scholarly journals Breath Hydrogen Produced by Ingestion of Commercial Hydrogen Water and Milk

2009 ◽  
Vol 4 ◽  
pp. BMI.S2209 ◽  
Author(s):  
Akito Shimouchi ◽  
Kazutoshi Nose ◽  
Makoto Yamaguchi ◽  
Hiroshi Ishiguro ◽  
Takaharu Kondo
Keyword(s):  
Baseline Level ◽  
Area Under The Curve ◽  
Distilled Water ◽  
Dependent Manner ◽  
Breath Hydrogen ◽  
Milk Intolerance ◽  
Maximal Level ◽  
Hydrogen Water ◽  
Dose Dependent ◽  
Sustained Increase

Objective To compare how and to what extent ingestion of hydrogen water and milk increase breath hydrogen in adults. Methods Five subjects without specific diseases, ingested distilled or hydrogen water and milk as a reference material that could increase breath hydrogen. Their end-alveolar breath hydrogen was measured. Results Ingestion of hydrogen water rapidly increased breath hydrogen to the maximal level of approximately 40 ppm 10–15 min after ingestion and thereafter rapidly decreased to the baseline level, whereas ingestion of the same amount of distilled water did not change breath hydrogen (p < 0.001). Ingestion of hydrogen water increased both hydrogen peaks and the area under the curve (AUC) of breath hydrogen in a dose-dependent manner. Ingestion of milk showed a delayed and sustained increase of breath hydrogen in subjects with milk intolerance for up to 540 min. Ingestion of hydrogen water produced breath hydrogen at AUC levels of 2 to 9 ppm hour, whereas milk increased breath hydrogen to AUC levels of 164 ppm hour for 540 min after drinking. Conclusion Hydrogen water caused a rapid increase in breath hydrogen in a dose-dependent manner; however, the rise in breath hydrogen was not sustained compared with milk.

scholarly journals Effect of heparin administration to sheep on the release profiles of circulating activin A and follistatin

2004 ◽  
Vol 181 (2) ◽  
pp. 307-314 ◽  
Author(s):  
KL Jones ◽  
DM De Kretser ◽  
DJ Phillips
Keyword(s):  
Area Under The Curve ◽  
Activin A ◽  
Size Exclusion ◽  
Dependent Manner ◽  
Large Pool ◽  
Heparin Administration ◽  
Repeat Administration ◽  
Clearance Mechanism ◽  
Exclusion Chromatography ◽  
Dose Dependent

Activin A and follistatin are normally present in relatively low amounts in the circulation. Heparin administration elicits a rapid and robust release of these proteins, although this phenomenon is poorly defined. In the present studies, the response to heparin administration was evaluated in the plasma of adult ewes in terms of whether it was dose-dependent, could be neutralized, was responsive to multiple stimulation, and the nature of the activin A and follistatin released. Activin A and follistatin were rapidly released by heparin in a dose-dependent manner (25, 100 or 250 IU/kg), with differences in the response as adjudged by peak concentration, timing of the peak and area under the curve. The heparin response could be blocked by pretreatment with protamine; conversely protamine injection alone (2 mg/kg) elicited release of follistatin but not activin A. Repeat administration of heparin at three-hourly intervals resulted in activin and follistatin responses to each injection, but each subsequent stimulation increased and extended the responses, consistent with saturation of the heparin clearance mechanism. Size exclusion chromatography of plasma samples confirmed that the majority of activin and follistatin released by heparin was a complex, whereas follistatin released by protamine was unbound. These data are consistent with a large pool of activin A and follistatin resident on extracellular matrices, with the rapid response implicating the vascular endothelium as the prime site of release following administration of these commonly used anticoagulant therapies.

scholarly journals Prebiotic fibres dose-dependently increase satiety hormones and alter Bacteroidetes and Firmicutes in lean and obese JCR:LA-cp rats

