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Journal articles on the topic 'Nitric monoxide'

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Author: Grafiati

Published: 11 March 2023

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1

Horváth, Béla, András Hrabák, Krisztina Káldi, Péter Sándor, and Zoltán Benyó. "Contribution of the Heme Oxygenase Pathway to the Maintenance of the Hypothalamic Blood Flow during Diminished Nitric Oxide Synthesis." Journal of Cerebral Blood Flow & Metabolism 23, no. 6 (June 2003): 653–57. http://dx.doi.org/10.1097/01.wcb.0000071890.63724.c9.

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The cerebrovascular effects of the heme oxygenase–carbon monoxide pathway were studied in the rat hypothalamus. Intraperitoneal administration of the heme oxygenase inhibitor zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG, 45 μmol/kg) had no significant effect on the resting cerebral blood flow, but increased hypothalamic nitric oxide synthase activity by 67% without changing the CSF cyclic GMP concentration. After pharmacologic inhibition of nitric oxide synthase, the diminished cerebral blood flow was further reduced by 22% after administration of ZnDPBG, and the effect showed direct correlation with the baseline perfusion level. Therefore, endogenous carbon monoxide may significantly contribute to the cerebral vasoregulation under resting conditions and in pathophysiologic states associated with diminished nitric oxide synthesis.

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2

Johnson, Fruzsina K., Federico J. Teran, Kay C. Coco, and Robert A. Johnson. "L-NAME, but not Phenylephrine Enhances the Effects of Endogenous Carbon Monoxide on Vascular Tone in Vivo and in Vitro." Hypertension 36, suppl_1 (October 2000): 678. http://dx.doi.org/10.1161/hyp.36.suppl_1.678-c.

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4 Vascular endothelium and smooth muscle express heme oxygenase, which metabolizes heme to form biliverdin, free iron and carbon monoxide. Carbon monoxide promotes endothelium-independent vasodilation, but also inhibits nitric oxide formation. We previously found, that heme-derived carbon monoxide dilates isolated gracilis arterioles pretreated with a nitric oxide synthase inhibitor, N ω -nitro-L-arginine methyl ester (L-NAME), and lowers blood pressure in hypertensive rat models. This current study examines the hypothesis that nitric oxide modifies the effects of endogenous carbon monoxide on vascular tone both in vitro and in vivo . For this purpose in vitro studies were conducted on rat isolated pressurized first-order gracilis arterioles superfused with oxygenated (14%O 2 /5%CO 2 balanced with N 2 ) modified Krebs’ buffer (CaCl 2 1.4mmol/L). A heme oxygenase inhibitor, chromium mesoporphyrin (CrMP, 15μmol/L), constricted gracilis arterioles (Δ-32±6μm, t 1/2max =5min; n=6, P<.05). This effect was markedly amplified by pretreatment with 1mmol/L L-NAME (Δ-65±11μm; t 1/2max =5min; n=7; P<.05), but not by preconstriction with 100nmol/L phenylephrine (n=6; P>.05). In addition, in vivo studies were performed in anesthetized rats instrumented with flow probes and arterial catheters. In these animals the heme oxygenase inhibitor CrMP (45μmol/Kg,IP) had no significant effect on hindlimb resistance (Δ 2.3±0.1 mmHg/mL/min; n=5; P>.05). But, in animals pretreated with L-NAME (100mg/Kg), CrMP increased hindlimb resistance (Δ10.7 ± 0.7 mmHg/mL/min; n=4; P<.05). In contrast, in animals infused with PE (3μg/min) to increase blood pressure and vascular tone, CrMP had no effect on hindlimb resistance (Δ1.8±0.2 mmHg/mL/min; n=5; P>.05). This study shows the vascular actions of an inhibitor of endogenous carbon monoxide formation are enhanced by an inhibitor of nitric oxide synthase, but not by an alternative vasoconstrictor. These findings suggest the endogenous heme-heme oxygenase-carbon monoxide system exerts vasodilatory influences on basal vascular tone which are uniquely enhanced in the absence of nitric oxide synthesis.

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3

Gil, Stanisław, and Wojciech Bialik. "Modelling of Nitric Oxide Formation During Liquid Fuel Combustion." Solid State Phenomena 246 (February 2016): 279–83. http://dx.doi.org/10.4028/www.scientific.net/ssp.246.279.

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A liquid fuel combustion process, being a source of many environmentally hazardous pollutants (e.g. nitric oxides, carbon monoxide, polycyclic aromatic hydrocarbons, soot and sulphur oxides), is a subject of extensive research aimed at reduction of their emissions. A high temperature of the combustion air tends to increase the content of NOX in exhaust gases. Based on the experimental data and literature as well as using the CFD tools, a model of light fuel oil combustion has been developed with an emphasis on nitric oxide formation. The model adequately reflects the impact of geometry changes in the flow of combustion substrates on concentrations of carbon monoxide and nitric oxides in the chamber. The quantitative results obtained are comparable to the experimental data.

