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Plasma Flow (plasma + flow)

Distribution by Scientific Domains
Medical Sciences71%

Kinds of Plasma Flow

  • renal plasma flow
    		•

    Selected Abstracts

    Mach Probe Measurements in Unmagnetized Plasmas with Subsonicand Supersonic Flow

    CONTRIBUTIONS TO PLASMA PHYSICS, Issue 5-6 2006
    A. Ando
    Abstract Characteristics of an up-down type Mach probe are investigated by using a directional Langmuir probe (DLP) in unmagnetized plasmas with subsonic and supersonic flow produced by a magneto-plasma-dynamic arcjet (MPDA). The ion acoustic Mach number Mi is derived from plasma flow velocity Up and ion temperature Ti measured by spectroscopy and electron temperature Te by Langmuir probe. The obtained values of Mi are compared to the DLP data in various conditions of plasma flow and the coefficient of Mc in the Mach probe formula,Mi = Mc ln(Jup/Jdown ) , is evaluated. The obtained data are also compared with Hutchinson's PIC simulation results in an unmagnetized plasma and are in good agreement with each other. The dependence of ln(Jup/Jdown ) on cos, can be expressed as a quadratic function under subsonic (Mi < 1) and supersonic (Mi > 1) flow, so that the up-down type Mach probe can detect the components of plasma flow vector even when the probe collection surface inclines to plasma flow direction. (© 2006 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source]

    Comparative Study of Flat and Round Collectors Using a Validated 1D Fluid Probe Model

    CONTRIBUTIONS TO PLASMA PHYSICS, Issue 5-6 2006
    P. Peleman
    Abstract In the literature two different types of Gundestrup-like probe designs are proposed: design with flat and with round collectors. In this paper we study the influence of different collector shapes of Gundestrup-like probes on the accuracy of the measurement of the parallel and perpendicular flows. A one dimensional fluid probe model is used for deducing both Mach numbers of the unperturbed flow from the probe data. An analytical expression relates the plasma flow to the measured ion saturation currents collected at the upstream and downstream collecting surfaces of the probe. For flat collectors, the analytical model is validated by comparing it to a two dimensional quasi-neutral Particle In Cell (PIC) simulation code. An extension of the theoretical model then allows us to study round collectors. We performed an accuracy study which showed that systematic errors are introduced when round collectors are employed for determination of the perpendicular flow which is systematically overestimated. The error can reach more than 70% when the perpendicular flow increases and when the angle of the collecting surface with respect to the magnetic field (, , 0)is small. The correct analytical expression is applied to experimental data from Gundestrup probe measurements with round collectors on the CASTOR tokamak. The analysis shows that for these measurements the error introduced by using the expression for flat collectors remains negligible, supporting our former use of the model for flat collectors. A new advanced Gundestrup-like probe design and the motivation for the choice of flat collectors are presented. (© 2006 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source]

    Losartan modifies glomerular hyperfiltration and insulin sensitivity in type 1 diabetes

