Continuous measurement of gastric nitric oxide production

1996 ◽  
Vol 271 (6) ◽  
pp. G1039-G1042
Author(s):  
A. Aneman ◽  
J. Snygg ◽  
L. Fandriks ◽  
A. Pettersson
Keyword(s):  
Nitric Oxide ◽  
Continuous Measurement ◽  
Gas Phases ◽  
No Formation ◽  
Double Lumen Catheter ◽  
Coefficients Of Variation ◽  
Lumen Catheter ◽  
On Line ◽  
Quantitative Analyses

With the use of a double-lumen catheter, nitric oxide (NO) was dialyzed across a Gore-Tex membrane into a gas phase and subsequently analyzed on-line by chemiluminescence. This new technique for the continuous measurement of NO was evaluated bench-side and applied in the human stomach in vivo to measure the nonenzymatic formation of NO generated from nitrite in an acidic milieu. A linear relation (r2 = 0.991, P < 0.0001) between concentrations of NO in aqueous solutions (2.5-52.5 mM) and NO in the corresponding gas phases obtained by the dialysis technique (50-1,000 parts per billion) validated the present method for quantitative analyses of NO. Interassay and intra-assay coefficients of variation at all concentrations of NO for six experiments were < 5%. High intragastric concentrations of NO (in the micromolar range) were found during basal conditions. The requirement of both nitrite from the saliva and an acidic environment for NO formation is indicated, since depletion of saliva as well as acid neutralization greatly reduced gastric NO concentrations. Furthermore, large amounts of gastric NO were formed after intake of sodium nitrate. With the use of this technique, NO can be continuously measured with accuracy experimentally and clinically in any organ accessible to intubation.

scholarly journals Nitric oxide interactions with cobalamins: biochemical and functional consequences

Blood ◽  
1996 ◽  
Vol 88 (5) ◽  
pp. 1857-1864 ◽  
Author(s):  
M Brouwer ◽  
W Chamulitrat ◽  
G Ferruzzi ◽  
DL Sauls ◽  
JB Weinberg
Keyword(s):  
Nitric Oxide ◽  
Electron Paramagnetic Resonance Spectroscopy ◽  
Resonance Spectroscopy ◽  
Paramagnetic Resonance ◽  
No Formation ◽  
Iron Nitrosyl ◽  
Wide Range ◽  
Functional Consequences

Abstract Nitric oxide (NO) is a paramagnetic gas that has been implicated in a wide range of biologic functions. The common pathway to evoke the functional response frequently involves the formation of an iron- nitrosyl complex in a target (heme) protein. In this study, we report on the interactions between NO and cobalt-containing vitamin B12 derivatives. Absorption spectroscopy showed that of the four Co(III) derivatives (cyanocobalamin [CN-Cbl], aquocobalamin [H2O-Cbl], adenosylcobalamin [Ado-Cbl], and methylcobalamin [MeCbl]), only the H2O- Cbl combined with NO. In addition, electron paramagnetic resonance spectroscopy of H2O-Cbl preparations showed the presence of a small amount of Cob-(II)alamin that was capable of combining with NO. The Co(III)-NO complex was very stable, but could transfer its NO moiety to hemoglobin (Hb). The transfer was accompanied by a reduction of the Co(III) to Co(II), indicating that NO+ (nitrosonium) was the leaving group. In accordance with this, the NO did not combine with the Hb Fe(II)-heme, but most likely with the Hb cysteine-thiolate. Similarly, the Co(III)-NO complex was capable of transferring its NO to glutathione. Ado-Cbl and Me-Cbl were susceptible to photolysis, but CN- Cbl and H2O-Cbl were not. The homolytic cleavage of the Co(III)-Ado or Co(III)-Me bond resulted in the reduction of the metal. When photolysis was performed in the presence of NO, formation of NO-Co(II) was observed. Co(II)-nitrosyl oxidized slowly to form Co(III)-nitrosyl. The capability of aquocobalamin to combine with NO had functional consequences. We found that nitrosylcobalamin had diminished ability to serve as a cofactor for the enzyme methionine synthase, and that aquocobalamin could quench NO-mediated inhibition of cell proliferation. Our in vitro studies therefore suggest that interactions between NO and cobalamins may have important consequences in vivo.