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4

van der Lee, Ivo, and Pieter Zanen. "Diffusion Capacity for Nitric Oxide and Carbon Monoxide." Chest 126, no. 5 (November 2004): 1708–9. http://dx.doi.org/10.1378/chest.126.5.1708.

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5

Spillers, Jana G. "Carbon Monoxide or Nitric Oxide: Which Came First?" Southern Medical Journal 104, no. 1 (January 2011): 9–10. http://dx.doi.org/10.1097/smj.0b013e3181fc1e25.

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6

Montuschi, Paolo, Sergei A. Kharitonov, and Peter J. Barnes. "Exhaled Carbon Monoxide and Nitric Oxide in COPD." Chest 120, no. 2 (August 2001): 496–501. http://dx.doi.org/10.1378/chest.120.2.496.

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7

Zavorsky, Gerald S. "Diffusion Capacity for Nitric Oxide and Carbon Monoxide." Chest 126, no. 5 (November 2004): 1709–10. http://dx.doi.org/10.1016/s0012-3692(15)31396-9.

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8

Furusawa, Takehiko, Mikio Tsunoda, Motoki Tsujimura, and Tadafumi Adschiri. "Nitric oxide reduction by char and carbon monoxide." Fuel 64, no. 9 (September 1985): 1306–9. http://dx.doi.org/10.1016/0016-2361(85)90193-0.

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9

Hartsfield, Cynthia L. "Cross Talk Between Carbon Monoxide and Nitric Oxide." Antioxidants & Redox Signaling 4, no. 2 (April 2002): 301–7. http://dx.doi.org/10.1089/152308602753666352.

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10

Arngrim, Nanna, Henrik W. Schytz, Mette K. Hauge, Messoud Ashina, and Jes Olesen. "Carbon monoxide may be an important molecule in migraine and other headaches." Cephalalgia 34, no. 14 (May 9, 2014): 1169–80. http://dx.doi.org/10.1177/0333102414534085.

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Introduction Carbon monoxide was previously considered to just be a toxic gas. A wealth of recent information has, however, shown that it is also an important endogenously produced signalling molecule involved in multiple biological processes. Endogenously produced carbon monoxide may thus play an important role in nociceptive processing and in regulation of cerebral arterial tone. Discussion Carbon monoxide-induced headache shares many characteristics with migraine and other headaches. The mechanisms whereby carbon monoxide causes headache may include hypoxia, nitric oxide signalling and activation of cyclic guanosine monophosphate pathways. Here, we review the literature about carbon monoxide-induced headache and its possible mechanisms. Conclusion We suggest, for the first time, that carbon monoxide may play an important role in the mechanisms of migraine and other headaches.

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11

Mardyukov, Artur, and Dominik Niedek. "Photochemical reactions of triplet phenylphosphinidene with carbon monoxide and nitric oxide." Chemical Communications 54, no. 97 (2018): 13694–97. http://dx.doi.org/10.1039/c8cc08664h.

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12

Park, Sarah S., Minyoung Hong, Yejin Ha, Jeongeun Sim, Gil-Ja Jhon, Youngmi Lee, and Minah Suh. "The real-time in vivo electrochemical measurement of nitric oxide and carbon monoxide release upon direct epidural electrical stimulation of the rat neocortex." Analyst 140, no. 10 (2015): 3415–21. http://dx.doi.org/10.1039/c5an00122f.

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13

Guglielminotti, E., and F. Boccuzzi. "Nitric Oxide Adsorption and Nitric Oxide-Carbon Monoxide Interaction on Ru/ZnO Catalyst." Journal of Catalysis 141, no. 2 (June 1993): 486–93. http://dx.doi.org/10.1006/jcat.1993.1157.

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14

Moinard, J., and H. Guenard. "Determination of lung capillary blood volume and membrane diffusing capacity in patients with COLD using the NO-CO method." European Respiratory Journal 3, no. 3 (March 1, 1990): 318–22. http://dx.doi.org/10.1183/09031936.93.03030318.

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Lung capillary blood volume (Qc) and the membrane diffusing capacity (Dm) can both be determined from the combined measurement of nitric oxide (NO) and carbon monoxide (CO) transfers using the single-breath method. In ten healthy subjects, no differences was observed between the values of transfer factor of the lungs for carbon monoxide (TLCO) recovered after a 3 s or 9 s breath-holding time (tBH). The NO-CO method could thus be used with a short tBH and a low fraction of inspired nitric oxide (FINO) (8 ppm). However, in ten patients with chronic obstructive lung disease (COLD), the values of both transfer factor of the lungs for nitric oxide (TLNO) and TLCO were underestimated by around 20% at a short tBH (3 s). In COLD patients, the NO-CO method therefore requires a longer tBH and a higher inspired fraction of NO (30 ppm) than in healthy subjects. Similar values of Dm and Qc were obtained using the NO-CO method and the two-step conventional method, at two levels of the oxygenation. The former method gave less scatter. Furthermore, TLNO is independent of the fraction of inspired oxygen (FIO2) and directly proportional to carbon monoxide membrane diffusing capacity (DmCO).