    DIABETES OBESITY & METABOLISM, Issue 6 2001
    S. Nielsen
    Aim: The effect of the angiotensin II receptor antagonist losartan on renal haemodynamics and insulin-mediated glucose disposal was examined in normotensive, normoalbuminuric type 1 diabetic patients using a double-blind, placebo-controlled, cross-over design. Methods: Diurnal blood pressure, glomerular filtration rate (GFR, determined using [125I]-iothalamate), renal plasma flow (RPF, determined using [131I]-hippuran) and urinary albumin excretion rate (UAE) were measured, and a hyperinsulinaemic, euglycaemic clamp with indirect calorimetry was performed in nine patients (age 30 ± 7 years (mean ±,s.d.), HbA1c 8.1 ± 1.1%) following 6 weeks' administration of either losartan 50 mg/day or placebo. Results: Diurnal blood pressure was significantly reduced after losartan compared with placebo (122/70 ± 11/8 vs. 130/76 ± 12/6 mmHg, p <,0.05). A significant decline in GFR (133 ± 23 vs. 140 ± 22 ml/min, p < 0.05) and filtration fraction (FF; GFR/RPF) (24.6 ± 3.5 vs. 26.2 ± 3.6%, p <,0.05) was observed in the losartan vs. placebo groups. RPF and UAE did not change. Isotopically determined glucose disposal rates were similar after losartan and placebo in the basal (2.61 ± 0.53 vs. 2.98 ± 0.93 mg/kg/min) and insulin-stimulated states (6.84 ± 2.52 vs. 6.97 ± 3.11 mg/kg/min). However, the glucose oxidation rate increased significantly after losartan vs. placebo in the basal state (1.72 ± 0.34 vs. 1.33 ± 0.18, mg/kg/min, p <,0.01) and during insulin stimulation (2.89 ± 0.75 vs. 2.40 ± 0.62 mg/kg/min, p <,0.03). Basal and insulin-stimulated non-oxidative glucose disposal tended to decrease after losartan; however, this was not significant. Endogenous glucose production and lipid oxidation were unchanged after treatment and similarly suppressed during hyperinsulinaemia. Glycaemic control, total cholesterol, high-density lipoprotein (HDL)-cholesterol and triglycerides were stable in both losartan and placebo groups. Conclusions: Losartan reduces blood pressure, glomerular hyperfiltration and FF, and improves basal and insulin-stimulated glucose oxidation in normotensive, normoalbuminuric type 1 diabetic patients. [source]

    Reduced plasma total homocysteine concentrations in Type 1 diabetes mellitus is determined by increased renal clearance

    DIABETIC MEDICINE, Issue 3 2005
    B. A. J. Veldman
    Abstract Introduction Elevated plasma levels of total homocysteine are related to the development of vascular complications. Patients with diabetes mellitus are particularly at risk for the development of these complications. Several factors determine plasma total homocysteine including renal function. Aims As early Type 1 diabetes is characterized by a relative glomerular hyperfiltration, increased renal clearance could contribute to decreased levels of homocysteine as observed in Type 1 diabetes mellitus. Therefore we investigated the relationship between plasma total homocysteine and the glomerular filtration rate (GFR). Methods In 92 Type 1 diabetes patients and 44 control subjects, we measured GFR and effective renal plasma flow (ERPF) by means of continuous infusion of inulin and p-aminohippurate. Fasting plasma total homocysteine was measured using high performance liquid chromatography. Results GFR (121 ± 21 resp. 104 ± 14 ml/min; P < 0.001) and ERPF (563 ± 127 resp. 516 ± 121 ml/min; P = 0.05) were significantly higher in Type 1 diabetes patients as compared with control subjects. Plasma total homocysteine was reduced in Type 1 diabetes patients as compared with control subjects (11.0 ± 4.5 resp. 13.4 ± 7 µmol/l; P = 0.01). Plasma total homocysteine was strongly correlated with GFR (Type 1 diabetes patients: r = ,0.43, P < 0.001; control subjects: r = ,0.39, P = 0.01). Conclusion GFR is a major determinant of plasma total homocysteine levels in Type 1 diabetes patients as well as control subjects. The reduced plasma total homocysteine levels in diabetes patients can be explained by an increased GFR. [source]

    Type 2 diabetes, obesity, and the renal response to blocking the renin system with irbesartan

    DIABETIC MEDICINE, Issue 10 2002
    D. A. Price
    Abstract Aim Our recent studies revealed a striking but variable enhancement of renal vasodilator responses to blockers of the renin-angiotensin system in subjects with diabetes mellitus, possibly reflecting the level of intrarenal activation of the renin-angiotensin system, and thus a risk of nephropathy. As obesity is a common finding in diabetic individuals, and obesity has been linked to an increase in plasma angiotensinogen levels, we enrolled diabetic subjects with a wide range of body mass index (BMI) for this study. Methods Twelve Type 2 diabetic subjects in balance on a low sodium diet participated after baseline renal plasma flow and glomerular filtration measurements were made. Each subject then received 150 mg irbesartan, and renal function was measured every 45 min for 4 h. Results The average vasodilator response to irbesartan was 174 ± 33 ml/min. No correlation was found between renal plasma flow response to irbesartan and duration of diabetes, baseline glucose, or HbA1c level. BMI, our measure of obesity, was highly correlated to the renal response to irbesartan (r = 0.7; P = 0.01). Conclusions Our findings suggest an important role for obesity in activating the intrarenal renin system, perhaps via production of angiotensinogen. BMI may be an indicator of risk of nephropathy. [source]