scholarly journals Constitutive nitric oxide production by rat alveolar macrophages

1998 ◽  
Vol 274 (3) ◽  
pp. L360-L368 ◽  
Author(s):  
P. R. Miles ◽  
L. Bowman ◽  
A. Rengasamy ◽  
L. Huffman
Keyword(s):  
Nitric Oxide ◽  
Alveolar Macrophage ◽  
Alveolar Macrophages ◽  
Lung Surfactant ◽  
Calcium Ionophore ◽  
Cell Types ◽  
Alveolar Type ◽  
No Production ◽  
No Formation

Results from previous studies suggest that alveolar macrophages must be exposed to inflammatory stimuli to produce nitric oxide (⋅ NO). In this study, we report that naive unstimulated rat alveolar macrophages do produce ⋅ NO and attempt to characterize this process. Western blot analysis demonstrates that the enzyme responsible is an endothelial nitric oxide synthase (eNOS). No brain or inducible NOS can be detected. The rate of ⋅ NO production is ∼0.07 nmol ⋅ 106cells−1 ⋅ h−1, an amount that is less than that produced by the eNOS found in alveolar type II or endothelial cells. Alveolar macrophage ⋅ NO formation is increased in the presence of extracellularl-arginine, incubation medium containing magnesium and no calcium, a calcium ionophore (A-23187), or methacholine. ⋅ NO production is inhibited by N G-nitro-l-arginine methyl ester (l-NAME) but not by N G-nitro-l-arginine,l- N 5-(1-iminomethyl)ornithine hydrochloride, or aminoguanidine. Incubation with ATP, ADP, or histamine also inhibits ⋅ NO formation. Some of these properties are similar to and some are different from properties of eNOS in other cell types. Cellular ⋅ NO levels do not appear to be related to ATP or lactate content. Alveolar macrophage production of ⋅ NO can be increased approximately threefold in the presence of lung surfactant or its major component, dipalmitoyl phosphatidylcholine (DPPC). The DPPC-induced increase in ⋅ NO formation is time and concentration dependent, can be completely inhibited by l-NAME, and does not appear to be related to the degradation of DPPC by alveolar macrophages. These results demonstrate that unstimulated alveolar macrophages produce ⋅ NO via an eNOS and that lung surfactant increases ⋅ NO formation. This latter effect may be important in maintaining an anti-inflammatory state in vivo.

In vivo and continuous measurement of bisulfide in the hippocampus of rat's brain by an on-line integrated microdialysis/droplet-based microfluidic system

The Analyst ◽  
2015 ◽  
Vol 140 (11) ◽  
pp. 3814-3819 ◽  
Author(s):  
Feidan Gu ◽  
Xiaoyu Zhou ◽  
Xiaocui Zhu ◽  
Meiping Zhao ◽  
Jie Hao ◽  
...  
Keyword(s):  
Continuous Measurement ◽  
Microfluidic System ◽  
System P ◽  
Continuous Approach ◽  
On Line

An on-line and continuous approach was demonstrated forin vivomeasurement of bisulfide in rat's brain.

scholarly journals Direct Evidence of in Vivo Nitric Oxide Production and Inducible Nitric Oxide Synthase mRNA Expression in the Brain of Living Rat during Experimental Meningitis

1999 ◽  
Vol 19 (11) ◽  
pp. 1175-1178 ◽  
Author(s):  
Yasuhiro Suzuki ◽  
Satoshi Fujii ◽  
Teiji Tominaga ◽  
Takashi Yoshimoto ◽  
Shigemoto Fujii ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mrna Expression ◽  
Interferon Γ ◽  
Iron Complex ◽  
Paramagnetic Resonance ◽  
No Formation ◽  
Endogenous Nitric Oxide ◽  
Oxide Synthase ◽  
The Brain

To detect endogenous nitric oxide (NO) produced in a rat bacterial meningitis model, the authors applied an electron paramagnetic resonance (EPR) NO-trapping technique. Iron complex with N,N-diethyldithiocarbamate were used as a trapping agent. Experimental meningitis was induced by a mixture of lipopolysaccharide and interferon-γ. Sequential changes of NO formation under meningitis were observed in rat brain tissue by using X-band (9 GHz) EPR spectroscopy, and endogenous NO was detected in the head of a living rat with a 700-MHz EPR system. Inducible NO synthase mRNA expression in the brain tissues also was proven by using a reverse transcriptase-polymerase chain reaction technique.

