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Biomedical subjects

D Ballantyne

Publications and source records attributed to D Ballantyne.

At least 55 records · Page 3Linked to original sources
PubMed1988

Left ventricular function and beta-blockers: does intrinsic sympathomimetic activity have any influence during chronic therapy?

A study comparing the chronic effects of propranolol (n = 21) and pindolol (n = 19) on male patients with stable angina pectoris was performed. Left ventricular function was assessed by serial radionuclide ventriculography. Radionuclide ventriculography was performed at rest and during cold pressor test. Both drugs improved symptoms of angina pectoris by at least one division of the New York Heart Association classification. Cold pressor testing caused increases in heart rate and blood pressure in both groups throughout the study. At rest, pretreatment ejection fraction was similar in both groups. During propranolol treatment this rose sequentially from 49% to 55% at 26 weeks. No change in the resting ejection fraction occurred in those taking pindolol. The difference in response between the groups reached significance at 26 weeks. In those with subnormal left ventricular ejection fraction (less than 50%), resting ejection fraction improved significantly throughout treatment with propranolol rising from a basal value of 39% to 51% at 26 weeks. In comparison, pindolol caused no significant change. There is no apparent advantage to intrinsic sympathomimetic activity in terms of preservation or improvement of left ventricular performance in patients with stable angina pectoris prescribed beta-blockers for extended periods of time.

Adrenergic beta-Antagonists↗
PubMed1988

The influence of beta-adrenoceptor blockers with and without intrinsic sympathomimetic activity on heart rate, arrhythmias and ST-T segments, using ambulatory electrocardiography.

1. Ambulatory electrocardiography was used to compare the effects of propranolol and pindolol on symptoms, heart rate, arrhythmias and ST segments. Seventeen males (mean age 54 years) with a diagnosis of chronic stable angina pectoris (New York Heart Association Class II-III) were studied. Patients were treated on a double-blind cross-over basis with propranolol 80 mg three times daily or pindolol 5 mg three times daily for 14 days each. During the last 48 h of each treatment period ambulatory electrocardiography was performed. 2. Propranolol resulted in a significantly lower mean hourly, mean 24 h and minimum heart rate. Likewise propranolol caused a lower mean daytime and nocturnal heart rate. There was no significant difference in the frequency of angina between the treatments. The number of episodes of ST segment depression was not significantly different between the two drugs, although there was a trend in favour of propranolol. 3. Both the mean 24 h ST level and the maximum ST segment depression were lower during treatment with pindolol. Propranolol was associated with a total of 117 nocturnal pauses or episodes of asystole ranging in length from 1.5 to 2.8 s. During treatment with pindolol only one such period occurred. The number of premature ventricular contractions occurring during treatment with pindolol (1316 beats) was less than on propranolol (2010) and the mean hourly frequency of premature ventricular contractions was significantly lower during pindolol administration. 4. Pindolol is not significantly different from propranolol in the control of symptomatic and asymptomatic myocardial ischaemia and is associated with fewer premature ventricular contractions. However, there is no advantage in using pindolol in chronic stable angina.

Adult↗
PubMed1988

Synaptic rhythm of caudal medullary expiratory neurones during stimulation of the hypothalamic defence area of the cat.

