Electron cyclotron emission spectra in X- and O-mode polarisation at JET: Martin-Puplett interferometer, absolute calibration, revised uncertainties, inboard/outboard temperature profile, and wall properties.

At the tokamak Joint European Torus (JET), the electron cyclotron emission spectra in O-mode and X-mode polarisations are diagnosed simultaneous in absolute terms for several harmonics with two Martin-Puplett interferometers. From the second harmonic range in X-mode polarisation, the electron temperature profile can be deduced for the outboard side (low magnetic field strength) of JET but only for some parts of the inboard side (high magnetic field strength). This spatial restriction can be bypassed, if a cutoff is not present inside the plasma for O-mode waves in the first harmonic range. Then, from this spectral domain, the profile on the entire inboard side is accessible. The profile determination relies on the new absolute and independent calibration for both interferometers. During the calibration procedure, the antenna pattern was investigated as well, and, potentially, an increase in the diagnostic responsivity of about 5% was found for the domain 100-300 GHz. This increase and other uncertainty sources are taken into account in the thorough revision of the uncertainty for the diagnostic absolute calibration. The uncertainty deduced and the convolution inherent for Fourier spectroscopy diagnostics have implications for the temperature profile inferred. Having probed the electron cyclotron emission spectra in orthogonal polarisation directions for the first harmonic range, a condition is derived for the reflection and polarisation-scrambling coefficients of the first wall on the outboard side of JET.

Influence of plasma diagnostics and constraints on the quality of equilibrium reconstructions on Joint European Torus.

One of the main approaches to thermonuclear fusion relies on confining high temperature plasmas with properly shaped magnetic fields. The determination of the magnetic topology is, therefore, essential for controlling the experiments and for achieving the required performance. In Tokamaks, the reconstruction of the fields is typically formulated as a free boundary equilibrium problem, described by the Grad-Shafranov equation in toroidal geometry and axisymmetric configurations. Unfortunately, this results in mathematically very ill posed problems and, therefore, the quality of the equilibrium reconstructions depends sensitively on the measurements used as inputs and on the imposed constraints. In this paper, it is shown how the different diagnostics (Magnetics Measurements, Polarimetry and Motional Stark Effect), together with the edge current density and plasma pressure constraints, can have a significant impact on the quality of the equilibrium on JET. Results show that both the Polarimetry and Motional Stark Effect internal diagnostics are crucial in order to obtain reasonable safety factor profiles. The impact of the edge current density constraint is significant when the plasma is in the H-mode of confinement. In this plasma scenario the strike point positions and the plasma last closed flux surface can change even by centimetres, depending on the edge constraints, with a significant impact on the remapping of the equilibrium-dependent diagnostics and of pedestal physics studies. On the other hand and quite counter intuitively, the pressure constraint can severely affect the quality of the magnetic reconstructions in the core. These trends have been verified with several JET discharges and consistent results have been found. An interpretation of these results, as interplay between degrees of freedom and available measurements, is provided. The systematic analysis described in the paper emphasizes the importance of having sufficient diagnostic inputs and of properly validating the results of the codes with independent measurements.

Electron cyclotron emission measurements on JET: Michelson interferometer, new absolute calibration, and determination of electron temperature.

At the fusion experiment JET, a Michelson interferometer is used to measure the spectrum of the electron cyclotron emission in the spectral range 70-500 GHz. The interferometer is absolutely calibrated using the hot/cold technique and, in consequence, the spatial profile of the plasma electron temperature is determined from the measurements. The current state of the interferometer hardware, the calibration setup, and the analysis technique for calibration and plasma operation are described. A new, full-system, absolute calibration employing continuous data acquisition has been performed recently and the calibration method and results are presented. The noise level in the measurement is very low and as a result the electron cyclotron emission spectrum and thus the spatial profile of the electron temperature are determined to within ±5% and in the most relevant region to within ±2%. The new calibration shows that the absolute response of the system has decreased by about 15% compared to that measured previously and possible reasons for this change are presented. Temperature profiles measured with the Michelson interferometer are compared with profiles measured independently using Thomson scattering diagnostics, which have also been recently refurbished and recalibrated, and agreement within experimental uncertainties is obtained.

Human cardiac beta1- or beta2-adrenergic receptor stimulation and the negative chronotropic effect of low-dose pirenzepine.