2011 ◽  
Vol 107 (4) ◽  
pp. 601-613 ◽  
Author(s):  
Jill A. Parnell ◽  
Raylene A. Reimer
Keyword(s):  
Gastric Emptying ◽  
Energy Expenditure ◽  
Gut Microbiota ◽  
Peptide Yy ◽  
Therapeutic Potential ◽  
Area Under The Curve ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Total Bacteria

There is a growing interest in modulating gut microbiota with diet in the context of obesity. The purpose of the present study was to evaluate the dose-dependent effects of prebiotics (inulin and oligofructose) on gut satiety hormones, energy expenditure, gastric emptying and gut microbiota. Male lean and obese JCR:LA-cp rats were randomised to either of the following: lean 0 % fibre (LC), lean 10 % fibre (LF), lean 20 % fibre (LHF), obese 0 % fibre (OC), obese 10 % fibre (OF) or obese 20 % fibre (OHF). Body composition, gastric emptying, energy expenditure, plasma satiety hormone concentrations and gut microbiota (using quantitative PCR) were measured. Caecal proglucagon and peptide YY mRNA levels were up-regulated 2-fold in the LF, OF and OHF groups and 3-fold in the LHF group. GhrelinO-acyltransferase mRNA levels were higher in obesev.lean rats and decreased in the OHF group. Plasma ghrelin response was attenuated in the LHF group. Microbial species measured in the Bacteroidetes division decreased, whereas those in the Firmicutes increased in obesev.lean rats and improved with prebiotic intake.BifidobacteriumandLactobacillusincreased in the OHFv.OC group.Bacteroidesand total bacteria negatively correlated with percentage of body fat and body weight. Enterobacteriaceae increased in conjunction with glucose area under the curve (AUC) and glucagon-like peptide-1 AUC.Bacteroidesand total bacteria correlated positively with ghrelin AUC yet negatively with insulin AUC and energy intake (P < 0·05). Several of the mechanisms through which prebiotics act (food intake, satiety hormones and alterations in gut microbiota) are regulated in a dose-dependent manner. The combined effects of prebiotics may have therapeutic potential for obesity.

Glibenclamide prevents coronary vasodilation induced by beta 1-adrenoceptor stimulation in dogs

1994 ◽  
Vol 266 (1) ◽  
pp. H84-H92 ◽  
Author(s):  
T. Narishige ◽  
K. Egashira ◽  
Y. Akatsuka ◽  
Y. Imamura ◽  
T. Takahashi ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Electromagnetic Flowmeter ◽  
Left Ventricular ◽  
K Channel ◽  
Dependent Manner ◽  
Coronary Vasodilation ◽  
Intracoronary Infusion ◽  
Before And After ◽  
Dose Dependent ◽  
Sustained Increase

This study aimed to determine whether a putative ATP-sensitive K(+)-channel blocker, glibenclamide (Glb), prevents metabolic coronary vasodilation associated with increased myocardial oxygen consumption (MVO2) caused by beta 1-adrenoceptor stimulation in anesthetized open-chest dogs. Isoproterenol (Iso) was infused selectively into the left circumflex coronary artery before and after Glb. Coronary blood flow (CBF) by an electromagnetic flowmeter, regional myocardial function by sonomicrometers, and left ventricular and arterial pressures were continuously measured. An intracoronary infusion of Iso (10 ng.kg-1 x min-1) resulted in the sustained increase in CBF as well as in the myocardial inotropic and chronotropic state. Glb (10, 30, and 100 micrograms/min ic) attenuated the Iso-induced increase in CBF in a dose-dependent manner, whereas inotropic and chronotropic responses to Iso were not affected by Glb. After beta 1-blockade with bisoprolol (0.3 mg/kg), which completely inhibited inotropic and chronotropic responses to Iso, the Iso-induced increase in CBF, presumably mediated by vascular beta 2-receptor stimulation, was not affected by Glb. Intracoronary denopamine (0.1 microgram.kg-1 x min-1), a beta 1-selective agonist, increased CBF, which was almost completely abolished by Glb. The increases in MVO2 induced by Iso or denopamine were similar before and after Glb, indicating that attenuation of the Iso- or denopamine-induced increase in CBF by Glb did not result from the decrease in MVO2. These results indicate that Glb prevented the increase in CBF associated with increased MVO2 caused by beta 1-adrenoceptor stimulation. It is suggested that ATP-sensitive K+ channels may play an important role in metabolic coronary vasodilation in dogs.