1. Intracellular recordings were made from caudal medullary expiratory neurones in anaesthetized, paralysed, artificially ventilated and vagotomized cats before during and after the tachypnoeic response evoked by stimulation of the perifornical region of the hypothalamus. 2. The tachypnoeic response was evoked in seven of ten cats tested, and was represented in the phrenic nerve by a rapid two- to threefold increase in the frequency of the respiratory rhythm. The shortened duration of inspiratory discharge in the phrenic nerve was accompanied by an increase in its rate of development. If initially present, post-inspiratory phrenic discharge was intensified and extended throughout the shortened expiratory interval. 3. Intracellular recordings were obtained from twenty-one expiratory neurones during intermittent hypothalamic stimulation with short trains of pulses. Eighteen neurones showed a regular, short-latency sequence of synaptic events which consisted of an initial depolarizing potential (presumed EPSP) and a following hyperpolarizing potential (Cl--mediated IPSP) of long duration (50-150 ms when measured in expiration). The IPSP was accompanied by a phasic cessation of phrenic nerve discharge of comparable duration which was succeeded by intensified discharge. In three neurones (one experiment) the IPSP response was absent. 4. Sixteen neurones showing the EPSP-IPSP sequence were held for sufficiently long to record changes in the respiratory-related membrane potential pattern accompanying stimulation. The reduced expiratory time accompanying the response resulted in a shortened expiratory burst. In four neurones showing evidence of IPSPs in early expiration (post-inspiratory IPSPs), stimulation resulted in a phasic weakening of this inhibition which resulted in a more rapid approach to threshold and a steady rather than delayed increase in discharge. A low level of post-inspiratory IPSPs extended throughout most of the shortened expiration, resulting in an alternating rhythm of inspiratory and post-inspiratory inhibition. In the twelve neurones lacking such post-inspiratory IPSPs stimulation had no obvious effect on the shape of the expiratory trajectory. 5. In neurones which received an IPSP from hypothalamic stimulation, the overall response was associated with reduced amplitude and increased rate of decline of inspiratory inhibition of expiratory neurones. Three neurones showed high-frequency (70-80 Hz) oscillation of the membrane potential during inspiration (Mitchell & Herbert, 1974b). Hypothalamic stimulation resulted in a transient suppression of this oscillation. 6. We conclude that the short-latency inhibitory component of the response to hypothalamic stimulation is widely distributed, including expiratory neurones, some fraction of the inspiratory population and the neurones responsible for inspiratory and post-inspiratory inhibition.

Animals↗
PubMed1987

The differential organization of medullary post-inspiratory activities.

Membrane potential trajectories of 68 bulbar respiratory neurones from the peri-solitary and peri-ambigual areas of the brain-stem were recorded in anaesthetized cats to explore the synaptic influences of post-inspiratory neurones upon the medullary inspiratory network. A declining wave of inhibitory postsynaptic potentials resembling the discharge of post-inspiratory neurones was seen in both bulbospinal and non-bulbospinal inspiratory neurones, including alpha- and beta-inspiratory, early-inspiratory, late-inspiratory and ramp-inspiratory neurones. Activation of laryngeal and high-threshold pulmonary receptor afferents excited bulbar post-inspiratory neurones, whilst in the case of inspiratory neurones such stimulation produced enhanced postsynaptic inhibition during the same period of the cycle. Activation of post-inspiratory neurones and enhanced post-inspiratory inhibition of inspiratory bulbospinal neurones was accompanied by suppression of the after-discharge of phrenic motoneurones. These results suggest that a population of post-inspiratory neurones exerts a widespread inhibitory function at the lower brain-stem level. Implications of such an inhibitory function for the organization of the respiratory network are discussed in relation to the generation of the respiratory rhythm.

Animals↗
PubMed1987

Lipoprotein analysis in bodybuilders.

The use of anabolic steroids to augment athletic performance is widespread. It is known that these drugs can adversely affect lipoproteins in normal volunteers, leading to increased cholesterol and low density lipoprotein and depressed high density lipoprotein. It has been shown that endurance type exercise can lead to beneficial effects on lipoproteins but the effects of power exercise are less clear-cut and made more difficult to interpret by prior anabolic steroid use. This paper details the lipoprotein results in 24 subjects, eight sedentary controls, eight non-steroid and eight steroid using bodybuilders. The results revealed no significant difference between sedentary controls and non-steroid bodybuilders suggesting that this form of training does not cause beneficial effects on lipoproteins. However, the steroid-using groups had higher cholesterol and low density lipoprotein, with lower high density lipoprotein, high density lipoprotein2, high density lipoprotein3 and high density lipoprotein2/high density lipoprotein3 ratios compared to the other two groups. The long-term effects of such results may be an increased risk of atherosclerosis and requires long-term follow-up.

Adult↗
PubMed1987

Beta-adrenoceptor blockade and plasma lipoproteins. Comparison of the effects of propranolol and pindolol on plasma lipoproteins including high-density lipoprotein subfractions.

