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Biomedical subjects

J M Elliott

Publications and source records attributed to J M Elliott.

At least 91 records · Page 5Linked to original sources
PubMed1987

Treatment of hypertension with enalapril and hydrochlorothiazide or enalapril and atenolol: contrasts in hypotensive interactions.

To determine the nature of the resultant effect on blood pressure when angiotensin converting enzyme (ACE) inhibitors are combined with other hypotensive agents in the treatment of uncomplicated essential hypertension, two randomized, double-blind, crossover trials were conducted. In each trial there were four treatment phases, each 4 weeks in duration, comprising a 2 X 2 factorial experiment. Twenty-one patients completed the first study in which the effects of enalapril (10 mg twice daily) were compared with hydrochlorothiazide (25 mg twice daily), with the two drugs in combination and with placebo. All blood pressure parameters were reduced in the three active treatment phases compared with placebo (P less than 0.001). Enalapril and hydrochlorothiazide were equally effective and in combination their hypotensive effects were fully additive. Sixteen patients completed the second study which compared the effects of enalapril (20 mg daily), atenolol (50 mg daily), the two drugs in combination and placebo. All blood pressure parameters were again reduced in all phases compared with placebo (P less than 0.001). Enalapril and atenolol were also equally effective, but in combination their hypotensive effects were less than fully additive, with attenuation of the potential additive response by 30-50%. These results indicate that a diuretic-ACE inhibitor combination can be expected to have a greater hypotensive effect than a beta-blocker-ACE inhibitor combination. Both hydrochlorothiazide and atenolol increased plasma atrial natriuretic peptide (ANP) concentrations (P less than 0.01), suggesting that ANP could contribute to the hypotensive effects of these two drug classes.

Angiotensin II↗
PubMed1986

Desipramine treatment in normal subjects. Effects on neuroendocrine responses to tryptophan and on platelet serotonin (5-HT)-related receptors.

Normal subjects took the tricyclic antidepressant, desipramine hydrochloride, for 16 days. Following treatment there was an increase in the number of specific binding sites on the platelet for both tritiated imipramine and tritiated LSD, the latter site probably representing a platelet serotonin (5-HT) receptor. During desipramine treatment the prolactin response to tryptophan (L-tryptophan) was enhanced, and this enhancement correlated with the increase in platelet LSD binding. The results confirm previous observations that desipramine administration increases certain 5-HT-mediated neuroendocrine responses. Our findings further indicate that desipramine may alter both 5-HT uptake and 5-HT receptor sensitivity, and suggest that the platelet LSD receptor may in certain conditions provide a useful model of 5-HT receptors in the brain.

Adult↗
PubMed1986

Increases in plasma neuropeptide Y concentrations during sympathetic activation in man.

Neuropeptide Y (NPY) coexists with noradrenaline in postganglionic sympathetic neurons. In order to test the hypothesis that NPY may be released along with catecholamines by activation of the sympathoadrenal system we measured plasma NPY-like immunoreactivity (NPY-LI) concentrations during cold pressor test, head up tilt and bicycle exercise in healthy volunteers. All 3 manoeuvres resulted in elevation of blood pressure, heart rate and plasma noradrenaline and adrenaline concentrations. These were accompanied by increases in plasma NPY-LI concentrations on cold pressor test and exercise, but not with head up tilt. The increases in both NPY-LI and catecholamines were greatest with exercise. These findings suggest that NPY is released at the same time as noradrenaline when sympathetic noradrenergic nerves are activated.

Adult↗
PubMed1986

Binding of yohimbine and imipramine to platelets in depressive illness.

Radioligand binding to intact platelets was carried out in antidepressant-free patients and the 1 mg dexamethasone suppression test (DST) was performed. There were no differences in binding characteristics between patients and controls for either [3H]yohimbine or [3H]imipramine. There were no differences in binding between patients classified as endogenous using the Newcastle Scale, compared with non-endogenous patients, and no difference between DST suppressors and non-suppressors. The severity of depression did not affect binding values. After 4-6 weeks antidepressant treatment [3H]yohimbine binding was significantly reduced but [3H]imipramine binding was unaffected.

Adult↗
PubMed1986

Plasma neuropeptide y levels rise in patients undergoing exercise tests for the investigation of chest pain.

Neuropeptide Y (NPY) is colocalised with noradrenaline in post-ganglionic sympathetic neurons. In order to examine the possibility that activation of the sympathetic nervous system might cause release of NPY into the plasma NPY levels were measured in 16 patients undergoing exercise tests for investigation of chest pain. Plasma NPY concentrations rose in 14 out of the 16 patients, and the mean level of plasma NPY increased from 335 (s.e.m. = 37) to 455 (s.e.m. = 41) pg/ml. Plasma noradrenaline and adrenaline levels increased four- and two-fold respectively. The increase in NPY correlated with the increase in noradrenaline, suggesting that NPY may be released with noradrenaline when sympathetic noradrenergic nerves are activated.

Adult↗
PubMed1986

Effects of enalapril and hydrochlorothiazide on blood pressure, renin-angiotensin system, and atrial natriuretic factor in essential hypertension: a double blind factorial cross-over study.

