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At least 19 recordsLinked to original sources

PubMed2000

Control of nitric oxide, nitrous oxide, and ammonia emissions using microwave plasmas

The subject of this paper is mitigation of the undesirable side-effects of selective non-catalytic reduction (SNCR) and selective catalytic reduction (SCR): ammonia slip, residual NO(x), and N(2)O emissions. The use of microwave-plasma discharge within the flue gas was explored as a potential pollution-control method. The key issues addressed were: (1) N(2)O, NH(3), and NO removal efficiencies; and (2) sustaining a stable plasma at atmospheric, or close to atmospheric, pressure. In non-oxidizing atmospheres, removal efficiencies were always close to 100% for all species. In the presence of oxygen, however, appreciable amounts of nitric oxide and ammonia were formed. Methods leading to preventing these undesirable effects were examined. In a number of runs, stable plasma operation was attained at pressures close to atmospheric.

Journal Article↗

PubMed1980

A comparison of the analgesic effects of methoxyflurane-nitrous oxide and nitrous oxide alone during labour related to the Eysenck personality inventory test.

One hundred and thirty-three paturients who had received either methoxyflurane-nitrous oxide or nitrous oxide analgesia with or without pudendal block, underwent the Eysenck Personality Inventory Test on the second postpartum day and evaluated their memory of the pain (Subjectively Evaluated Pain Suffering Scores) during labor. Parturients who had received methoxyflurance-nitrous oxide analgesia reported significantly lower pain suffering than parturients who had had nitrous oxide analgesia. Subdivision according to Personality Inventory factors showed that at the introvert end of the Extroversion-Introversion scale, methoxyflurance-nitrous oxide analgesia with or without additional pudendal block resulted in significantly lower pain suffering than did not nitrous oxide analgesia. On the other hand, nitrous oxide analgesia without additional pudendal block gave significantly lower pain suffering at the extrovert end of the scale. Among the extroverts there was a tendency, though not statistically significant, towards non-approval of the pudendal block.

Anesthesia, Inhalation↗

PubMed2003

Toxicity of nitrous oxide.

Nitrous oxide interacts with vitamin B12 resulting in selective inhibition of methionine synthase, a key enzyme in methionine and folate metabolism. Thus, nitrous oxide may alter one-carbon and methyl-group transfer most important for DNA, purine and thymidylate synthesis. Long-term exposure to high concentrations of nitrous oxide may cause megaloblastic bone-marrow depression and neurological symptoms. Exposure to higher doses for less than 6 hours, as in clinical anaesthesia, are considered harmless. Recent studies seem to suggest a correlation between nitrous oxide anaesthesia and hyperhomocysteinaemia which is accepted to be an independent risk factor for coronary artery disease. As for today, available data do not support the notion that exposure to trace amounts of nitrous oxide is associated with impaired fertility or an increased risk of developing cancer. Emission of nitrous oxide from medical use is estimated to contribute less than 0.05% to total annual greenhouse gas emission.

Animals↗

PubMed1970

Production of nitric oxide and nitrous oxide during denitrification by Corynebacterium nephridii.

Resting cells of Corynebacterium nephridii reduce nitrate, nitrite, and nitric oxide to nitrous oxide under anaerobic conditions. Nitrous oxide production from nitrite was optimal from pH 7.0 to 7.4. The stoichiometry of nitrous oxide production from nitrite was 99% of the theoretical-two moles of nitrite was used for each mole of nitrous oxide detected. Hydroxylamine increases gas evolution from nitrite but inhibits the reduction of nitric oxide to nitrous oxide. Hydroxylamine is converted to nitrogenous gas(es) by resting cells only in the presence of nitrite. Under certain conditions nitric oxide, as well as nitrous oxide, was detected.

Chromatography, Gas↗

PubMed1993

Metabolic evidence of cobalamin deficiency in bone marrow cells harvested for transplantation from donors given nitrous oxide.