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15

Jing, Ming, Saiid Bina, Ajay Verma, Jayne L. Hart, and Sheila M. Muldoon. "Effects of Halothane and Isoflurane on Carbon Monoxide-induced Relaxations in the Rat Aorta." Anesthesiology 85, no. 2 (August 1, 1996): 347–54. http://dx.doi.org/10.1097/00000542-199608000-00017.

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Background Halothane and isoflurane previously were reported to attenuate endothelium-derived relaxing factor/nitric oxide-mediated vasodilation and cyclic guanosine monophosphate (cGMP) formation in isolated rat aortic rings. Carbon monoxide has many chemical and physiologic similarities to nitric oxide. This study was designed to investigate the effects of halothane and isoflurane on carbon monoxide-induced relaxations and cGMP formation in the isolated rat aorta. Methods Isometric tension was recorded continuously from endothelium denuded rat aortic rings suspended in Krebs-filled organ baths. Rings precontracted with submaximal concentrations of norepinephrine were exposed to cumulative concentrations of carbon monoxide (26-176 microM). This procedure was repeated three times, with anesthetics delivered 10 min before the second procedure. Carbon monoxide responses of rings contracted with the same concentration of norepinephrine (10(-6) M and 2 x 10(-6) M) used in the anesthetic-exposed preparations also were examined. The concentrations of cGMP were determined in denuded rings using radioimmunoassay. The rings were treated with carbon monoxide (176 microM, 30 s) alone, or carbon monoxide after a 10-min incubation with halothane (0.34 mM or 0.72 mM). To determine whether the sequence of anesthetic delivery influenced results, vascular rings pretreated with halothane were compared with nonpretreated rings. Results Carbon monoxide (26-176 microM) caused a dose-dependent reduction of norepinephrine-induced tension, with a maximal relaxation of 1.51 +/- 0.07 g (85 +/- 7% of norepinephrine-induced contraction). Halothane (0.34 mM and 0.72 mM) significantly attenuated the carbon monoxide-induced relaxations, but only the highest concentration of isoflurane (0.53 mM) significantly attenuated the carbon monoxide-induced relaxations. Carbon monoxide (176 microM) significantly increased cGMP content (+88.1 +/- 7.1%) and preincubation of the aortic rings with halothane (0.34 mM and 0.72 mM) inhibited this increase (-70.7 +/- 6.8% and -108.1 +/- 10.6%, respectively). When aortic rings and carbon monoxide were added simultaneously to Krebs solution equilibrated with halothane (0.72 mM), no inhibition of cGMP formation occurred. Conclusion Carbon monoxide-induced endothelium-independent relaxations of rat aortic rings were decreased by clinically relevant concentrations of halothane and isoflurane. The carbon monoxide-induced elevations of cGMP were attenuated by halothane only when the anesthetic was incubated with aortic rings before carbon monoxide treatment. The possible clinical significance of the actions of the anesthetics on this endogenous vasodilator is yet to be determined.

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16

Nohl, H., K. Staniek, B. Sobhian, S. Bahrami, H. Redl, and A. V. Kozlov. "Mitochondria recycle nitrite back to the bioregulator nitric monoxide." Acta Biochimica Polonica 47, no. 4 (December 31, 2000): 913–21. http://dx.doi.org/10.18388/abp.2000_3946.

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Nitric monoxide (NO) exerts a great variety of physiological functions. L-Arginine supplies amino groups which are transformed to NO in various NO-synthase-active isoenzyme complexes. NO-synthesis is stimulated under various conditions increasing the tissue of stable NO-metabolites. The major oxidation product found is nitrite. Elevated nitrite levels were reported to exist in a variety of diseases including HIV, reperfusion injury and hypovolemic shock. Denitrifying bacteria such as Paracoccus denitrificans have a membrane bound set of cytochromes (cyt cd1, cyt bc) which were shown to be involved in nitrite reduction activities. Mammalian mitochondria have similar cytochromes which form part of the respiratory chain. Like in bacteria quinols are used as reductants of these types of cytochromes. The observation of one-e- divergence from this redox-couple to external dioxygen made us to study whether this site of the respiratory chain may also recycle nitrite back to its bioactive form NO. Thus, the aim of the present study was therefore to confirm the existence of a reductive pathway which reestablishes the existence of the bioregulator NO from its main metabolite NO2-. Our results show that respiring mitochondria readily reduce added nitrite to NO which was made visible by nitrosylation of deoxyhemoglobin. The adduct gives characteristic triplet-ESR-signals. Using inhibitors of the respiratory chain for chemical sequestration of respiratory segments we were able to identify the site where nitrite is reduced. The results confirm the ubiquinone/cyt be1 couple as the reductant site where nitrite is recycled. The high affinity of NO to the heme-iron of cytochrome oxidase will result in an impairment of mitochondrial energy-production. "Nitrite tolerance" of angina pectoris patients using NO-donors may be explained in that way.

