Behaviour of nitric oxide metabolites in unprofessional athletes before and after a cardiopulmonary test

2010 ◽  
Vol 44 (4) ◽  
pp. 283-286
Author(s):  
Gregorio Caimi ◽  
Baldassare Canino ◽  
Rosalia Lo Presti
Keyword(s):  
Nitric Oxide ◽  
Before And After ◽  
Nitric Oxide Metabolites

Erythrocyte Deformability and Nitric Oxide Metabolites in Athletes Before and After a Cardiopulmonary Test

2009 ◽  
Vol 19 (4) ◽  
pp. 306-310 ◽  
Author(s):  
Gregorio Caimi ◽  
Baldassare Canino ◽  
Gabriella Amodeo ◽  
Paolo Ingargiola ◽  
Daniela Lucido ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Erythrocyte Deformability ◽  
Before And After ◽  
Nitric Oxide Metabolites

Effects of 7 Days of Arginine-Alpha-Ketoglutarate Supplementation on Blood Flow, Plasma L-Arginine, Nitric Oxide Metabolites, and Asymmetric Dimethyl Arginine After Resistance Exercise

2011 ◽  
Vol 21 (4) ◽  
pp. 291-299 ◽  
Author(s):  
Darryn S. Willoughby ◽  
Tony Boucher ◽  
Jeremy Reid ◽  
Garson Skelton ◽  
Mandy Clark
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Resistance Exercise ◽  
Brachial Artery ◽  
Exercise Session ◽  
Artery Blood Flow ◽  
Before And After ◽  
Asymmetric Dimethyl Arginine ◽  
Nitric Oxide Metabolites ◽  
Dimethyl Arginine

Background:Arginine-alpha-ketoglutarate (AAKG) supplements are alleged to increase nitric oxide production, thereby resulting in vasodilation during resistance exercise. This study sought to determine the effects of AAKG supplementation on hemodynamics and brachial-artery blood flow and the circulating levels of L-arginine, nitric oxide metabolites (NOx; nitrate/nitrite), asymmetric dimethyl arginine (ADMA), and L-arginine:ADMA ratio after resistance exercise.Methods:Twenty-four physically active men underwent 7 days of AAKG supplementation with 12 g/day of either NO2 Platinum or placebo (PLC). Before and after supplementation, a resistance-exercise session involving the elbow flexors was performed involving 3 sets of 15 repetitions with 70–75% of 1-repetition maximum. Data were collected immediately before, immediately after (PST), and 30 min after (30PST) each exercise session. Data were analyzed with factorial ANOVA (p < .05).Results:Heart rate, blood pressure, and blood flow were increased in both groups at PST (p = .001) but not different between groups. Plasma L-arginine was increased in the NO2 group (p = .001). NOx was shown to increase in both groups at PST (p = .001) and at 30PST (p = .001) but was not different between groups. ADMA was not affected between tests (p = .26) or time points (p = .31); however, the L-arginine:ADMA ratio was increased in the NO2 group (p = .03).Conclusion:NO2 Platinum increased plasma L-arginine levels; however, the effects observed in hemodynamics, brachial-artery blood flow, and NOx can only be attributed to the resistance exercise.

scholarly journals Reduced Levels of Nitric Oxide Metabolites in Cerebrospinal Fluid Are Associated with Equine Protozoal Myeloencephalitis

2002 ◽  
Vol 9 (3) ◽  
pp. 605-610 ◽  
Author(s):  
Chinedu J. Njoku ◽  
William J. A. Saville ◽  
Stephen M. Reed ◽  
Michael J. Oglesbee ◽  
Päivi J. Rajala-Schultz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebrospinal Fluid ◽  
Natural Infection ◽  
Clinical Signs ◽  
Sarcocystis Neurona ◽  
Immune Effector ◽  
Equine Protozoal Myeloencephalitis ◽  
Clinically Normal ◽  
Before And After ◽  
Nitric Oxide Metabolites

ABSTRACT Equine protozoal myeloencephalitis (EPM) is a disease of horses that is primarily associated with infection with the apicomplexan Sarcocystis neurona. Infection with this parasite alone is not sufficient to induce the disease, and the mechanism of neuropathogenesis associated with EPM has not been reported. Nitric oxide (NO) functions as a neurotransmitter, a vasodilator, and an immune effector and is produced in response to several parasitic protozoa. The purpose of this work was to determine if the concentration of NO metabolites (NO x −) in the cerebrospinal fluid (CSF) is correlated with the development of EPM. CSF NO x − levels were measured before and after transport-stressed, acclimated, or dexamethasone-treated horses (n = 3 per group) were experimentally infected with S. neurona sporocysts. CSF NO x − levels were also compared between horses that were diagnosed with EPM after natural infection with S. neurona and horses that did not have clinical signs of disease or that showed no evidence of infection with the parasite (n = 105). Among the experimentally infected animals, the mean CSF NO x − levels of the transport-stressed group, which had the most severe clinical signs, was reduced after infection, while these values were found to increase after infection in the remaining groups that had less severe signs of EPM. Under natural conditions, horses with EPM (n = 65) had a lower mean CSF NO x − concentration than clinically normal horses with antibodies (Abs) against S. neurona (n = 15) in CSF, and horses that developed ataxia (n = 81) had a significantly lower mean CSF NO x − concentration than horses that did not have neurologic signs (n = 24). In conclusion, lower CSF NO x − levels were associated with clinical EPM, suggesting that measurement of CSF NO x − levels could improve the accuracy of diagnostic tests that are based upon detection of S. neurona-specific Abs in CSF alone and that reduced NO levels could be causatively related to the development of EPM.