scholarly journals Endothelial-derived hyperpolarization contributes to acetylcholine-mediated vasodilation in human skin in a dose-dependent manner

2015 ◽  
Vol 119 (9) ◽  
pp. 1015-1022 ◽  
Author(s):  
Vienna E. Brunt ◽  
Naoto Fujii ◽  
Christopher T. Minson
Keyword(s):  
Area Under The Curve ◽  
No Synthase ◽  
Dependent Manner ◽  
Cox Inhibitors ◽  
Relative Contribution ◽  
Calcium Activated Potassium Channel ◽  
Cutaneous Vascular Conductance ◽  
Dose Dependent ◽  
Infusion Protocol ◽  
Hyperemic Response

Cutaneous acetylcholine (ACh)-mediated dilation is commonly used to assess microvascular function, but the mechanisms of dilation are poorly understood. Depending on dose and method of administration, nitric oxide (NO) and prostanoids are involved to varying extents and the roles of endothelial-derived hyperpolarizing factors (EDHFs) are unclear. In the present study, five incremental doses of ACh (0.01-100 mM) were delivered either as a 1-min bolus ( protocol 1, n = 12) or as a ≥20-min continuous infusion ( protocol 2, n = 10) via microdialysis fibers infused with 1) lactated Ringer, 2) tetraethylammonium (TEA) [a calcium-activated potassium channel (KCa) and EDHF inhibitor], 3) L-NNA+ketorolac [NO synthase (NOS) and cyclooxygenase (COX) inhibitors], and 4) TEA+L-NNA+Ketorolac. The hyperemic response was characterized as peak and area under the curve (AUC) cutaneous vascular conductance (CVC) for bolus infusions or plateau CVC for continuous infusions, and reported as %maximal CVC. In protocol 1, TEA, alone and combined with NOS+COX inhibition, attenuated peak CVC (100 mM Ringer 59 ± 6% vs. TEA 43 ± 5%, P < 0.05; L-NNA+ketorolac 35 ± 4% vs. TEA+L-NNA+ketorolac 25 ± 4%, P < 0.05) and AUC (Ringer 25,414 ± 3,528 vs. TEA 21,403 ± 3,416%·s, P < 0.05; L-NNA+ketorolac 25,628 ± 3,828%.s vs. TEA+L-NNA+ketorolac 20,772 ± 3,711%·s, P < 0.05), although these effects were only significant at the highest dose of ACh. At lower doses, TEA lengthened the total time of the hyperemic response (10 mM Ringer 609 ± 78 s vs. TEA 860 ± 67 s, P < 0.05). In protocol 2, TEA alone did not affect plateau CVC, but attenuated plateau in combination with NOS+COX inhibition (100 mM 50.4 ± 6.6% vs. 30.9 ± 6.3%, P < 0.05). Therefore, EDHFs contribute to cutaneous ACh-mediated dilation, but their relative contribution is altered by the dose and infusion procedure.