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17

Antus, Balázs, and Ildikó Horváth. "Exhaled nitric oxide and carbon monoxide in respiratory diseases." Journal of Breath Research 1, no. 2 (December 1, 2007): 024002. http://dx.doi.org/10.1088/1752-7155/1/2/024002.

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18

Temleitner, L., and L. Pusztai. "Orientational correlations in liquid carbon monoxide and nitric oxide." Journal of Physics: Condensed Matter 17, no. 5 (January 22, 2005): S47—S57. http://dx.doi.org/10.1088/0953-8984/17/5/006.

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19

Dressel, Holger, Laura Filser, Rainald Fischer, Dorothea de la Motte, Werner Steinhaeusser, Rudolf M. Huber, Dennis Nowak, and Rudolf A. Jörres. "Lung Diffusing Capacity for Nitric Oxide and Carbon Monoxide." Chest 133, no. 5 (May 2008): 1149–54. http://dx.doi.org/10.1378/chest.07-2388.

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20

Siriussawakul, Arunotai, Lucinda I. Chen, and John D. Lang. "Medical Gases: A Novel Strategy for Attenuating Ischemia—Reperfusion Injury in Organ Transplantation?" Journal of Transplantation 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/819382.

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Ischemia reperfusion injury (IRI) is an inevitable clinical consequence in organ transplantation. It can lead to early graft nonfunction and contribute to acute and chronic graft rejection. Advanced molecular biology has revealed the highly complex nature of this phenomenon and few definitive therapies exist. This paper reviews factors involved in the pathophysiology of IRI and potential ways to attenuate it. In recent years, inhaled nitric oxide, carbon monoxide, and hydrogen sulfide have been increasingly explored as plausible novel medical gases that can attenuate IRI via multiple mechanisms, including microvascular vasorelaxation, reduced inflammation, and mitochondrial modulation. Here, we review recent advances in research utilizing inhaled nitric oxide, carbon monoxide, and hydrogen sulfide in animal and human studies of IRI and postulate on its future applications specific to solid organ transplantation.

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21

Marks, Gerald S., Kanji Nakatsu, and James F. Brien. "Does endogenous zinc protoporphyrin modulate carbon monoxide formation from heme? Implications for long-term potentiation, memory, and cognitive function." Canadian Journal of Physiology and Pharmacology 71, no. 10-11 (October 1, 1993): 753–54. http://dx.doi.org/10.1139/y93-112.

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Carbon monoxide, which is formed endogenously from heme catabolism catalyzed by heme oxygenase and shares some of the chemical and biological properties of nitric oxide, may play a similar role as a widespread signal transduction mechanism for the regulation of cell function and communication. Zinc protoporphyrin, an inhibitor of heme oxygenase, prevents induction of long-term potentiation. Zinc protoporphyrin is an endogenous substance and we suggest that it has a physiological role, by modulating heme oxygenase activity and, therefore, formation of carbon monoxide from heme. This in turn would modulate long-term potentiation, memory, and cognitive function.Key words: zinc protoporphyrin, carbon monoxide, heme oxygenase, long-term potentiation.

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22

Gollahalli, S. R., and R. Puri. "Flame Structure and Pollutant Emission Characteristics of a Burning Kerosene Spray With Injection of Diluents." Journal of Energy Resources Technology 114, no. 3 (September 1, 1992): 209–15. http://dx.doi.org/10.1115/1.2905943.

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An experimental study of the effects of diluent gas injection on the structure and pollutant emissions of a kerosene spray from a twin fluid atomizer is presented. Nitrogen and carbon dioxide were used as the diluents. Flame length, radiation emission, axial and radial temperature profiles, and the radial profiles of carbon monoxide, oxygen, nitric oxide, and soot in flame gas samples were studied. The emission index, defined as the mass ratio of the rate of the species emitted to the fuel input rate, was determined from the experimental data. Results show, at a diluent injection rate approximately equal to the atomizing air flow rate, nitrogen was more effective than carbon dioxide in reducing flame length, flame radiation, and the emission indices of carbon monoxide and soot. Although both diluents increased nitric oxide emission, the effect of carbon dioxide was weaker.

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23

Ehsanipoor, Robert M., Wilbert Fortson, Laura E. Fitzmaurice, Wu-Xiang Liao, Deborah A. Wing, Dong-bao Chen, and Kenneth Chan. "Nitric Oxide and Carbon Monoxide Production and Metabolism in Preeclampsia." Reproductive Sciences 20, no. 5 (September 25, 2012): 542–48. http://dx.doi.org/10.1177/1933719112459231.

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24

Leffler, Charles W., Liliya Balabanova, Alexander L. Fedinec, and Helena Parfenova. "Nitric oxide increases carbon monoxide production by piglet cerebral microvessels." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 4 (October 2005): H1442—H1447. http://dx.doi.org/10.1152/ajpheart.00464.2005.

