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Biomedical subjects

R Bannister

Publications and source records attributed to R Bannister.

At least 55 records · Page 3Linked to original sources
PubMed1985

Unmasking of the cardiovascular effects of carbohydrate in subjects with sympathetic denervation.

The cardiovascular, biochemical and hormonal effects of a standard meal and two differing carbohydrates have been studied in normal subjects and in patients with autonomic failure (AF) and impaired cardiovascular reflexes. In the normal subjects blood pressure (BP) was unchanged after a meal and oral glucose. In AF patients, however, there was a marked and prolonged fall in BP after the meal. A similar fall occurred after oral glucose with only a small fall after oral xylose. In normal subjects, the meal and glucose raised plasma noradrenaline levels, unlike in AF patients, in whom noradrenaline and adrenaline levels were unchanged. In normal subjects with intact autonomic reflexes there are minimal cardiovascular effects induced by a meal or glucose. In AF subjects neural mechanisms are impaired, which probably unmasks the primary effects of food ingestion. The ability of glucose, but not xylose, to induce a similar degree of hypotension suggests that insulin may play an important role in postcibal hypotension.

Aged↗
PubMed1984

Growth hormone response to clonidine is impaired in patients with central sympathetic degeneration.

Serum growth hormone (GH) levels before and after intravenous clonidine (1.5 mcg/Kg) were measured in normal subjects and patients with chronic idiopathic autonomic failure (AF) due to central sympathetic degeneration. Normal subjects showed a rise in plasma GH from 2 +/- 1 mU/l to 27 +/- 12 mU/l. Basal levels were similar but there was no rise in GH levels in the AF patients. There was no difference in sedation in the two groups, indicating similar central nervous system penetration of the drug. Systolic blood pressure fell in both groups. Diastolic blood pressure fell significantly in normals but not in the AF patients. Clonidine-induced growth hormone release may be a potentially useful neuroendocrine marker indicating derangement of certain components of the central alpha-adrenergic system in man.

Autonomic Nervous System Diseases↗
PubMed1984

Plasma volume regulation in patients with progressive autonomic failure during changes in salt intake or posture.

Blood pressure in patients with progressive autonomic failure falls during salt restriction or orthostasis. We contrasted the regulation of plasma volume in patients with progressive autonomic failure with that of controls to determine whether hypovolemia contributes to this hypotension. When sitting, the plasma volume (measured from distribution of human serum albumin) was normal. During 1 week of low Na+ intake, patients with progressive autonomic failure lost three times as much body weight as controls; however, changes in plasma volume were strictly comparable. Therefore, the extra fluid lost in the patients must have derived primarily from the interstitial space. During alteration in Na+ intake, mean blood pressure values were closely related to plasma volume in the patients (r = 0.80, p less than 0.01) but not in controls. Changes in plasma volume in the head-up tilt position were assessed from the hematocrit values. During tilting, the blood pressure in controls was unchanged, but their plasma volume fell by 10.3% +/- 1.8% (p less than 0.001). In contrast, the mean blood pressure of the patients with progressive autonomic failure fell by 40 +/- 6 mm Hg; yet, their plasma volume was unchanged. Thus, in progressive autonomic failure, plasma volume measured during sitting is normal, but dynamic regulation of plasma volume during salt restriction or orthostasis is abnormal and hypovolemia is offset by partitioning of interstitial fluid into the plasma. Also, because the blood pressure is unusually dependent on volume, this fluid redistribution could be an important defense against severe hypotension in patients lacking cardiovascular reflex control.

Adult↗
PubMed1983

Genetic control of progressive autonomic failure: evidence for an association with an HLA antigen.

In 16 patients with progressive autonomic failure, a rare disease of unknown cause, the frequency of the HLA antigen Aw32 was 13 times more common than in healthy controls, giving a relative risk of progressive autonomic failure with Aw32 of 28.7. Such genetic predisposition to the disease might cause a defect of catecholamine metabolism In the brain or possibly affect the immune response to a virus.

Autonomic Nervous System Diseases↗
PubMed1983

Blood pressure and vasopressin in progressive autonomic failure. Response to postural stimulation, L-dopa and naloxone.

