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Biomedical subjects

J Dempster

Publications and source records attributed to J Dempster.

28 records · Page 2Linked to original sources
PubMed1987

The effect of fetal heart rate on umbilical artery flow velocity waveforms.

Umbilical artery flow velocity waveforms were obtained using continuous wave Doppler ultrasound in 85 normal pregnancies (25 antepartum, 60 intrapartum) to examine the relation between fetal heart rate, end systolic/end diastolic ratio (A/B ratio) and resistance index (RI). Our results demonstrated a significant negative correlation between fetal heart rate, A/B ratio and RI (in the antepartum group r = -0.49, and in the labouring group r = -0.65). It is therefore important when performing mathematical analysis of umbilical artery flow velocity profiles to make a statistical allowance for fetal heart rate.

Blood Flow Velocity↗
PubMed1987

A kinetic analysis of the endplate ion channel blocking action of disopyramide and its optical isomers.

The effects of the antiarrhythmic agent disopyramide was studied on responses from voltage-clamped endplates at the neuromuscular junction of the garter snake. Disopyramide reduced endplate current amplitude and decay time constant in a concentration- and voltage-dependent manner. Endplate current decays remained monophasic in the presence of the drug. These results were interpreted in terms of the drug blocking the open form of the acetylcholine receptor-ion channel complex. Disopyramide produced a greater reduction of the amplitude of endplate currents than of miniature endplate currents. The reduction in miniature endplate current amplitude was not voltage-dependent. Analysis of endplate current driving functions showed that this was due to the rapid occurrence of channel block during the rising phase of the endplate current. The residual reduction, apart from that produced by channel block, is most probably due to receptor block. Disopyramide had a voltage-dependent blocking rate constant of about 10(7) M-1 S-1 at -90 mV. The unblocking rate constant was estimated from the results of experiments using paired ionophoretically applied pulses of acetylcholine. This value was again voltage-dependent and approximately 1 s-1. The actions of the (+)- and (-)-stereoisomers of disopyramide on endplate current decay were identical, indicating that the channel binding site at the neuromuscular junction is not stereoselective.

Acetylcholine↗
PubMed1987

Survival after ovarian granulosa and theca cell tumours.

Ninety-two cases of ovarian granulosa and theca cell tumours were recorded in the Tayside Gynaecological Tumour Registry during the 30 year period 1948-78. A high follow-up rate was achieved through this centralised registry and exhaustive annual recall. At 20 years after initial treatment patient actuarial survival was 92% for the theca cell tumours and 34% for granulosa cell tumours.

Adult↗
PubMed1986

The use of the driving function in the analysis of endplate current kinetics.

The time course of transmitter release at the neuromuscular junction is non-instantaneous and is more prolonged for nerve-evoked endplate currents (EPCs) than for miniature endplate currents (MEPCs). This creates difficulties in the interpretation of the effects of ion channel blocking drugs which greatly increase the rate of EPC decay, resulting in a substantial number of channels being blocked during the EPC rising phase. Apparent changes in peak current and in the EPC/MEPC peak current ratio can be erroneously interpreted as receptor block or effects on quantal content. A method is described for a more precise assessment of receptor block or quantal content in the presence of ion channel block, by calculation of the EPC driving function. The driving function is a measure of the rate of opening of the ion channels in response to transmitter release, and is independent of ion channel block effects. Simulated EPCs with the same decay rate can be created from the driving functions of EPCs in control and in the presence of the drug. The peak current of such EPCs can be compared to reveal any additional receptor block or quantal content effects independent of a drug's ion channel blocking effects.

Animals↗
PubMed1986

The effects of chloramphenicol isomers on the motor end-plate nicotinic receptor-ion channel complex.