Nitric Oxide Metabolites Before and After Spinal Anesthesia with Lidocaine

1998 ◽  
Vol 89 (Supplement) ◽  
pp. 1414A
Author(s):  
Ashwani K. Chhibber ◽  
Michael P. Eaton ◽  
Stewart J. Lustik ◽  
Salvatore Mauro ◽  
Jeremy Hogan
Keyword(s):  
Nitric Oxide ◽  
Spinal Anesthesia ◽  
Before And After ◽  
Nitric Oxide Metabolites

scholarly journals Levels of nitric oxide metabolites in patients with asthma and concomitant hypertension

2010 ◽  
Vol 16 (3) ◽  
pp. 266-269
Author(s):  
A. G. Kozyrev ◽  
A. U. Gichkin ◽  
A. A. Zhloba
Keyword(s):  
Nitric Oxide ◽  
Arterial Hypertension ◽  
Plasma Levels ◽  
Healthy Subjects ◽  
Asthma Exacerbation ◽  
Asthma Severity ◽  
Asthmatic Patients ◽  
Before And After ◽  
Nitric Oxide Metabolites ◽  
Concomitant Hypertension

Objective. To investigate plasma levels of nitrates/nitrites (NO2+NO3) and S-nitrosothiols in asthmatic patients, including patients with concomitant arterial hypertension. Methods. The data were obtained by Greiss method before and after treatment of asthma exacerbation in asthmatic patients and healthy subjects. Results. This study has shown that evaluation of NO2+NO3 and S-nitrosothiols should consider asthma severity and the presence of concomitant arterial hypertension. The level of NO metabolites was higher in mild asthma and in patients with concomitant hypertension of grade 1.

Plasma Nitric Oxide Metabolites and Lipid Peroxide Levels in Preeclamptic Pregnant Women before and after Delivery

1999 ◽  
Vol 48 (4) ◽  
pp. 247-250 ◽  
Author(s):  
Ü. Mutlu-Türkoglu ◽  
G. Aykaç-Toker ◽  
L. Ibrahimoglu ◽  
E. Ademoglu ◽  
M. Uysal
Keyword(s):  
Nitric Oxide ◽  
Pregnant Women ◽  
Lipid Peroxide ◽  
Before And After ◽  
Nitric Oxide Metabolites

The Effect on Health of Some Cardiovascular Risk Factors

2017 ◽  
Vol 68 (10) ◽  
pp. 2237-2242
Author(s):  
Germaine Savoiu Balint ◽  
Mihaiela Andoni ◽  
Ramona Amina Popovici ◽  
Laura Cristina Rusu ◽  
Ioana Citu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Reactivity ◽  
Vascular Wall ◽  
Dose Effect ◽  
Organ Bath ◽  
Before And After ◽  
Specific Receptors ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Relaxing Response

Arterial endothelium produces a large ramge of active factors which are indispensable for modulation of vasomotor tone and maintenance of vascular wall integrity. From these factors, nitric oxide (NO), wich is released by the endothelial cells as a response to acetylcholine or adenosine action on specific receptors, plays an important role.NO is the result of oxidation process of L-arginine into L-citrulline, under the action of endothelial nitric oxide synthase (NOSe), wich is activated by intracelluar Ca2+ - calmodulin complex . Our study, performed in isolated organ bath, analyzed vascular reactivity of 12 guinea pigs� thoracic aorta rings. After phenylephrine -PHE 10-5 mol/L precontraction, the dose-effect curves for acetylcoline � ACH, adenosine 5� phosphate - 5�ADP and sodium nitroprusside � SNP were determined, before and after incubation of preparation, for 1 hour, with 5% hydrosoluble cigarettes smoke extract (CSE). Statistic analysis, performed with the use of t pair test and ANOVA parametric test, showed that incubation of vascular preparation with 5% CSE has increased the contractile response to PHE 10-5 mol/L (p[0.05), has reduced the endothelium-dependent relaxing response to ATP 10-5 mol/L (p[0.001) and 5�ADP 10-5 molo/L (p[0.001), but has not significantly modified the endothelium-independent relaxing response to SNP 10-5 mol/L (p=0.05). As a conclusion, vascular rings incubation with 5% CSE induced a decrease of endothelium NO synthesis under the action of AXH and 5�ADP, but did not change the smooth muscle fiber respomse in the presence of NO released by SNP.

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Cardiac Output ◽  
No Synthase ◽  
Before And After ◽  
Regional Hemodynamics ◽  
Autonomic Blockade ◽  
Infusion Of Norepinephrine ◽  
Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

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