OBJECTIVES: The M1-muscarinic receptor antagonist pirenzepine in low doses (<1 mg intravenously) decreases heart rate. We investigated whether these effects of pirenzepine differ in volunteers with activated cardiac beta1-adrenergic receptors versus activated cardiac beta2-adrenergic receptors. METHODS: In 17 male volunteers (25 +/- 1 years) we studied effects of pirenzepine infusion (0.5 mg intravenous bolus followed by continuous infusion of 0.15 microg/kg/min) on heart rate and heart rate-corrected duration of electromechanical systole (QS2c, as a measure of inotropism) that had been stimulated by activation of cardiac beta1-adrenergic receptors (bicycle exercise in the supine position for 60 minutes at 25 W) or cardiac beta2-adrenergic receptors (continuous intravenous infusion of 100 ng/kg/min terbutaline). RESULTS: Bicycle exercise and terbutaline infusion significantly increased heart rate and shortened QS2c. When pirenzepine was infused 20 minutes after the beginning of the exercise or terbutaline infusion, heart rate decreased in both settings by approximately the same extent (approximately -10 to -14 beats/min), although exercise and terbutaline infusion continued; however, QS2c was not affected. Pirenzepine (0.05 to 1 mg intravenous bolus)-induced decrease in heart rate was abolished after 6 days of transdermal scopolamine treatment of volunteers. CONCLUSIONS: Low-dose pirenzepine decreased heart rate by muscarinic receptor stimulation, because this was blocked by scopolamine. Moreover, low-dose pirenzepine did not differentiate between cardiac beta1- or beta2-adrenergic receptor stimulation; however, low-dose pirenzepine did not affect cardiac contractility as measured by QS2c. Low-dose pirenzepine therefore exerted a unique pattern of action in the human heart: it decreased heart rate (basal and beta1- and/or beta2-adrenergic receptor-stimulated) without affecting contractility.

Cardiac effects of beta-adrenoceptor antagonists with intrinsic sympathomimetic activity in humans: beta1- and/or beta2-adrenoceptor mediated?

The aim of this study was to find out whether cardiac responses to the beta-adrenoceptor antagonists with intrinsic sympathomimetic activity (ISA) xamoterol and celiprolol are mediated by cardiac beta1- or beta2-adrenoceptors or both. For this purpose we assessed, in six healthy male volunteers, the effects of xamoterol (100 and 200 mg, p.o.) and celiprolol (200, 600, and 1,200 mg, p.o.) on blood pressure, heart rate, and heart rate-corrected duration of the electromechanical systole (QS2c, as a measure of inotropism). Xamoterol, in both doses, increased systolic blood pressure and heart rate, transiently decreased diastolic blood pressure, and shortened QS2c; all these effects were attenuated after pretreatment of the volunteers with the beta1-adrenoceptor antagonist bisoprolol. Celiprolol, in all three doses, increased heart rate, decreased diastolic blood pressure, and shortened QS2c but only marginally increased systolic blood pressure. Bisoprolol did not attenuate these celiprolol effects but rather enhanced celiprolol effects on systolic blood pressure and heart rate. In a further set of experiments, we studied cardiovascular effects of celiprolol in six healthy volunteers whose beta2-adrenoceptors had been desensitized by a 2-week treatment with 3x5 mg/day terbutaline. Under these conditions, celiprolol failed to increase heart rate or to shorten QS2c. We conclude that, under resting conditions, in healthy volunteers, beta-adrenoceptor antagonists with ISA can exert increases in heart rate and contractility that are mediated by either cardiac beta1-adrenoceptor (xamoterol) or cardiac beta2-adrenoceptor (celiprolol) stimulation. Thus in the human heart, the ISA of beta-adrenoceptor antagonists can be a beta1- or beta2-adrenoceptor agonistic component.

Influence of atropine on the cardiovascular effects of noradrenaline and tyramine in elder volunteers.

The aim of this study, carried out in six elder healthy volunteers (mean age: 61 years), was to determine the influence of muscarinic receptor blockade with atropine (15 microg/kg i.v. loading dose followed by 0.15 microg/kg/min by i.v. infusion) on the effects of i.v. infusions of noradrenaline (5 incremental doses of 10-120 ng/kg/min) or tyramine, that releases endogenous noradrenaline (4 incremental doses of 5-20 microg/kg/min), on blood pressure, heart rate and systolic time intervals (STI's, as a measure of positive inotropism). These results were compared with those recently published for young healthy volunteers (mean age: 26 years; Schäfers et al. 1997). Noradrenaline caused increases in systolic and diastolic blood pressure, decreases in heart rate and a shortening of STI's that were not different from those in young volunteers. Atropine did not significantly affect these hemodynamic responses to noradrenaline, while in young volunteers it significantly enhanced noradrenaline-induced blood pressure increases and converted the heart rate decrease into an increase. In the present study in elder volunteers, tyramine caused a smaller increase in systolic blood pressure than in the previous study in young volunteers; in addition, it slightly increased diastolic blood pressure while it decreased diastolic blood pressure in young volunteers. Atropine did not significantly affect the hemodynamic effects of tyramine in the elder volunteers, while in the young volunteers it enhanced the increase in systolic blood pressure and converted the decreases in diastolic blood pressure and heart rate into increases. These results indicate a) that ageing is accompanied by a blunted baroreflex-mediated parasympathetic activation resulting in reduced cholinergic vasodilation and decreases in heart rate, and b) that ageing is associated with a decreased responsiveness of (cardiac) beta-adrenoceptors and (vascular) alpha1-adrenoceptors which is only unmasked when the counterregulatory action of parasympathetic activation is removed.