Nitrous oxide inactivates cobalamin, but clinically apparent sequelae ensue in nondeficient individuals only when exposure is prolonged. The gas is widely used in anesthesia, therefore, and is commonly given to donors during harvesting of their bone marrow cells for transplantation. The present study shows that nitrous oxide administered for only 75-120 minutes induced mild but unequivocal DNA synthetic abnormalities attributable to cobalamin deficiency in the harvested marrow cells of 4 out of 5 donors; the deoxyuridine suppression test in these 4 patients showed abnormal results more than 4 standard deviations above the reference mean. Metabolic evidence of cobalamin deficiency in cryopreserved cells diminished only slightly when they were thawed and retested 1 day later, but was no longer detectable in cells thawed and tested on the 3rd day. In contrast, cells harvested under nitrous oxide-free anesthesia in 4 subjects showed no evidence of cobalamin deficiency in the deoxyuridine suppression test. These results demonstrate that even relatively brief exposure to nitrous oxide induces cobalamin deficiency in harvested bone marrow cells, and that the cells remain metabolically impaired for more than 24 hours. Although clinical sequelae are not apparent at this time, the several potential implications of our findings indicate that the use of nitrous oxide in bone marrow transplantation needs to be evaluated further.

Anesthesia↗

PubMed1997

Stable isotope enrichment in stratospheric nitrous oxide

Nitrous oxide is a greenhouse gas that also plays a role in the cycling of stratospheric ozone. Air samples from the lower stratosphere exhibit 15N/14N and 18O/16O enrichment in nitrous oxide, which can be accounted for with a simple model describing an irreversible destruction process. The observed enrichments are quite large and incompatible with those determined for the main stratospheric nitrous oxide loss processes of photolysis and reaction with excited atomic oxygen. Thus, although no stratospheric source needs to be invoked, the data indicate that present understanding of stratospheric nitrous oxide chemistry is incomplete.

Journal Article↗

PubMed1991

Vecuronium infusion requirements in children during halothane-narcotic-nitrous oxide, isoflurane-narcotic-nitrous oxide, and narcotic-nitrous oxide anesthesia.

We were interested in determining the infusion rate of vecuronium required to maintain approximately 95% neuromuscular blockade in children during halothane-narcotic-nitrous oxide (0.8% end-tidal concentration), isoflurane-narcotic-nitrous oxide (1.0% end-tidal concentration), or narcotic-nitrous oxide anesthesia. Neuromuscular blockade was monitored by recording the electromyographic activity (Datex NMT) of the adductor pollicis muscle resulting from supramaximal stimulation of the ulnar nerve at 2 Hz for 2 s at 10-s intervals. Effective vecuronium infusion requirements averaged 1.5 +/- 0.1 micrograms.kg-1.min-1 (mean +/- SEM) during isoflurane-narcotic-nitrous oxide anesthesia, 1.9 +/- 0.1 micrograms.kg-1.min-1 during halothane-narcotic-nitrous oxide anesthesia, and 2.4 +/- 0.3 micrograms.kg-1.min-1 during narcotic-nitrous oxide anesthesia. Infusion requirements significantly decreased after the first 30 min of infusion in the presence of both potent inhalation anesthetics, but did not change with time during narcotic-nitrous oxide anesthesia. There was no evidence of decreasing infusion requirements during prolonged vecuronium infusion (2.5 h). There was no difference in the rate of spontaneous or pharmacologically induced recovery between anesthetic groups. The mean recovery index (T25-75) after termination of the infusion was 13.7 min.

Anesthesia, General↗

PubMed1992

Advantages and guidelines for using nitrous oxide.

Nitrous oxide is useful as an adjunct to methoxyflurane anesthesia and prolonged halothane anesthesia. Nitrous oxide is also useful in the debilitated patient in which the potent volatile anesthetics induce excessive cardiovascular depression. Finally nitrous oxide is useful for smoothing an inadequate anesthetic plane induced by the potent volatile anesthetics.

Adjuvants, Anesthesia↗

PubMed1993

[Decreased pressure of endotracheal tube cuff in general anesthesia without nitrous oxide].