Four enantiomers of chloramphenicol have been tested for their effects on end-plate current and miniature end-plate current decay and amplitude characteristics in the voltage-clamped costocutaneous nerve-muscle preparation of the garter snake. All four enantiomers exhibited effects on end-plate current and miniature end-plate current decay at similar concentrations (0.2-1.0 mM), indicating that the measured effect was not related to the antibacterial action of the compounds in which D-threo chloramphenicol is known to be at least 50 times more powerful than the L-threo and D- and L-erythro isomers. The compounds slightly increased end-plate current but not miniature end-plate current amplitude, indicating that they produce an increase in end-plate current quantal content. This effect was verified by an analysis of end-plate current driving functions (see Appendix) for one of the chloramphenicol isomers. In addition to this presynaptic action, all four compounds converted end-plate current and miniature end-plate current decays from single to double exponential functions. This effect was both concentration and voltage dependent. For all four compounds, hyperpolarization resulted in a progressive decrease in tau f and an increase in tau s. The relative amplitudes of the fast and slow decay components were independent of membrane potential. The results are interpreted in terms of the drugs blocking the open form of the acetylcholine-activated receptor-ion channel complex. However, in addition to affecting decay characteristics, all four compounds increased the charge passed during both end-plate and miniature end-plate currents. This effect was concentration but not voltage dependent and is inconsistent with the predictions of the sequential model for open ion channel blockade. By using an extension of Ruff's analysis of the sequential model of open end-plate ion channel blockade, we have been able to show that the action of the chloramphenicols on end-plate current amplitude and time course can be explained by the combination of two distinct mechanisms. First is an open channel block conforming to the sequential model and with calculated channel blocking affinity constants ranging from 0.3-1.0 mM. The channel blocking actions of all four isomers were shown to be independent of membrane voltage. Second is an action to slow channel closing, resulting in prolonged open time and hence increased charge passed during the end-plate current. This effect was strongly concentration dependent, but not voltage dependent.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Inward rectifier current noise in frog skeletal muscle.

Inwardly rectifying K+ currents were studied in cut muscle fibres from frogs using the Vaseline-gap voltage-clamp method. Both faces of the membrane were exposed to 120 mM-K+ methylsulphate solution. At small negative potentials, -10 and -21 mV, the current noise spectrum, after subtraction of a control spectrum at the zero current potential, could be fitted by a Lorentzian spectral component, usually with an additional 1/f component, where f is the frequency. At more negative potentials the 1/f component predominated. The zero frequency amplitude of the Lorentzian averaged 2.6 X 10(-24) A2 Hz-1 at -10 mV and 4.6 X 10(-24) A2 Hz-1 at -21 mV, with a mean half-power frequency, fc, of 34 Hz and 45 Hz, respectively. The time constant of the K+ current activation upon hyperpolarization agrees with that calculated from fc, and the Lorentzian disappears upon replacement of external K+ by tetraethylammonium (TEA+) or Rb+. Thus, the Lorentzian component appears to be ascribable to fluctuations originating in the inwardly rectifying mechanism. The noise spectra and macroscopic currents were interpreted by assuming that the inwardly rectifying K+ conductance is proportional to the product of two parameters: ps representing the state of the mechanism that gives rise to the observable macroscopic current relaxations and to the current fluctuations resulting in the observed Lorentzian spectra, and pf describing the instantaneous rectification of the single-channel conductance. Alternatively, pf may represent another mechanism in series with ps, but which fluctuates too rapidly to measure. Using this model the limiting single-channel conductance, gamma, was found to be approximately 9 pS. The corresponding specific density of channels is about 1 micron-2, assuming uniform distribution over all regions of the membrane. A preliminary value for gamma ( DeCoursey & Hutter , 1982) was derived without consideration of instantaneous rectification. Systematic errors in these results due to voltage decrement in the T-tubules are evaluated in an Appendix, and are found to be tolerably small in the voltage range studied.

Animals↗
PubMedDate not supplied

Epidural analgesia and its effect on umbilical artery flow velocity waveform patterns in uncomplicated labour and labour complicated by pregnancy-induced hypertension.

Umbilical artery flow velocity waveforms were obtained using continuous-wave Doppler ultrasound to examine the effect of epidural analgesia on peak systolic/least diastolic ratio (A/B ratio) in 38 women in uncomplicated labour, and 12 women with pregnancy-induced hypertension (PIH). In the uncomplicated group there was no significant change in A/B ratio after epidural analgesia, but in the PIH group there was significant correlation between the fall in mean blood pressure and the fall in A/B ratio at 30 min after induction of epidural analgesia (r = 0.85, p less than 0.001). This suggests that epidural analgesia in PIH is associated with a reduction in placental resistance and may be beneficial to the fetus.

Analgesia, Epidural↗