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Carbon monoxide (CO) and nitric oxide (NO) can be involved in the regulation of cerebral circulation. Inhibition of production of either one of these gaseous intercellular messengers inhibits newborn pig cerebral arteriolar dilation to the excitatory amino acid glutamate. Glutamate can increase NO production. Therefore, the present study tests the hypothesis that NO, which is increased by glutamate, stimulates the production of CO by cerebral microvessels. Experiments used freshly isolated cerebral microvessels from piglets that express only heme oxygenase-2 (HO-2). CO production was measured by gas chromatography-mass spectrometry. Although inhibition of nitric oxide synthase (NOS) with Nω-nitro-l-arginine (l-NNA) did not alter basal HO-2 catalytic activity or CO production, l-NNA blocked glutamate stimulation of HO-2 activity and CO production. Furthermore, the NO donor sodium nitroprusside mimicked the actions of glutamate on HO-2 and CO production. The action of NO appears to be via cGMP because 8-bromo-cGMP mimics and 1 H-[1,2,4]oxadiazole-[4,3- a]quinoxalin-1-one (ODQ) blocks glutamate stimulation of CO production and HO-2 catalytic activity. Inhibitors of neither casein kinase nor phosphotidylinositol 3-kinase altered HO-2 catalytic activity. Conversely, inhibition of calmodulin with calmidazolium chloride blocked glutamate stimulation of CO production and reduced HO-2 catalytic activity. These data suggest that glutamate may activate NOS producing NO that leads to CO synthesis via a cGMP-dependent elevation of HO-2 catalytic activity. These results are consistent with the findings in vivo that either HO or NOS inhibition blocks cerebrovascular dilation to glutamate in piglets.

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25

El-Sallab, Shadia, Hesham Abdel-Hady ., Ekbal Abu-Hashim ., and Mohamed Matter . "Implications of Nitric Oxide and Carbon Monoxide in Neonatal Sepsis." Journal of Medical Sciences 2, no. 4 (June 15, 2002): 177–81. http://dx.doi.org/10.3923/jms.2002.177.181.

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26

Tetreau, Catherine, Martine Tourbez, Antonius Gorren, Bernd Mayer, and Daniel Lavalette. "Dynamics of Carbon Monoxide Binding with Neuronal Nitric Oxide Synthase." Biochemistry 38, no. 22 (June 1999): 7210–18. http://dx.doi.org/10.1021/bi9901026.

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27

Li, S. R., Y. F. Huang, Z. Liu, M. H. Sui, J. M. Liu, and K. P. Yan. "Production of medically useful nitric monoxide using AC arc discharge." Nitric Oxide 73 (February 2018): 89–95. http://dx.doi.org/10.1016/j.niox.2017.06.006.

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28

Cameli, P., E. Bargagli, A. Fossi, D. Bennett, L. Voltolini, R. M. Refini, G. Gotti, and P. Rottoli. "Exhaled nitric oxide and carbon monoxide in lung transplanted patients." Respiratory Medicine 109, no. 9 (September 2015): 1224–29. http://dx.doi.org/10.1016/j.rmed.2015.07.005.

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29

Kituyi, E., L. Marufu, S. O. Wandiga, I. O. Jumba, M. O. Andreae, and G. Helas. "Carbon monoxide and nitric oxide from biofuel fires in Kenya." Energy Conversion and Management 42, no. 13 (September 2001): 1517–42. http://dx.doi.org/10.1016/s0196-8904(00)00158-8.

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30

Rodriguez, Francisca, Brian D. Lamon, Weiying Gong, Rowena Kemp, and Alberto Nasjletti. "Nitric Oxide Synthesis Inhibition Promotes Renal Production of Carbon Monoxide." Hypertension 43, no. 2 (February 2004): 347–51. http://dx.doi.org/10.1161/01.hyp.0000111721.97169.97.

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31

Pauwels, Bart, Charlotte Boydens, Laura Vanden Daele, and Johan Van de Voorde. "Ruthenium-based nitric oxide-donating and carbon monoxide-donating molecules." Journal of Pharmacy and Pharmacology 68, no. 3 (January 15, 2016): 293–304. http://dx.doi.org/10.1111/jphp.12511.

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32

Takizawa, Shunya, Hitoshi Fujita, Saori Ogawa, and Yukito Shinohara. "Carbon Monoxide, a Novel Neural Messenger, Does Not Modulate Extracellular Glutamate Concentration in Forebrain Ischemia." Journal of Cerebral Blood Flow & Metabolism 16, no. 5 (September 1996): 1075–78. http://dx.doi.org/10.1097/00004647-199609000-00033.