scholarly journals Estimation of total rate of formation of nitric oxide in the rat

1998 ◽  
Vol 330 (1) ◽  
pp. 527-532 ◽  
Author(s):  
Augustinas SAKINIS ◽  
Åke WENNMALM
Keyword(s):  
Nitric Oxide ◽  
Spectrometric Analysis ◽  
Total Rate ◽  
Cage System ◽  
No Formation ◽  
Organ Systems ◽  
Anaesthetized Rats ◽  
Male Wistar Rats ◽  
Controlled Breathing

Nitric oxide (NO) is a powerful mediator with important actions in several organ systems. NO is synthesized during the enzymatic conversion of L-arginine and molecular oxygen to l-citrulline. About 90% of the NO formed is degraded to nitrate. Utilizing this information we have developed a method for assessment of the total rate of formation of NO in the rat. Male Wistar rats were kept in a closed-cage system allowing controlled breathing of a mixture of 18O2 and 16O2 in N2 for up to 5 h. Blood samples for mass spectrometric analysis of nitrate residues with varying numbers of 18O atoms incorporated were drawn before and during the exposure to 18O2. By comparing the relative incorporation of 18O into nitrate residues to the 16O2/18O2 ratio in the breathing gas mixture in the cage system it was possible to calculate the absolute rate of NO formation in the animal. The rate of formation of NO in anaesthetized rats ranged from 0.33 to 0.85 μmol·kg-1·h-1. The rate of formation did not differ significantly in rats which were awake during the experiment (range 0.36-0.72 μmol·kg-1·h-1). The L-arginine analogue Nω-nitro-L-arginine methyl ester (L-NAME) dose-dependently inhibited the formation of NO, at a dose of 100 mg/kg by more than 99%. The technique presented allows estimation of the total rate of formation of NO in vivo in rats. Application of the technique may yield important information about the physiological and pathophysiological roles of NO. It may also be utilized to evaluate the effect of pharmacological treatment on NO formation.

Role of L-arginine-derived nitric oxide in cholinergic dilation of gastric arterioles

1993 ◽  
Vol 265 (6) ◽  
pp. H2110-H2116
Author(s):  
R. Y. Chen ◽  
G. Ross ◽  
K. Y. Chyu ◽  
P. H. Guth
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Topical Administration ◽  
Microscopy Technique ◽  
No Formation ◽  
Resistance Vessels ◽  
Gastric Circulation ◽  
Arteriolar Diameter

The role of L-arginine-derived nitric oxide (NO) in cholinergic vasodilation of resistance vessels was studied in the intact stomach of the rat, utilizing an in vivo microscopy technique. Two L-arginine analogues, NG-monomethyl-L-arginine (L-NMMA) and nitro-L-arginine methyl ester (L-NAME), were used to block NO synthesis. Cholinergic dilation of gastric submucosal arterioles was induced by topical application of various concentrations of acetylcholine (ACh) (10(-7)-10(-4) M). Intravenous but not topical administration of L-NMMA and L-NAME caused an increase in arterial pressure. Intravenous or topical L-NAME reduces resting arteriolar diameter. These findings support the contention that NO formation modulates basal vascular tone and suggest that NO release may play a significant role in the regulation of the gastric circulation. L-Arginine analogues attenuated the arteriolar dilating effect of ACh but not adenosine or nitroglycerin. Substantial arteriolar responses to ACh remained after systemic or topical treatment with either L-NMMA or L-NAME. These results indicate that the L-arginine-NO pathway accounts only in part for ACh-induced vasodilation in gastric resistance vessels in vivo.