Beta-Adrenoceptor blocker therapy is known to cause disturbances of the lipoprotein profile. The long-term effects of beta-adrenoceptor blockers and the influence of intrinsic sympathomimetic activity (ISA) has not been clearly defined. We measured serum lipoproteins during chronic beta-adrenoceptor blockade in patients with stable angina pectoris treated with propranolol (without ISA) (n = 21) or pindolol (with ISA) (n = 19). No significant changes occurred in the lipoprotein profile of the patients taking pindolol. In those taking propranolol, very low density lipoprotein (VLDL) increased at 52 weeks (P less than 0.05) and total high density lipoprotein (HDL) decreased at 26 weeks (P less than 0.01) and at 52 weeks (P less than 0.05). However, HDL2 rose significantly at 52 weeks (P less than 0.05). There was a corresponding increase in HDL2/HDL3 ratio. We conclude that pindolol is less likely to exert a harmful effect on plasma lipoproteins than beta-adrenoceptor blockers without ISA.

Adult↗
PubMed1986

The effect of sotalol on plasma lipoproteins and apolipoproteins.

Plasma lipoproteins were estimated in ten hypertensive subjects (mean age 51 +/- 11.2 yr), before, 6 wk and 6 mth following treatment with Sotalol 320 mg/day. Heart rate fell sequentially throughout the study (p less than 0.01) and although there was a sequential fall in mean blood pressure this did not reach statistical significance. There was a significant increase in plasma triglyceride concentration from a basal value of 1.87 +/- 1.064 to 2.50 +/- 0.877 mmol/l (p less than 0.005) at 6 mth. No significant change was found in very low density, low density and high density lipoprotein cholesterol or apolipoprotein concentrations (Apo A-I, Apo A-II, Apo B). We conclude that Sotalol exerts a similar influence on plasma lipoproteins as other non-cardioselective beta-adrenoceptor blockers without intrinsic sympathomimetic activity and its use does not constitute an increased risk of developing atherosclerosis, when compared with other beta-blockers.

Adult↗
PubMed1986

Influence of intrinsic sympathomimetic activity on respiratory function during chronic beta blockade: comparison of propranolol and pindolol.

The long term effect of beta blockers and the influence of intrinsic sympathomimetic activity on respiratory function were assessed in patients with chronic stable angina pectoris randomised to receive treatment with propranolol (n = 21) or pindolol (n = 19) for one year. Forced expiratory volume in one second (FEV1) had fallen by a mean of 240 ml after one year (p less than 0.001) in those treated with propranolol compared with 120 ml in those treated with pindolol (p less than 0.05). The difference between the groups was significant (p less than 0.01). Vital capacity fell significantly only in those treated with propranolol (p less than 0.05 at one year). In those in whom the basal ratio of FEV1 to forced vital capacity was low (less than 70%) propranolol, but not pindolol, caused a significant (p less than 0.05) fall in FEV1 throughout treatment. Long term administration of pindolol has a less adverse effect on respiratory function than propranolol, which results in a progressive deterioration in respiratory function over one year.

Forced Expiratory Volume↗
PubMed1986

Reflex prolongation of stage I of expiration.

Experiments were performed on anesthetized cats to test the theory that the interval between phrenic bursts is comprised of two phases, stage I and stage II of expiration. Evidence that these represent two separate neural phases of the central respiratory rhythm was provided by the extent to which stage duration is controlled individually when tested by superior laryngeal, vagus and carotid sinus nerve stimulation. Membrane potential trajectories of bulbar postinspiratory neurons were used to identify the timing of respiratory phases. Stimulation of the superior laryngeal, vagus and carotid sinus nerves during stage I of expiration prolonged the period of depolarization in postinspiratory neurons without significantly changing the durations of either stage II expiratory or inspiratory inhibition, indicating a fairly selective prolongation of the first stage of expiration. Changes in subglottic pressure, insufflation of smoke into the upper airway, application of water to the larynx or rapid inflation of the lungs produced similar effects. Sustained tetanic stimulation of superior laryngeal and vagus nerves arrested the respiratory rhythm in stage I of expiration. Membrane potentials in postinspiratory, inspiratory and expiratory neurons were indicative of a prolonged postinspiratory period. Thus, such an arrhythmia can be described as a postinspiratory apneic state of the central oscillator. The effects of carotid sinus nerve stimulation reversed when the stimulus was applied during stage II expiration. This was accompanied by corresponding changes in the membrane potential trajectories in postinspiratory neurons. The results manifest a ternary central respiratory cycle with two individually controlled phases occurring between inspiratory bursts.