The hypotensive and hormonal effects of the angiotensin converting enzyme (ACE) inhibitor enalapril (10 mg twice daily) were compared with those of hydrochlorothiazide (25 mg twice daily), with the two drugs in combination and with placebo in 21 patients with essential hypertension. For each patient there were four randomised double-blind treatment phases, each of four weeks' duration, which comprised a 2 X 2 factorial experiment. All blood pressure parameters were reduced in the three active treatment phases compared to placebo (p less than 0.001). Supine mean blood pressures were 119 mmHg (placebo), 113 mmHg (hydrochlorothiazide), 108 mmHg (enalapril), and 98 mmHg (hydrochlorothiazide plus enalapril) (SEM 3 mmHg, ANOVA). Enalapril and hydrochlorothiazide were equally effective and well tolerated and their hypotensive effects were additive. Enalapril increased plasma renin activity (PRA), reduced plasma angiotensin II (AII) and aldosterone concentrations, and reduced ACE activity, whereas hydrochlorothiazide increased PRA, plasma AII, and aldosterone concentrations without altering ACE activity. With combination treatment the effects of enalapril on PRA and plasma AII concentrations were potentiated whereas those on plasma aldosterone concentration and ACE activity were additive. Atrial natriuretic factor plasma concentration in the placebo phase was 92 pg/ml and increased to 145 pg/ml in the hydrochlorothiazide phase (p less than 0.001, SEM 13 pg/ml), but there was no significant change in either the enalapril or combination phases.

Aged↗
PubMed1986

Measurement of kinaesthetic sensitivity.

Two recent papers (Laszlo and Bairstow 1980, Bairstow and Laszlo 1981) have used the method of constant stimuli to measure kinaesthetic difference thresholds. If this method is used, however, certain constraints must be observed: these concern the values of the stimuli relative to the threshold, and the numbers of observations made at each value. Laszlo and Bairstow appear to have neglected these constraints, which must cast doubt on their results. In any case, the method of constant stimuli has largely been superseded by staircase techniques for threshold estimation, on grounds of economy of trials for a given level of accuracy in estimation. It is concluded, therefore, that the details of the method as described by Laszlo and Bairstow are unsuitable for testing kinaesthetic sensitivity, and that other methods are preferable.

Humans↗
PubMed1985

Increased platelet membrane [3H]-LSD binding in patients on chronic neuroleptic treatment.

Using a [3H]-lysergic acid diethylamide [( 3H]-LSD) binding technique, platelet 5-hydroxytryptamine (5-HT) receptor number and affinity were compared in schizophrenics treated with depot thioxanthenes and phenothiazines and controls. There was an approximately 30% increase in platelet receptor number (Bmax) in the patient group. There was a decrease in affinity (increase in Kd) of about 30% in the patient group. This was probably due to the persistence of the neuroleptic in the platelet membrane preparation. There was a weak positive correlation between receptor number and total neuroleptic dosage. The increased number of 5-HT receptors is consistent with the previously reported enhancement of 5-HT-induced platelet aggregation in patients treated with long-term phenothiazines and thioxanthenes. Our findings are compatible with 5-HT up-regulation in human platelets produced by depot neuroleptic therapy. It is not known whether parallel changes may be occurring in brain 5-HT receptors.

Adult↗
PubMed1985

The mechanism of hypertension and bradycardia following lesions of the caudal ventrolateral medulla in the rabbit: the role of sympathetic nerves, circulating adrenaline, vasopressin and renin.

Lesions of the ventrolateral medulla of the rabbit, coinciding with the A1 noradrenaline cell bodies (A1 lesions) produced fortyfold increases in the plasma levels of vasopressin and adrenaline, a twofold increase in plasma noradrenaline and a substantial increase in plasma renin activity. These increases accompanied the hypertension and bradycardia that follow A1 lesions. The vasoconstriction and hypertension were completely abolished by phentolamine, an alpha-adrenoceptor antagonist, when it was administered before lesions and were markedly reduced when it was given after lesions. On the other hand, administration of an antagonist to the vasoconstrictor action of vasopressin (d(CH2)5Tyr(Me)AVP) or an angiotensin converting enzyme inhibitor had little effect. Prior removal of the adrenal glands prevented any rise in plasma adrenaline levels but had no effect on the pressure response to subsequent A1 lesions. These results indicate that the vasoconstriction and hypertension were predominantly mediated by alpha-adrenoceptor stimulation, acting mainly through sympathetic vasoconstrictor nerves. The fall in heart rate following A1 lesions was approximately halved by pretreatment either with d(CH2)5Tyr(Me)AVP alone, or by blockade of the vagus and sympathetic with scopolamine and propranolol; it was completely abolished by combined pretreatment with all three agents. The experiments show that vasopressin release makes a major contribution to the bradycardia acting at least in part through mechanisms that are independent of cardiac vagal or sympathetic nerves.

Adrenalectomy↗
PubMed1984

The schematic representation of effector function underlying perceptual-motor skill.