Direct pituitary inhibition of prolactin secretion by dopamine and noradrenaline in sheep

1989 ◽  
Vol 123 (3) ◽  
pp. 393-402 ◽  
Author(s):  
G. B. Thomas ◽  
J. T. Cummins ◽  
B. W. Doughton ◽  
N. Griffin ◽  
G. A. Smythe ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Prolactin Secretion ◽  
Plasma Prolactin ◽  
Dependent Manner ◽  
Dopamine Receptor Antagonist ◽  
Peripheral Plasma ◽  
Series Of Experiments ◽  
Dose Dependent ◽  
Inhibitory Regulation ◽  
Sustained Increase

ABSTRACT The effects of dopamine, noradrenaline and 3,4-dihydroxyphenylacetic acid (DOPAC) on the release of prolactin were examined in ovariectomized ewes. Infusion of dopamine (0·5 or 1 μg/kg per min for 2 h i.v.) reduced plasma prolactin concentrations in a dose-dependent manner, whereas DOPAC (5 or 10 μg/kg per min for 2 h i.v.) had no effect. In a further series of experiments, ovariectomized hypothalamo-pituitary disconnected ewes were given dopamine or noradrenaline (each at 0·5 or 1 μg/kg per min for 2 h i.v.), and both amines reduced mean plasma concentrations of prolactin with similar potency in a dose-dependent manner. These effects were blocked by treatment with pimozide and prazosin respectively. During the infusion of dopamine, the peripheral plasma concentrations of DOPAC and 3,4-dihydroxyphenylethyleneglycol (DHPG) were increased (DOPAC, 22 ± 7 (s.e.m.) to 131 ± 11 nmol/l; DHPG, 2·9 ± 0·3 to 6·4 ± 0·2 nmol/l), but plasma concentrations of dopamine and noradrenaline did not change. Finally, administration of domperidone, a specific dopamine receptor antagonist that does not cross the blood-brain barrier, resulted in a sustained increase in plasma prolactin concentrations in ovariectomized ewes. We conclude that the secretion of prolactin from the pituitary gland is under dual inhibitory regulation by both dopamine and noradrenaline in the sheep. Journal of Endocrinology (1989) 123, 393–402

scholarly journals Biotransformation of Oral Dehydroepiandrosterone in Elderly Men: Significant Increase in Circulating Estrogens

1999 ◽  
Vol 84 (6) ◽  
pp. 2170-2176 ◽  
Author(s):  
Wiebke Arlt ◽  
Joachim Haas ◽  
Frank Callies ◽  
Martin Reincke ◽  
Doris Hübler ◽  
...  
Keyword(s):  
Area Under The Curve ◽  
Inverse Correlation ◽  
Serum Testosterone ◽  
Epidemiological Studies ◽  
Dependent Manner ◽  
Elderly Men ◽  
Beneficial Effects ◽  
Adult Men ◽  
17Β Estradiol ◽  
Dose Dependent

The most abundant human steroids, dehydroepiandrosterone (DHEA) and its sulfate ester DHEAS, may have a multitude of beneficial effects, but decline with age. DHEA possibly prevents immunosenescence, and as a neuroactive steroid it may influence processes of cognition and memory. Epidemiological studies revealed an inverse correlation between DHEAS levels and the incidence of cardiovascular disease in men, but not in women. To define a suitable dose for DHEA substitution in elderly men we studied pharmacokinetics and biotransformation of orally administered DHEA in 14 healthy male volunteers (mean age, 58.8 ± 5.1 yr; mean body mass index, 25.5 ± 1.5 kg/m2) with serum DHEAS concentrations below 4.1 μmol/L (1500 ng/mL). Diurnal blood sampling was performed on 3 occasions in a single dose, randomized, cross-over design (oral administration of placebo, 50 mg DHEA, or 100 mg DHEA). The intake of 50 mg DHEA led to an increase in serum DHEAS to mean levels of young adult men, whereas 100 mg DHEA induced supraphysiological concentrations [placebo vs. 50 mg DHEA vs. 100 mg DHEA; area under the curve (AUC) 0–12 h (mean ± sd) for DHEA, 108 ± 22 vs. 252 ± 45 vs. 349 ± 72 nmol/L·h; AUC 0–12 h for DHEAS, 33 ± 9 vs. 114 ±. 19 vs. 164± 36 μmol/L·h]. Serum testosterone and dihydrotestosterone remained unchanged after DHEA administration. In contrast, 17β-estradiol and estrone significantly increased in a dose-dependent manner to concentrations still within the upper normal range for men[ placebo vs. 50 mg DHEA vs. 100 mg DHEA; AUC 0–12 h for 17β-estradiol, 510 ± 198 vs. 635 ± 156 vs. 700 ± 209 pmol/L·h (P &lt; 0.0001); AUC 0–12 h for estrone, 1443 ± 269 vs. 2537 ± 434 vs. 3254 ± 671 pmol/L·h (P&lt; 0.0001)]. In conclusion, 50 mg DHEA seems to be a suitable substitution dose in elderly men, as it leads to serum DHEAS concentrations usually measured in young healthy adults. The DHEA-induced increase in circulating estrogens may contribute to beneficial effects of DHEA in men.