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We investigated the role of carbon monoxide as a neural modulator of extracellular glutamate concentration in rat hippocampus CA1 in transient forebrain ischemia by using metalloporphyrins, which block the production of carbon monoxide through the inhibition of heme oxygenase (HO) activity. Infusion of 10 and 100 μ M zinc protoporphyrin IX, which inhibits nitric oxide synthase activity as well as HO activity, significantly increased glutamate concentration compared with that on the vehicle-treated side. However, infusion of 100 μ M tin mesoporphyrin IX, which inhibits only HO activity, did not affect glutamate concentration in ischemia. Our results therefore do not support the hypothesis that carbon monoxide acts as a neural messenger through the modulation of extracellular glutamate concentration in ischemia.

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33

Kadinov, Boris, and Dimitar Itzev. "Influence between NO and CO in guinea pig stomach fundus." Pharmacia 67, no. 3 (September 15, 2020): 161–68. http://dx.doi.org/10.3897/pharmacia.67.e52474.

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The interaction between carbon monoxide and nitric oxide and their role in modulation of stomach fundus excitability was studied. The presence and colocalization of heme oxygenase 1 (HO-1) and nitric oxide synthase (NOS) was verified in myentheric ganglia by immunohistochemistry. The role of inducible heme oxygenase isoenzyme was investigated after in vivo treatment of animals with CoCl2 (80 mg kg-1 b.w.) injected subcutaneously 24 hours before euthanasia. This treatment resulted in positive staining for the inducible isoform in stomach smooth muscle.

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34

SRINIVASAN, ANAND, and CHRISTOPHER DEPCIK. "REVIEW OF CHEMICAL REACTIONS IN THE NO REDUCTION BY CO ON PLATINUM/ALUMINA CATALYSTS." Surface Review and Letters 19, no. 01 (February 2012): 1230001. http://dx.doi.org/10.1142/s0218625x12300018.

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The emissions of nitric oxide and carbon monoxide from internal combustion engines generate a large impact on the environment and on people's health. Catalytic reduction of these species using platinum group metals has already shown significant potential for emissions control. Since catalysts often use carbon monoxide to reduce nitric oxide in these devices, accurate models of their interaction are required to advance catalyst simulations in order to meet increasingly stringent emissions regulations. As a result, this paper reviews the literature of the NO–CO reaction over platinum in order to develop more precise detailed and global reaction mechanisms for use in exhaust after-treatment modeling activities. Moreover, it is found that the reaction between NO and CO over platinum yields carbon dioxide and nitrogen as main products and nitrous oxide as an important side product. Hence, this paper additionally describes the mechanism for nitrous oxide production in advance of greenhouse gas regulations.

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35

Yacoub, Y. M., and R. M. Bata. "Development and Validation of a Thermodynamic Model for an SI Single-Cylinder Engine." Journal of Engineering for Gas Turbines and Power 120, no. 1 (January 1, 1998): 209–16. http://dx.doi.org/10.1115/1.2818078.

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A multizone quasi-dimensional model that illustrates the intake, compression, combustion, expansion, and exhaust processes has been developed for a single-cylinder four-stroke spark-ignition engine. The model takes into consideration mass and energy conservation in the engine cylinder, intake and exhaust plenums, and crank-case plenum. The model calculates instantaneous variations in gas thermodynamic states, gas properties, heat release rates, in-cylinder turbulence, piston ring motion, blowby, nitric oxide, and carbon monoxide formation. The cycle simulation accounts for the induced gas velocities due to flame propagation in the turbulence model (k–ε type), which is applied separately to each gas zone. This allows for the natural evolution of the averaged mean and turbulent velocities in burned and unburned gas regions. The present model predictions of thermal efficiency, indicated mean effective pressure, peak values of gas pressure, ignition delay, concentrations of nitric oxide, carbon monoxide, and carbon dioxide are proven to be in agreement with experimental data.

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36

Farrés, Judith, Susanna Burckhardt-Herold, Jan Scherrer, Alexander D. Frey, and Pauli T. Kallio. "Analysis of the contribution of the globin and reductase domains to the ligand-binding properties of bacterial haemoglobins." Biochemical Journal 407, no. 1 (September 12, 2007): 15–22. http://dx.doi.org/10.1042/bj20070668.

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Bacterial Hbs (haemoglobins), like VHb (Vitreoscilla sp. Hb), and flavoHbs (flavohaemoglobins), such as FHP (Ralstonia eutropha flavoHb), have different autoxidation and ligand-binding rates. To determine the influence of each domain of flavoHbs on ligand binding, we have studied the kinetic ligand-binding properties of oxygen, carbon monoxide and nitric oxide to the chimaeric proteins, FHPg (truncated form of FHP comprising the globin domain alone) and VHb-Red (fusion protein between VHb and the C-terminal reductase domain of FHP) and compared them with those of their natural counterparts, FHP and VHb. Moreover, we also analysed polarity and solvent accessibility to the haem pocket of these proteins. The rate constants for the engineered proteins, VHb-Red and FHPg, do not differ significantly from those of their natural counterparts, VHb and FHP respectively. Our results suggest that the globin domain structure controls the reactivity towards oxygen, carbon monoxide and nitric oxide. The presence or absence of a reductase domain does not affect the affinity to these ligands.