Conceptual and methodological problems related to Schmidt' (1975) motor schema theory are discussed. In particular, the motor schema is interpreted as representing the dynamics of the system being controlled, which may or may not be associated with a referent movement pattern. Furthermore, it is suggested that prior familiarity with a control system's dynamics is a critical but uncontrolled factor in tests of the theory, and largely accounts for their equivocal findings. These ideas are examined by two experiments in which subjects had to bimanually control the movement of a computer-displayed cursor along a track on a CRT screen. Different track orientations required different patterns of movement not entailing a single generalized motor program. Experiment 1 shows that variable track performance with a given control system, results in better transfer to novel tracks than does fixed practice. Experiment 2 demonstrates that altering the control system disrupts performance whether or not the required movements remain the same. These results indicate the need for a fundamental modification of schema theory, such that a schematic representation of effector-environment relations (effector function) is available independently of particular movement patterns used in its acquisition.

Journal Article↗
PubMed1984

A classification of manipulative hand movements.

The nature of manual manipulation of objects is discussed. It is argued that a functional distinction should be made between palmar grips which immobilise an object in the hand, and digital patterns which permit manipulation. Such a distinction is separate from any anatomically defined power and precision configurations. Manipulative hand movements may be grouped into three classes, based on differences between sequenced patterns of movement and synergies, the latter being further subdivided into simple and reciprocal patterns. Within each of the three classes, a number of individual movement patterns are described. These differ mainly in the number of digits involved and the way in which the thumb is employed. The classification is concerned with movements of the digits directed at manipulating an object within the hand. It is not concerned with movements of the hand as a whole, using the wrist or more proximal joints, while holding an immobilised object.

Child↗
PubMed1984

Criteria for detection of Clostridium difficile toxin production by counterimmunoelectrophoresis.

Counterimmunoelectrophoresis (CIE) was compared with a cytotoxicity assay and isolation of toxin-producing Clostridium difficile for the diagnosis of antibiotic-associated diarrhea. Standardized criteria for CIE positivity were established as two major precipitin lines with specific C. difficile antitoxin. Using these criteria on 425 fecal specimens, we determined the sensitivity of CIE (80%) to be comparable to that of the cytotoxicity assay (82%). Both methods were highly specific. With carefully controlled techniques, CIE can be used in routine diagnostic laboratories to screen for toxigenic C. difficile.

Animals↗
PubMed1984

Decreased platelet 3H-imipramine binding sites in classical migraine.

Patients with classical migraine investigated between attacks had significantly fewer platelet 3H-imipramine binding sites than control subjects and this finding was more marked in males than in females. There was no abnormality of binding characteristics of platelet 5-hydroxytryptamine receptors or of platelet alpha 2-adrenoceptors. Because the reduced 3H-imipramine binding capacity was found in classical migraineurs who were investigated between attacks, it may reflect a predisposition to migraine rather than being a consequence of attacks.

Blood Platelets↗
PubMed1984

Cardiac performance in the conscious rabbit with acute hypertension following brainstem lesions coinciding with the A1 group of catecholamine neurons.

Electrolytic lesions of the ventrolateral medulla, coinciding with the A1 catecholamine cells of the conscious rabbit (A1 lesions) cause acute hypertension and bradycardia and in some animals, pulmonary oedema. We have assessed the change in cardiac performance after an A1 lesion, the role of cardiac autonomic effectors in this change; and the mechanism of the pulmonary oedema. Following A1 lesions there was a profound (over 100%) rise in total peripheral resistance and a fall in cardiac output which was mainly due to a fall in stroke volume since it occurred even in animals in which the heart rate was held constant by atrial pacing. This reduced stroke volume occurred despite a 40% increase in myocardial contractility (peak LV dP/dt) and elevation of left ventricular end diastolic pressure. beta-Adrenoceptor blockade with propranolol abolished the rise in peak LV dP/dt, while vagal blockade with methylscopolamine abolished the bradycardia and combined blockade with propranolol and methylscopolamine abolished the rise in peak LV dP/dt and reduced the bradycardia. In rabbits which developed pulmonary oedema, left ventricular end diastolic pressure rose to 35 +/- 3.5 compared to 16 +/- 2.7 mmHg in those which did not, suggesting that the pulmonary oedema was due to raised left ventricular filling pressure.

Adrenergic beta-Antagonists↗
PubMed1983

Changes in platelet alpha 2-adrenoceptor binding post partum: possible relation to maternity blues.

Platelet alpha 2-adrenoceptor binding characteristics were investigated in 28 healthy women during the peripartum period. The number of platelet alpha 2-adrenoceptors fell after childbirth, corresponding to a fall in the circulating levels of oestrogen and progesterone. Two-thirds of the women had an episode of maternity blues. At 7-10 days post partum the platelet alpha 2-adrenoceptor capacity in these subjects was significantly higher than in those women who did not show signs of maternity blues and significantly higher than a control group of normally menstruating women. We conclude that platelet alpha 2-adrenoceptors may be affected by the circulating levels of endogenous oestrogen and progesterone and that a delayed or diminished fall in platelet alpha 2-adrenoceptor capacity after childbirth may be associated with the development of maternity blues.

Blood Platelets↗