scholarly journals Acetyl-cholinesterase Inhibitory Activity of Methoxyflavones Isolated from Kaempferia parviflora

2017 ◽  
Vol 12 (1) ◽  
pp. 1934578X1701200
Author(s):  
Sang-Hwan Seo ◽  
Young-Choon Lee ◽  
Hyung-In Moon
Keyword(s):  
Spectral Analysis ◽  
Pc12 Cell ◽  
Acetylcholinesterase Activity ◽  
Distilled Water ◽  
Dependent Manner ◽  
Kaempferia Parviflora ◽  
Acetyl Cholinesterase ◽  
Pc12 Cell Line ◽  
Cholinesterase Inhibitory Activity ◽  
Dose Dependent

MeOH extracts of Kaempferia parviflora Wall. ex. Baker, family Zingiberaceae, were consecutively partitioned with CHCl3, EtOAc, and n-BuOH. The CHCl3 fractions were diluted in distilled water with n-hexane–CH2Cl2 and three methoxyflavones were isolated from the CH2Cl2 extract. Based on spectral analysis and comparison of the spectral data with literature values, the compounds were identified as 3,5,7,3′,4′-pentamethoxyflavone (KP1), 5,7-dimethoxyflavone (KP2), and 5,7,4′-trimethoxyflavone (KP3). In relation to their possible effectiveness against Alzheimer's disease, these compounds were tested for their ability to inhibit acetylcholinesterase activity and neurite outgrowth in the PC12 cell line. Of the three compounds, KP1 was the only one to inhibit significantly the acetylcholinesterase activity in a dose-dependent manner.

scholarly journals A Single Injection of Pegylated Murine Megakaryocyte Growth and Development Factor (MGDF ) Into Mice Is Sufficient to Produce a Profound Stimulation of Megakaryocyte Frequency, Size, and Ploidization

Blood ◽  
1997 ◽  
Vol 89 (3) ◽  
pp. 823-833 ◽  
Author(s):  
Julie T. Arnold ◽  
Najat C. Daw ◽  
Paula E. Stenberg ◽  
Deepthi Jayawardene ◽  
Deo Kumar Srivastava ◽  
...  
Keyword(s):  
Growth And Development ◽  
Single Injection ◽  
Membrane System ◽  
Dependent Manner ◽  
Development Factor ◽  
Typical Distribution ◽  
Kinetics Of ◽  
Dose Dependent ◽  
Sustained Increase

