoms/subunit of Mr = 88,000, was studied by electron paramagnetic resonance (EPR) at 9.2 GHz from 6 to 80 K [35].
• Nitrous oxide inactivates the enzyme methionine synthase by oxidation of enzyme bound cobalamin, which is formed from the cofactor methylcobalamin during the catalytic cycle [36].
• RESULTS: Nitrous oxide depresses C5a- or FMLP-induced generation of reactive oxygen derivatives in a concentration-dependent manner [23].

Analytical, diagnostic and therapeutic context of nitrous oxide

• Nitrous oxide produced a dose-related "analgesia" in mice (median effective dose, 55 percent) [37].
• Nitrous oxide analgesia was used in the management of the terminal hospitalization of four adolescents and one child with disseminated cancer [2].
• Nitrous oxide is purged from the water sample and trapped cryogenically using an automated system with subsequent release into a gas chromatography column [38].
• Nitrous oxide cryotherapy was applied in a double rapid-freeze/slow-thaw manner for either 30 or 60 seconds [39].
• Nitrous oxide self-administration by the squirrel monkey [40].

References