Nitrous oxide diffuses into endotracheal tube cuff and then overexpand the cuff. This causes upper airway obstruction and trauma in intubated patients during general anesthesia. On the other hand, pressure of endotracheal cuff is reported to decrease in time-related fashion under artificial ventilation with oxygen and air. We evaluated the changes in the pressure of endotracheal cuff in intubated patient who underwent general anesthesia without nitrous oxide. After the intubation, endotracheal tube cuff was inflated until no leak of oxygen and air was recognized under positive airway pressure ventilation. This pressure was defined as clinically sealing pressure. Beyond the sealing pressure, the cuff was further inflated by air to 19 mmHg. This is defined as initial pressure. Pressure of the inflated cuff was recorded at an interval of 30 min until the extubation. Clinically sealing pressure was 11.6 +/- 1.0 mmHg and necessary volume of air was 5.5 +/- 1.8 ml. The initial pressure of the inflated cuff gradually decreased to clinical sealing pressure during 130.9 +/- 30.5 min. In conclusion, when regurgitation should be prevented at the point of the clinically sealing pressure, pressure and volume of inflated cuff by air should be re-checked at an interval of about 2 hrs in intubated patients under general anesthesia without nitrous oxide.

Adult↗

PubMed1971

Separate nitrite, nitric oxide, and nitrous oxide reducing fractions from Pseudomonas perfectomarinus.

Pseudomonas perfectomarinus was found to grow anaerobically at the expense of nitrate, nitrite, or nitrous oxide but not chlorate or nitric oxide. In several repetitive experiments, anaerobic incubation in culture media containing nitrate revealed that an average of 82% of the cells in aerobically grown populations were converted to the capacity for respiration of nitrate. Although they did not form colonies under these conditions, the bacteria synthesized the denitrifying enzymes within 3 hr in the absence of oxygen or another acceptable inorganic oxidant. This was demonstrated by the ability, after anaerobic incubation, of cells and of extracts to reduce nitrite, nitric oxide, and nitrous oxide to nitrogen. From crude extracts of cells grown on nitrate, nitrite, or nitrous oxide, separate complex fractions were obtained that utilized reduced nicotinamide adenine dinucleotide as the source of electrons for the reduction of (i) nitrite to nitric oxide, (ii) nitric oxide to nitrous oxide, and (iii) nitrous oxide to nitrogen. Gas chromatographic analyses revealed that each of these fractions reduced only one of the nitrogenous oxides.

Cell-Free System↗

PubMed2002

Comparison of sevoflurane and nitrous oxide mixture with nitrous oxide alone for inhalation conscious sedation in children having dental treatment: a randomised controlled trial.

We studied 411 children aged 3-10 years who were referred for dental treatment. They were randomly allocated to have inhalation conscious sedation with either sevoflurane/nitrous oxide mixture or nitrous oxide alone. Dental treatment was satisfactorily completed in 215/241 children who were given sevoflurane/nitrous oxide mixture (89%) compared with 89/170 who were given nitrous oxide alone (52%) (Chi square 70.3, p < 0.0001). All children remained conscious and responsive to verbal contact throughout the treatment and in the recovery room. No adverse side-effects were recorded in either group and there were no significant differences in oxygen saturation, heart rate, recovery profile, or time to discharge home between the groups. The study concluded that, for every 100 children treated with sevoflurane/nitrous oxide mixture, 37 children would be saved a general anaesthetic if given combined sevoflurane and nitrous oxide mixture rather than nitrous oxide alone. The use of sevoflurane in low concentrations 0.1-0.3% to supplement nitrous oxide and oxygen for inhalation conscious sedation is safe, practical, and significantly more effective than nitrous oxide alone in children having dental treatment.

Administration, Inhalation↗

PubMed1986

In vitro inactivation of methionine synthase by nitrous oxide.