Abstract Despite numerous studies investigating the action of c-mpl ligand, no reports have defined the in vivo changes in megakaryocytopoiesis in response to a single injection of this cytokine. Here we compare the kinetics of the megakaryocytopoietic response in C57Bl/6J mice administered 25 μg/kg or 250 μg/kg of pegylated (PEG) murine megakaryocyte growth and development factor (MGDF ) as a single intravenous injection. Megakaryocytes of mice treated with MGDF had normal ultrastructure, showing a typical distribution of the demarcation membrane system, α-granules, and other cytoplasmic organelles. Megakaryocyte ploidy, size, and frequency were markedly increased with both MGDF doses. Megakaryocyte ploidy was maximally increased from a modal value of 16N to 64N on day 3, with both doses of MGDF. Similarly, a comparable increase in megakaryocyte size occurred in the two MGDF groups. Increased megakaryocyte size was coupled to the increase in megakaryocyte ploidy, and no evidence for independent regulation of megakaryocyte size within individual ploidy classes was apparent. In contrast to megakaryocyte ploidy and size, the increase in megakaryocyte frequency was markedly different with the two doses of MGDF. The proportion of 2N and 4N cells was increased from a baseline of 0.035% to 0.430% by day 4 in mice treated with the higher dose of MGDF, but only to 0.175% in mice administered 25 μg/kg of MGDF. The marked increase in the pool of these immature megakaryocytes translated to a sustained elevation in the frequency of polyploid megakaryocytes (8N cells and greater). In contrast to the sustained increase in the frequency of polyploid cells, the level of polyploidization was downregulated on days 6 to 10, but normalized by day 14. We conclude that a single injection of MGDF is able to expand the megakaryocytic pool in a dose-dependent manner, which, with subsequent maturation, should lead to an increased rate of platelet production.

Activation of 5-HT1A receptors attenuates tachycardia induced by restraint stress in rats

2008 ◽  
Vol 294 (1) ◽  
pp. R132-R141 ◽  
Author(s):  
Sukonthar Ngampramuan ◽  
Mathias Baumert ◽  
Mirza Irfan Beig ◽  
Naiphinich Kotchabhakdi ◽  
Eugene Nalivaiko
Keyword(s):  
Sympathetic Activity ◽  
Restraint Stress ◽  
Transient Increase ◽  
Dependent Manner ◽  
Initial Transient ◽  
Way 100635 ◽  
Medullary Raphe ◽  
Dose Dependent ◽  
Sustained Increase ◽  
Vagal Withdrawal

To better understand the central mechanisms that mediate increases in heart rate (HR) during psychological stress, we examined the effects of systemic and intramedullary (raphe region) administration of the serotonin-1A (5-HT1A) receptor agonist 8-hydroxy-2-(di- n-propylamino)tetraline (8-OH-DPAT) on cardiac changes elicited by restraint in hooded Wistar rats with preimplanted ECG telemetric transmitters. 8-OH-DPAT reduced basal HR from 356 ± 12 to 284 ± 12 beats/min, predominantly via a nonadrenergic, noncholinergic mechanism. Restraint stress caused tachycardia (an initial transient increase from 318 ± 3 to 492 ± 21 beats/min with a sustained component of 379 ± 12 beats/min). β-Adrenoreceptor blockade with atenolol suppressed the sustained component, whereas muscarinic blockade with methylscopolamine (50 μg/kg) abolished the initial transient increase, indicating that sympathetic activation and vagal withdrawal were responsible for the tachycardia. Systemic administration of 8-OH-DPAT (10, 30, and 100 μg/kg) attenuated stress-induced tachycardia in a dose-dependent manner, and this effect was suppressed by the 5-HT1A antagonist WAY-100635 (100 μg/kg). Given alone, the antagonist had no effect. Systemically injected 8-OH-DPAT (100 μg/kg) attenuated the sympathetically mediated sustained component (from +85 ± 19 to +32 ± 9 beats/min) and the vagally mediated transient (from +62 ± 5 to +25 ± 3 beats/min). Activation of 5-HT1A receptors in the medullary raphe by microinjection of 8-OH-DPAT mimicked the antitachycardic effect of the systemically administered drug but did not affect basal HR. We conclude that tachycardia induced by restraint stress is due to a sustained increase in cardiac sympathetic activity associated with a transient vagal withdrawal. Activation of central 5-HT1A receptors attenuates this tachycardia by suppressing autonomic effects. At least some of the relevant receptors are located in the medullary raphe-parapyramidal area.

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