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37

Leffler, Charles W., Helena Parfenova, and Jonathan H. Jaggar. "Carbon monoxide as an endogenous vascular modulator." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 1 (July 2011): H1—H11. http://dx.doi.org/10.1152/ajpheart.00230.2011.

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Carbon monoxide (CO) is produced by heme oxygenase (HO)-catalyzed heme degradation to CO, iron, and biliverdin. HO has two active isoforms, HO-1 (inducible) and HO-2 (constitutive). HO-2, but not HO-1, is highly expressed in endothelial and smooth muscle cells and in adjacent astrocytes in the brain. HO-1 is expressed basally only in the spleen and liver but can be induced to a varying extent in most tissues. Elevating heme, protein phosphorylation, Ca2+ influx, and Ca2+/calmodulin-dependent processes increase HO-2 activity. CO dilates cerebral arterioles and may constrict or dilate skeletal muscle and renal arterioles. Selected vasodilatory stimuli, including seizures, glutamatergic stimulation, hypoxia, hypotension, and ADP, increase CO, and the inhibition of HO attenuates the dilation to these stimuli. Astrocytic HO-2-derived CO causes glutamatergic dilation of pial arterioles. CO dilates by activating smooth muscle cell large-conductance Ca2+-activated K+ (BKCa) channels. CO binds to BKCa channel-bound heme, leading to an increase in Ca2+ sparks-to-BKCa channel coupling. Also, CO may bind directly to the BKCa channel at several locations. Endothelial nitric oxide and prostacyclin interact with HO/CO in circulatory regulation. In cerebral arterioles in vivo, in contrast to dilation to acute CO, a prolonged exposure of cerebral arterioles to elevated CO produces progressive constriction by inhibiting nitric oxide synthase. The HO/CO system is highly protective to the vasculature. CO suppresses apoptosis and inhibits components of endogenous oxidant-generating pathways. Bilirubin is a potent reactive oxygen species scavenger. Still many questions remain about the physiology and biochemistry of HO/CO in the circulatory system and about the function and dysfunction of this gaseous mediator system.

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Iselin, C. E., L. Ny, B. Larsson, N. C. Schaad, P. Alm, P. Graber, D. R. Morel, and K. E. Andersson. "The Nitric Oxide Synthase/ Nitric Oxide and Heme Oxygenase/ Carbon Monoxide Pathways in the Human Ureter." European Urology 33, no. 2 (1998): 214–21. http://dx.doi.org/10.1159/000019539.

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Mehandjiev, D., D. Panayotov, G. Tiuliev, I. Mitov, and I. Dragieva. "Reaction of nitric oxide and nitric oxide + carbon monoxide with amorphous Fe-Co-B alloy powders." Applied Catalysis B: Environmental 5, no. 3 (February 1995): 199–219. http://dx.doi.org/10.1016/0926-3373(94)00045-x.

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40

Caton, J. A., and D. L. Siebers. "Reduction of Nitrogen Oxides in Engine Exhaust Gases by the Addition of Cyanuric Acid." Journal of Engineering for Gas Turbines and Power 111, no. 3 (July 1, 1989): 387–93. http://dx.doi.org/10.1115/1.3240266.

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Nitric oxide concentrations in a portion of the exhaust of a diesel engine operated with equivalence ratios between 0.25 and 0.75 were reduced by up to 98 percent by the addition of cyanuric acid. The cyanuric acid was combined with the exhaust gas in an electrically heated quartz flow reactor. The effects of the key process parameters (temperature, exhaust gas composition and residence time, and the overall engine equivalence ratio) on NO reduction by cyanuric acid were investigated. Nitric oxide reduction was evident at flow reactor temperatures above 700 K. The maximum nitric oxide reduction varied from 80 percent for a reactor temperature of 1180 K and an engine equivalence ratio of 0.25 to 98 percent for a temperature of 1120 K and an equivalence ratio of 0.75. The temperature range over which 60 percent or greater nitric oxide reduction was obtained was 1100 to 1340 K. Increasing the exhaust gas carbon monoxide concentration lowered the required reactor temperature and increased the temperature range for significant nitric oxide reduction. Increasing the exhaust gas nitric oxide concentration lowered the ratio of cyanuric acid to nitric oxide required for maximum nitric oxide reduction.

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Baltrenas, Pranas, Danguole Kaziukoniene, and Mindaugas Kvasauskas. "AIR POLLUTION AT PARKING‐LOTS OF VILNIUS." JOURNAL OF ENVIRONMENTAL ENGINEERING AND LANDSCAPE MANAGEMENT 12, no. 1 (March 31, 2004): 38–43. http://dx.doi.org/10.3846/16486897.2004.9636813.