Nitrous oxide (N2O) is commonly used as an anesthetic agent. Prolonged exposure to N2O leads to megaloblastic anemia in humans and to loss of methionine synthase activity in vertebrates. We now report that purified preparations of cobalamin-dependent methionine synthase (5-methyltetrahydrofolate-homocysteine methyltransferase, EC 2.1.1.13) from both Escherichia coli and pig liver are irreversibly inactivated during turnover in buffers saturated with N2O. Inactivation by N2O occurs only in the presence of all components required for turnover: homocysteine, methyltetrahydrofolate, adenosylmethionine, and a reducing system. Reisolation of the inactivated E. coli enzyme after turnover in the presence of N2O resulted in significant losses of bound cobalamin and of protein as compared to controls where the enzyme was subjected to turnover in N2-equilibrated buffers before reisolation. However, N2O inactivation was not associated with major changes in the visible absorbance spectrum of the remaining enzyme-bound cobalamin. We postulate that N2O acts by one-electron oxidation of the cob(I)alamin form of the enzyme which is generated transiently during turnover with the formation of cob(II)alamin, N2, and hydroxyl radical. Generation of hydroxyl radical at the active site of the enzyme could explain the observed irreversible loss of enzyme activity.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗

PubMed1991

The relationship between the anoxic sensitivity and the extent of sensitization by nitrous oxide.

Nitrous oxide reacts during irradiation to increase the yield of .OH, a radical many believe to be a major cause of lethality. Logically, one would expect N2O to be a radiation sensitizer. In some instances it is, while in others it is not. In some cases we can explain why N2O fails to sensitize; factors such as dose rate, cell concentration, buffer composition and ionic strength all influence when N2O will sensitize and, if it sensitizes, by what magnitude. Based on the results presented here with multiple strains of procaryotic and eucaryotic cells, we believe the anoxic sensitivity is another critical factor that governs whether N2O will sensitize. Our data, with data from the literature, show a relationship between the anoxic sensitivity and the N2O enhancement ratio. N2O does not sensitize in vitro unless the anoxic sensitivity (inactivation constant, k) is less than approximately 0.2 daGy-1.

Animals↗

PubMed1990

No finding of increased myocardial ischemia during or after carotid endarterectomy under anesthesia with nitrous oxide.

Nitrous oxide (N2O) has been implicated as a cause of myocardial ischemia. We investigated whether substitution of N2O for a portion of the anesthesia supplied by isoflurane increased myocardial ischemia in patients at risk for such ischemia. Seventy patients having carotid endarterectomies (63 patients) or other carotid surgery (seven patients) were prospectively, randomly assigned to an anesthetic regimen that included or excluded N2O. All other aspects of anesthetic management were similar, except for greater concentrations of oxygen and isoflurane in patients not given N2O. Perioperative monitoring for myocardial ischemia and infarction included 12- or 5-lead electrocardiography, transesophageal echocardiography, and creatine kinase isoenzyme levels. By transesophageal echocardiographic or electrocardiographic criteria, 44% of patients given oxygen but only 21% of those given N2O had myocardial ischemia intraoperatively (P = 0.065). Similarly, myocardial infarction, identified by changes in creatine kinase isoenzymes, occurred in only one patient given N2O but in three given oxygen (not significantly different). Thus we found no trend indicating a greater incidence of myocardial ischemia or infarction associated with the use of N2O.

Aged↗

PubMedDate not supplied

[Oxidation of nitrous oxide during decomposition of hydrogen peroxide by catalase].

Possible involvement of the catalase mechanism in the elimination of nitrous oxide was studied in model experiments. The concentration of N2O in the gaseous phase was found to decrease due to the decomposition of hydrogen peroxide by catalase. The concentration of NO increased accompanying the removal of N2O from the gaseous phase in the pressure of H2O2 and catalase. Though the observed effect is slight, the oxidation of nitrous oxide during the decomposition of H2O2 by catalase might be one of the mechanisms for biological elimination of N2O under the oxidating conditions.

Catalase↗

PubMed1990

Effects of intravenous administration of local anesthetics on the renal sympathetic nerve activity during nitrous oxide and nitrous oxide-halothane anesthesia in the cat.