Animals↗
PubMed1986

Presynaptic depolarization in myelinated vagal afferent fibres terminating in the nucleus of the tractus solitarius in the cat.

The presynaptic influences that act on terminals of slowly adapting lung stretch receptor afferents and aortic baroreceptor afferents within the nucleus of the solitary tract were assessed using intracellular recording and antidromic stimulation techniques. Central respiratory influences on the excitability of lung stretch receptor terminals were observed in 29% (4 of 14) of measurements. These were confirmed in intracellular recordings where membrane depolarizations in synchrony with phrenic nerve discharge were seen in 17% (4 of 24) of fibres. In three cases membrane depolarization also occurred synchronously with artificial lung inflation. Neither tests of excitability nor intracellular recording revealed any evidence for equivalent presynaptic influences on 16 myelinated aortic baroreceptor terminals. Stimulation of the superior laryngeal nerve evoked depolarizations in 50% (7 of 14) of lung stretch receptor terminals. These took the form of complex waves of depolarization with both short (3-8 ms) and long latency (27-35 ms) components. The amplitude of the long latency response increased during the period of phrenic nerve discharge, i.e. during "central inspiration". These effects are discussed in relation to the central respiratory influences on both respiratory and cardiovascular reflexes.

Animals↗
PubMed1986

Continuous 24-hour electrocardiography in thyrotoxicosis before and after treatment.

Ten thyrotoxic individuals, who otherwise had no evidence of cardiovascular disease, underwent continuous ambulatory 24-hour ECG monitoring, before and after antithyroid treatment. The mean age of the subjects was 41 +/- 14.4 years (mean +/- SD) with a range of 22 to 66 years. When subjects were thyrotoxic, the mean heart rate for the group was 104 +/- 10.8 bpm. This fell to 82 +/- 6.8 bpm when the subjects were rendered euthyroid (p less than 0.001). Circadian rhythm of heart rate response was maintained in the thyrotoxic state, although heart rate variability was significantly increased (p less than 0.001). The prevalence of ventricular premature contractions was not significantly different before and after treatment, although premature atrial contractions were more prevalent during the middle third of the day (p less than 0.01) when subjects were euthyroid. These findings support the view that normal adrenergic responsiveness persists in hyperthyroidism, and for most individuals treatment does not significantly alter the prevalence of ectopic activity.

Adult↗
PubMed1986

Cardiac adaptations to training: relevance to angina pectoris.

Exercise training has for many years been suggested as a useful adjunct to medical therapy for patients with ischaemic heart disease. While its popularity amongst the general public continues to grow, limitations in our ability to assess its effects on the heart have meant that, as cardiologists, our desire to encourage this popular upsurge in physical activity has been tempered by our inability to provide convincing evidence of its value to our patients. In particular the role of exercise in the rehabilitation of patients with angina pectoris is as yet unclear. This review addresses this question and states what has been proven to date and also the questions which remain to be answered. It also suggests some reasons why we have failed to provide answers so far, and ways in which new technology may be used in the future. Studies in animals, asymptomatic humans, and patients with ischaemic heart disease have demonstrated that training reduces the resting heart rate and double product of heart rate times blood pressure at any given level of exercise. This has the benefit of reducing myocardial oxygen consumption during exercise. There is also evidence that it increases end-diastolic volume and left ventricular wall thickness. Evidence for an increase in maximal myocardial oxygen consumption in angina is limited to one or two studies showing an improved maximum double product and to the occasional patient proven by echocardiography or nuclear studies to increase ejection fraction by training. Better selection of patients and use of new imaging techniques should provide further information in the near future.

Adaptation, Physiological↗
PubMed1986

Echocardiographic diagnoses in elderly patients with systolic murmurs and cardiac disease.

