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Nitric oxide concentration profiles

Fig. 22. (a) Vau-iation in translational temperature profiles along the stagnation streamline as a function of altitude, (b) Variation in vibrational temperature profiles along the stagnation streamline as a function of altitude, (c) Variation in nitric oxide concentration profiles along the stagnation streamline as a function of altitude. [Pg.125]

Levine and coworkers first reported on the real-time profiling of kidney tubular fluid nitric oxide concentration in vivo [89, 91], In the 2001 publication, a modified version of a combination NO electrode (WPI, ISONOP007) was successfully used to measure NO concentration profiles along the length of a single nephron of a rat kidney tubular segment. Since it was shown that the electrode is sensitive to NO in the rat tubule it was used to detect NO concentration differences in rat kidney tubules before and after 5/6 nephrectomy. The results clearly showed that the NO concentration was much higher in nephrectomized rats vs unnephrectomized rats. [Pg.37]

D.Z. Levine, M. Iacovitti, K.D. Burns, and XJ. Zhang, Real-time profiling of kidney tubular fluid nitric oxide concentrations in vivo. Am. J. Physiol.-Renal Physiol. 281, FI 89-194 (2001). [Pg.50]

Pro-inflammatory cytokines (see p. 432 et seq.) can also induce sleep, the effect depending on the concentration of the cytokine and the time of day. The effect on the sleep profile (increased non-REM and decreased REM sleep) appears to depend on the increased synthesis of prostaglandin D2 and nitric oxide which then alter the circadian rhythm. It is also known that some pro-inflammatory cytokines can affect the reuptake of 5-HT which plays an important role in regulating the sleep-wake profile. The endogenous fatty acid, oleamide, can cause sedation and induce sleep by activating cannabinoid receptors but also by potentiating the action of benzodiazepines on their receptor sites. Whether such action is of physiological relevance is presently unknown. [Pg.452]

The temperature and density structure of the troposphere, along with the concentrations of major constituents, are well documented and altitude profiles have been measured over a wide range of seasons and latitudes for the minor species water, carbon dioxide, and ozone. A few profiles are available for carbon monoxide, nitrous oxide, methane, and molecular hydrogen, while only surface or low-altitude measurements have been made for nitric oxide, nitrogen dioxide, ammonia, sulfur dioxide, hydrogen sulfide, and nonmethane hydrocarbons. No direct measurements of nitric acid and formaldehyde are available, though indirect information does exist. The concentrations of a number of other important species, such as peroxides and oxy and peroxy radicals, have never been determined. Therefore, while considerable information concerning trace constituent concentrations is available, the picture is far from complete. [Pg.373]

The major source of nitric oxide in a certain urban area is auto exhaust. At 6 00 A.M. the NOx concentration (mixing ratio) is 0.3 ppb(v). During the morning rush hour, automobiles collectively emit 1000 g of NOx (measured as N) per square kilometer of land area. The 10 00 A.M. temperature profile is shown next. By neglecting possible sinks for NOx, what mixing ratio do you expect in ambient air at 10 00 A.M. ... [Pg.408]

The metabolic countermeasures are characterized by the regulatory role of ascorbate for metabolic systems determining the clinical risk profile for CVD. The common aim of these metabolic regulations is to decrease the vascular permeability in ascorbate deficiency. Low ascorbate concentrations therefore induce vasoconstriction and hemostasis and affect vascular wall metabolism in favor of atherosclerogenesis. Towards this end ascorbate interacts with lipoproteins, coagulation factors, prostaglandins, nitric oxide, and second messenger systems such as cyclic monophosphates (for review see 1, 3-5). It... [Pg.619]

SAFETY PROFILE Moderately toxic by inhalation. A weak sensitizer and allergen. Local contact may cause contact dermatitis. A flammable liquid and dangerous fire hazard when exposed to heat or flame can react vigorously with oxidizing materials. Hypergolic reaction with concentrated nitric acid. To fight fire, use foam, CO2, dry chemical. See also MERCAPTANS. [Pg.1076]

SAFETY PROFILE Poison by inhalation. Potentially explosive decomposition at 200°C. Flammable when exposed to heat or flame. Explosive reaction with ammonia + heat, chlorine, concentrated nitric acid, ozone. Incompatible with oxidants. The decomposition products are hydrogen and metallic antimony. When heated to decomposition it emits toxic fumes of Sb. Used as a fumigating agent. See also ANTIMONY COMPOUNDS and HYDRIDES. [Pg.1277]

DOT CLASSIFICATION 4.3 Label Dangerous When Wet, Poison SAFETY PROFILE Human poison by ingestion causing nausea, vomiting, death. Flammable when exposed to heat or flame. This material is stable while kept dry. In moist air, it decomposes slowly. Reacts violently with acids or acid fumes to emit the highly toxic and flammable phosphine. Violent reaction with concentrated sulfuric acid, nitric acid, and oxidizing materials. Incompatible with HCl, H2SO4. When heated to decomposition it emits toxic fumes of POx and ZnO. Used as an acute rodenticide. See also PHOSPHIDES and... [Pg.1451]


See other pages where Nitric oxide concentration profiles is mentioned: [Pg.126]    [Pg.207]    [Pg.105]    [Pg.144]    [Pg.145]    [Pg.498]    [Pg.102]    [Pg.451]    [Pg.210]    [Pg.213]    [Pg.94]    [Pg.672]    [Pg.1127]    [Pg.734]    [Pg.535]    [Pg.642]    [Pg.448]    [Pg.444]    [Pg.279]    [Pg.610]    [Pg.297]    [Pg.1424]    [Pg.279]    [Pg.243]    [Pg.463]   
See also in sourсe #XX -- [ Pg.375 ]




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