The effects of subseizure doses of lidocaine and bupivacaine administered intravenously (i.v.) on mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were studied in cats anesthetized with nitrous oxide (N2O)-O2 and N2O-O2-halothane (1%). In cats anesthetized with N2O-O2, MAP decreased briefly (P less than 0.01) and then returned to the initial level within a minute after the i.v. injection of lidocaine (5 mg/kg, 10 mg/kg). RSNA increased at first and then decreased slightly. In cats with denervated baroreceptors, the change in RSNA after lidocaine 5 mg/kg i.v. was similar to that in cats with intact baroreceptors. In contrast, MAP, HR and RSNA decreased significantly (P less than 0.01) after i.v. injection of lidocaine during N2O-O2-halothane anesthesia. The effects of bupivacaine on RSNA were similar to those of lidocaine. It is concluded that cardiovascular depression following intravenous local anesthetics during N2O-O2-halothane anesthesia may be caused by both a decreased sympathetic activity and a direct depressant effect on the myocardium.

Anesthesia, Inhalation↗

PubMed1995

Cytochrome c oxidase catalysis of the reduction of nitric oxide to nitrous oxide.

Reduction of nitric oxide (NO) to nitrous oxide (N2O) is catalyzed by bovine heart cytochrome c oxidase (CcO) in anaerobic solutions at pH 7.2 and 20 degrees C. Cyanide inhibits and forms Fea3(3+)CN. The mononitrosyl (Fea3(2+)NO), but not the dinitrosyl (Fea3(2+)NO; CuB+NO), is a likely intermediate in N2O formation. One-electron reduction of NO at Fea3(2+) could yield N2O via HNO. However, a two-electron reduction of the NO ligand to give an intermediate that reacts with a second NO to give N2O and H2O appears more likely. Conversion of NO to N2O is favored by low levels of both NO and O2, higher NO levels can inhibit both cytochrome c oxidase and NO reductase activities. Raising the O2 level will favor catalysis of NO oxidation to NO2 by CcO. The reactions of NO and the specific CcO activity that occur in tissue will be critically dependent on NO, O2, and CcO levels.

Animals↗

PubMed2002

Assessing nitrate metabolism in the intestinal tract by measuring breath nitric oxide and nitrous oxide, and its clinical significance.

BACKGROUND: The toxicity of dietary nitrate (NO3-) is controversial. One reason is nitrate metabolism in the intestine is so complicated that it is far from fully understood. There is no study measuring breath nitric oxide (NO) and nitrous oxide (N2O) after ingesting vegetables and high-nitrate food at the same time. METHODS: Breath samples from 10 healthy young and 10 healthy old subjects were collected at 15-min intervals for 5 h after ingestion of 100 g of lettuce and during fasting (control). Breath NO and N2O were analyzed by a chemiluminescence and an IR-PAS analyzer respectively. RESULTS: N2O maximum concentration and excretions increased significantly after ingesting lettuce in each group [303 (30) vs. 750 (81) ppb, 771 (72) vs. 1668 (146) microg in young; 442 (52) vs. 1092 (109) ppb, 1088 (125) vs. 2100 (183) microg in old subjects; mean (SE), P<0.01], while NO did not. In addition, breath NO was strongly influenced by ambient NO, which varied greatly. N2O maximum level in old subjects after ingesting lettuce was higher than that of young subjects (750 vs. 1092 ppb, P<0.05), and significantly higher N2O concentration levels were seen at 30, 45, 60, and 105 min in old subjects. CONCLUSIONS: A large amount of N2O produced in the intestine and normal nitrate intake do not influence the breath NO concentration, probably due to its relatively small production. Higher maximum N2O concentration after ingesting lettuce in old subject is probably because more bacteria, which rapidly reduce dietary nitrate in the upper intestinal tract, inhabit the gut in old age. Our results suggested that breath N2O is a useful noninvasive maker to estimate dietary nitrate reduction in the intestinal tract.

Adult↗