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The expansion of Vilnius creates the need for the installation of new parking facilities. This problem could be solved by establishing guarded parking‐lots or modern underground and multi‐storey garages, in order to economize useful land and comply with the requirements of environmentalists. Investigation was carried out on parking‐lots of Vilnius. All the guarded parking‐lots are divided into three types in accordance with the size of the lot and the type of vehicles parked on it. Measurements were carried out at a lot of each type. The concentrations of hydrocarbons, nitric oxide, carbon monoxide and dust were measured. Guarded parking‐lots located at the crossroad of Ateities and L. Giros streets, on Architektu and Č. Sugiharos streets were selected for the investigation. The parking‐lot located at the crossroad of Ateities and L. Giros streets had the highest concentration of nitric oxide overrunning the permitted concentration up to 1,9 times. Besides, the concentration of carbon monoxide and hydrocarbons also overran the permitted norms. The lowest concentrations were found after measuring dust concentration in the air.

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NOMENOĞLU, Tuğçe, and Emine DEMİREL YILMAZ. "Gas Mediators in the Nervous System: Nitric Oxide, Hydrogen Sulfide and Carbon Monoxide." Turkiye Klinikleri Journal of Neurology 12, no. 3 (2017): 71–88. http://dx.doi.org/10.5336/neuro.2017-58770.

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43

Vialatte, A., M. Barthélemy, and J. Lilensten. "Impact of Energetic Electron Precipitation on the Upper Atmosphere: Nitric Monoxide." Open Atmospheric Science Journal 11, no. 1 (July 27, 2017): 88–104. http://dx.doi.org/10.2174/1874282301711010088.

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Background:Nitric oxide concentration in the upper atmosphere is known to be highly dependent on the solar activity. It can be transported to the stratosphere by the atmospheric circulation. In the stratosphere it is responsible for the destruction of ozone and consequently stratospheric heating rates are affected. This is one of the mechanisms by which solar variability has been suspected to drive variability in the energetic budget of the Earth climate. Therefore, it is essential to know every physical and chemical processes leading to the production or to a destruction of nitric oxide.Aim:The aim of this work is to calculate the production rate of NO+and some of the NO electronic states created by electron impact on NO at night in the auroral zone using an electron transport code.Conclusion:We study this variability under different precipitation conditions and taking into account the variability of the neutral atmosphere with the geomagnetic and solar activity. We find that the energetic electron precipitation has a very small effect on the absolute value of the NO+and NO* production rates. In order to help further research to consider the effect of NO+and NO*, we provide a table of all the production rates in a medium solar and geomagnetic activity case.

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Namihira, T., S. Tsukamoto, D. Wang, S. Katsuki, R. Hackam, K. Okamoto, and H. Akiyama. "Production of nitric monoxide using pulsed discharges for a medical application." IEEE Transactions on Plasma Science 28, no. 1 (2000): 109–14. http://dx.doi.org/10.1109/27.842877.

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Weinberg, J. Brice, Bert K. Lopansri, Esther Mwaikambo, and Donald L. Granger. "Arginine, nitric oxide, carbon monoxide, and endothelial function in severe malaria." Current Opinion in Infectious Diseases 21, no. 5 (October 2008): 468–75. http://dx.doi.org/10.1097/qco.0b013e32830ef5cf.

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Marazioti, Antonia, Mariarosaria Bucci, Ciro Coletta, Valentina Vellecco, Padmamalini Baskaran, Csaba Szabó, Giuseppe Cirino, et al. "Inhibition of Nitric Oxide–Stimulated Vasorelaxation by Carbon Monoxide-Releasing Molecules." Arteriosclerosis, Thrombosis, and Vascular Biology 31, no. 11 (November 2011): 2570–76. http://dx.doi.org/10.1161/atvbaha.111.229039.

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Naseem, Khalid M., and K. Richard Bruckdorfer. "INHIBITION OF PLATELET ACTIVATION BY CARBON MONOXIDE: COMPARISON WITH NITRIC OXIDE." Biochemical Society Transactions 25, no. 3 (August 1, 1997): 396S. http://dx.doi.org/10.1042/bst025396s.

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Hogg, Neil. "Nitric Oxide expands scope to cover hydrogen sulfide and carbon monoxide." Nitric Oxide 35 (November 2013): 1. http://dx.doi.org/10.1016/j.niox.2013.06.003.

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Reade, Michael C., J. Duncan Young, and C. A. R. Boyd. "Nitric Oxide and Carbon Monoxide: Pathogenic Factors in Human Septic Shock?" Clinical Science 104, s49 (April 1, 2003): 55P—56P. http://dx.doi.org/10.1042/cs104055pb.

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Hartmann, Nathaniel J., Guang Wu, and Trevor W. Hayton. "Reactivity of a Nickel Sulfide with Carbon Monoxide and Nitric Oxide." Journal of the American Chemical Society 138, no. 38 (September 14, 2016): 12352–55. http://dx.doi.org/10.1021/jacs.6b08084.

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