M-mode and 'real-time' echocardiography was employed to study 100 elderly with systolic murmurs and cardiac disease. Technically adequate recordings were obtained in 89 patients. Independent assessment of the echocardiographs showed good reproducibility. Aortic sclerosis was the most prevalent lesion, but did not by itself impair left ventricular function. The echocardiographic diagnosis of mitral regurgitation was significantly related to heart failure and atrial fibrillation. A link between murmur and cardiac disease was postulated in 40% of cases.

Aged↗
PubMed1986

The non-uniform character of expiratory synaptic activity in expiratory bulbospinal neurones of the cat.

Intracellular recordings were made from caudal medullary expiratory neurones in pentobarbitone-anaesthetized, vagotomized and artificially ventilated cats. The sample consisted of thirty-three bulbospinal neurones and seven neurones which were not antidromically excited from either the spinal cord (C2-C3) or vagus nerve. Their rhythmic activity consisted of an alternating inspiratory hyperpolarization due to Cl(-)-dependent inhibitory post-synaptic potentials (i.p.s.p.s) (Mitchell & Herbert, 1974) and an expiratory depolarization. The precise shape of the expiratory depolarizing wave varied within a given neurone depending on the over-all pattern of respiration. This variation extended from a smoothly developing depolarization, continuous throughout its course, through an intermediate state in which depolarization proceeded in two stages with a definite transition between them, to a final state in which the early part of expiration was occupied by a distinct hyperpolarizing component to the membrane potential trajectory. Under conditions of a brisk phrenic nerve discharge, these variations in the shape of the membrane potential profile were related to the time course and intensity of post-inspiratory discharge in the nerve. However, other factors (depth of anaesthesia and stimulation of laryngeal receptors) could influence the time course of the membrane potential profile of expiratory neurones independently of post-inspiratory phrenic discharge. In five of fifteen neurones which were tested, early expiration was occupied by a rapidly developing, decrementing wave of Cl(-)-dependent i.p.s.p.s (post-inspiratory i.p.s.p.s). These i.p.s.p.s were present only under conditions of a strong phrenic rhythm (large amplitude, fairly rapid phrenic discharge). They became weaker and ultimately disappeared when the level of anaesthesia was deepened and the phrenic rhythm became slower. Under these conditions, the post-inspiratory wave of i.p.s.p.s could be restored by stimulation of the superior laryngeal nerve. Adequate stimulation of presumed 'irritant' laryngeal receptors elicited post-inspiratory i.p.s.p.s in seven of ten neurones tested which initially showed either no post-inspiratory i.p.s.p.s or possibly just a weak pattern. In ten of fifteen neurones tested, the responses to current injection revealed clear differences in membrane potential behaviour in early and late expiration, which became intensified following stimulation of the superior laryngeal nerve.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1986

Increased left ventricular mass in a bodybuilder using anabolic steroids.

As the effects of anabolic steroids on left ventricular structure and function are unknown, we carried out clinical examination, 12 lead electrocardiography and echocardiography on a 23 year old male bodybuilder using these drugs. In this subject we found values of ECG voltage criteria, left ventricular-mass, posterior wall and interventricular septal thickness which exceeded those found in normal subjects and also in other competitive, power athletes. Despite these values, however, ejection fraction remained normal. This would suggest that anabolic steroids perhaps have a direct effect on the myocardium, in addition to the effects of training, but whether this is of pathological significance is unclear.

Adult↗
PubMed1986

Sudden death and vigorous exercise--a study of 60 deaths associated with squash.

The circumstances surrounding 60 sudden deaths (59 men, one woman) associated with squash playing are described. The mean age (SD) of those who died was 46 (10.3) years (range 22-66 years). Necropsy reports were available in 51. The certified cause of death was coronary artery disease in 51 cases, valvar heart disease in four, cardiac arrhythmia in two cases, and hypertrophic cardiomyopathy in one case. There were only two deaths from non-cardiac causes. Forty five of those who died had reported prodromal symptoms, the most common of which was chest pain, and 22 were known to have had at least one medical condition related to the cardiovascular system during life, the most common of which was systemic hypertension (14 subjects). Those dying from coronary artery disease had a high frequency of risk factors. Some of these deaths might have been prevented by appropriate counselling of players after prospective medical screening, which would have detected most of the patients with overt cardiovascular disease and some of those with subclinical coronary artery disease.

Adult↗