    Lack of renal improvement with nonselective endothelin antagonism with tezosentan in type 2 hepatorenal syndrome,,

    HEPATOLOGY, Issue 1 2008
    Florence Wong
    Renal vasoconstriction is a key factor in the development of hepatorenal syndrome (HRS) and may be secondary to increased activities of endothelin-1, a potent renal vasoconstrictor. To assess the effects of tezosentan, a nonselective endothelin receptor antagonist, on renal function in patients with type 2 HRS, six male patients, 56.3 ± 2.5 years old, with cirrhosis and type 2 HRS were treated with tezosentan; ascending doses of 0.3, 1.0, and 3.0 mg/hour, each for 24 hours, were used for the initial 2 patients, but a constant dose of 0.3 mg/hour for up to 7 days was used for the remaining 4 patients. The glomerular filtration rate, renal plasma flow, 24-hour urinary volume, mean arterial pressure (MAP), heart rate, tezosentan levels, and vasoactive hormones were measured daily. Albumin was given as required. The study was stopped early because of concerns about the safety of tezosentan in type 2 HRS. Five patients discontinued the study early; one stopped within 4 hours because of systemic hypotension (MAP < 70 mm Hg), and 4 patients stopped at ,4 days because of concerns about worsening renal function (serum creatinine increased from 180 ± 21 to 222 ± 58 ,mol/L, P > 0.05) and decreasing urine volume (P = 0.03) but without a significant change in MAP. The plasma tezosentan concentrations were 79 ± 34 ng/mL at a steady state during infusion at 0.3 mg/hour. The plasma endothelin-1 concentrations increased from 2.7 ± 0.3 pg/mL at the baseline to 19.1 ± 7.3 pg/mL (P < 0.05). Conclusion: An endothelin receptor blockade potentially can cause a deterioration in renal function in patients with cirrhosis and type 2 HRS. Caution should be taken in future studies using endothelin receptor antagonists in these patients. (HEPATOLOGY 2007.) [source]

    Contribution of Gastric Oxidation to Ethanol First Pass Metabolism in Baboons

    ALCOHOLISM, Issue 7 2000
    Enrique Baraona
    Background: A portion of ingested alcohol does not reach the systemic blood, undergoing a first-pass metabolism (FPM) during gastric and hepatic circulation. Methods: To determine whether the stomach can metabolize sufficient ethanol to account for the FPM, and to what extent gastric alcohol dehydrogenase (ADH) activity is responsible, the hepatic vein, the portal vein, and the aorta were cannulated nonocclusively in baboons to measure the conversion of ethanol to acetate in vivo. 14C-ethanol (300 mg/kg as a 15% solution) was given intragastrically (IG) whereas 3Hacetate was continuously infused intravenously (IV).14C-acetate was measured after exhaustive evaporation of ethanol. Simultaneous sampling of hepaticvenous, portal and arterial blood was carried out for 3 hr, at the end of which the same alcohol dose was given IV to calculate the Michaelis-Menten parameters of elimination. Results: Analysis of the IV and IG ethanol curves revealed a FPM of 94 ± 11 mg/kg (31% of dose). The portal-arterial differences were negative for 3H-acetate (indicating net extraction) and positive for 14Cethanol and 14C-acetate (indicating net output). Portal acetate production (extraction plus net output multiplied by the portal plasma flow) increased with time and accounted, over the first 3 hr (82 ± 13 mg/kg), for 87% of the FPM. Alcohol oxidation by gastric ADH activity (28.7 ± 7.2 mg/kg) accounted for only 31% of the FPM. Conclusions: The in vivo oxidation of ethanol to acetate in the upper digestive tract accounts for the FPM of ethanol and is mediated, at least in part, by ADH activity. [source]