Nitric oxide and prostaglandins are involved in the macula densa control of the renin system

1995 ◽  
Vol 269 (6) ◽  
pp. F825-F830 ◽  
Author(s):  
K. Schricker ◽  
M. Hamann ◽  
A. Kurtz
Keyword(s):  
Nitric Oxide ◽  
Plasma Renin ◽  
Macula Densa ◽  
Salt Transport ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
No Formation ◽  
Sprague Dawley Rats ◽  
Renin Mrna

This study sought to examine the involvement of prostaglandins and of nitric oxide (NO) in the macula densa-dependent activation of the renin system in vivo. For this purpose, male Sprague-Dawley rats were chronically infused with furosemide (12 mg/day) for 6 days to inhibit macula densa salt transport. To inhibit the synthesis of prostaglandins and of NO, animals were injected with indomethacin (2 mg/kg twice daily) and with nitro-L-arginine methyl ester (L-NAME; 40 mg/kg twice daily) for the last 2 days of the experiment, respectively. Furosemide infusion increased plasma renin activity (PRA) from 8.8 +/- 1.4 to 41 +/- 5.2 ng angiotensin I (ANG I).h-1.ml-1 and renin mRNA levels from 112 +/- 8 of standard to 249 +/- 18% of standard. After treatment with indomethacin, the furosemide-induced increases in renin mRNA levels was attenuated to 190 +/- 11% of standard. After injections of L-NAME, both the furosemide-induced increases of renin mRNA levels and of PRA were reduced to 126 +/- 14% of standard and 22 +/- 5 ng ANG I.h-1.ml-1, respectively. These findings suggest that activation of renin gene expression by blockade of the macula densa function is dependent on intact NO and prostaglandin formation, whereas for stimulation of renin secretion mainly intact NO formation appears to be necessary.

Use of electrochemical sensors for on-line monitoring of ionized calcium, potassium, and glucose in whole blood of living dogs.

1980 ◽  
Vol 26 (10) ◽  
pp. 1425-1429 ◽  
Author(s):  
E J Fogt ◽  
A R Eddy ◽  
A H Clemens ◽  
J Fox ◽  
H Heath
Keyword(s):  
Whole Blood ◽  
Electrochemical Sensors ◽  
Venous Blood ◽  
Ionized Calcium ◽  
Pump System ◽  
Modular Concept ◽  
Double Lumen Catheter ◽  
Lumen Catheter ◽  
On Line

Abstract We report the development and evaluation of electrochemical sensors for continuous on-line measurement of whole-blood ionized calcium, potassium, and glucose in living animals. Ionized calcium and potassium are measured with ion-selective electrodes, by using a unique differential approach. A polarographic sensor coupled with a membrane with bound glucose oxidase is used in the glucose analyzer. The modular concept of instrument design permits one mainframe, computer, and pump system to house any analyzer module or a combination of modules. A small volume of venous blood (about 2 mL/h) is continuously withdrawn from the subject through a double-lumen catheter and pumped through the analyzer(s). Results of in vitro correlation studies and studies in normal dogs (including responses of ionized calcium, potassium, and glucose to various stresses) support the validity of the measurements.

Dependence of intestinal arteriolar regulation on flow-mediated nitric oxide formation

2000 ◽  
Vol 279 (5) ◽  
pp. H2249-H2258 ◽  
Author(s):  
H. Glenn Bohlen ◽  
Geoffrey P. Nase
Keyword(s):  
Nitric Oxide ◽  
Shear Rate ◽  
Flow Velocity ◽  
Large Fraction ◽  
Sodium Absorption ◽  
Nitric Oxide Formation ◽  
No Formation ◽  
Relationship Of ◽  
The Relationship

Our hypothesis was that a large fraction of resting nitric oxide (NO) formation is driven by flow-mediated mechanisms in the intestinal microvasculature of the rat. NO-sensitive microelectrodes measured the in vivo perivascular NO concentration ([NO]). Flow was increased by forcing the arterioles to perfuse additional nearby arterioles; flow was decreased by lowering the mucosal metabolic rate by reducing sodium absorption. Resting periarteriolar [NO] of large arterioles (first order; 1A) and intermediate-sized arterioles (second order; 2A) was 337 ± 20 and 318 ± 21 nM. The resting [NO] was higher than the dissociation constant for the NO-guanylate cyclase reaction of vascular smooth muscle; therefore, resting [NO] should be a potent dilatory signal at rest. Over flow velocity and shear rate ranges of ∼40–180% of control, periarteriolar [NO] changed 5–8% for each 10% change in flow velocity and shear rate. The relationship of [NO] to flow velocity and shear rate demonstrated that 60–80% of resting [NO] depended on flow-mediated mechanisms. Therefore, moment-to-moment regulation of [NO] at rest is an ongoing process that is highly dependent on flow-dependent mechanisms.

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