UNLABELLED: We showed previously that patients with progressive autonomic failure with multiple system atrophy (MSA) failed to excrete a water load while they were standing, suggesting abnormal postural regulation of vasopressin release. The rise of plasma arginine vasopressin (AVP) with upright posture is modulated by central dopamine and opioid receptors. Patients with MSA may have depletion of brain dopamine and opioid peptides. We measured the plasma levels of AVP in patients with MSA and control subjects during postural stimulation by head-up tilt and the inhibition of this rise in AVP by L-DOPA (dopamine precursor) and naloxone (opiate antagonist). Since L-DOPA and naxolone can alleviate hypotension, we also studied the effects of these agents on orthostatic hypotension. Plasma AVP concentration of normal subjects rose progressively over 90 min of head-up tilt and this postural rise in AVP was abolished by L-DOPA and naloxone. Patients with MSA had similar levels of AVP while horizontal. However, they showed a severely blunted postural AVP response since their levels rose to only 10 per cent of the rise in the normal subjects despite the additional stimulus to AVP secretion of considerable postural hypotension. They also showed no inhibition of AVP secretion by L-DOPA or naloxone. Naloxone did not alter the blood pressure of either group. Although L-DOPA did not change the blood pressure of normal subjects, it lowered it in patients with MSA both while they were horizontal and tilted. IN CONCLUSION: (1) the postural stimulation of AVP release is blunted in MSA; (2) this postural rise in AVP is not inhibited by a dopamine agonist or opioid antagonist in MSA suggesting loss of dopaminergic and opioid pathways involved in AVP release; (3) endogenous opioids do not contribute to orthostatic hypotension in MSA; (4) patients with MSA are supersensitive to the hypotensive effects of an acute L-DOPA infusion.

Aged↗
PubMed1983

Non-obstructive detrusor failure. A urodynamic, electromyographic, neurohistochemical and autonomic study.

Twenty-eight patients presenting with persistent loss of the voiding reflex have been evaluated. Those with cauda equina lesions or pelvic nerve injury were distinguished from a group with idiopathic detrusor failure by their abnormal urethral behaviour during filling, and by urethral sphincter electromyography (EMG). Bladder muscle biopsies revealed the presence of presumptive cholinergic fibres in all three groups, indistinguishable in quantity and distribution from normal controls. The implications of these findings for the diagnosis and management of these patients is discussed.

Adult↗
PubMed1983

Circadian variation of blood pressure in autonomic failure.

We have monitored ambulant intra-arterial blood pressure with the Oxford system in six subjects with autonomic failure who exhibited postural hypotension. Plotting pooled hourly mean values we have demonstrated a consistent circadian trend in blood pressure that was the inverse of the normal pattern, with the highest pressures at night and the lowest in the morning. In four subjects, confinement to bed did not substantially alter this pattern. Heart rate variability was much reduced in four of the subjects, but relatively normal in two in whom blood pressure variation was also less abnormal. There was a correlation of the nadir of the blood pressure measurements with the reported time of peak incidence of orthostatic symptoms. These findings are of importance in both the management and physiologic testing of patients with this condition.

Adult↗
PubMed1982

Extrahypothalamic vasopressin is unchanged in Parkinson's disease and Huntington's disease.

Vasopressin immunoreactivity was measured post-mortem in the locus coeruleus and substantia nigra of 16 cases of Parkinson's disease and multisystem atrophy, 10 cases of Huntington's chorea and 28 normal controls. Amounts of vasopressin did not differ significantly (P greater than 0.05) between the 3 groups. Immunohistochemistry demonstrated vasopressin within nerve terminals. These data are consistent with an extrinsic vasopressin system in the human locus coeruleus and substantia nigra.

Adult↗
PubMed1982

Methacholine pupillary responses in third nerve palsy and Adie's syndrome.

In order to examine the clinical usefulness of methacholine in assessing the site of ocular parasympathetic lesions, pupillary responses in man were measured in postganglionic (Adie's syndrome) and preganglionic third nerve lesions involving the pupil and in controls. From previous work with methacholine it might have been expected that greater constriction would occur in the postganglionic lesions but similar responses were found in both. Corneal hypoxia due to ptosis appeared unlikely to affect corneal permeability significantly and it is probable that these results reflect an increase responsiveness of the iris at, or distal to, the site of muscarinic acetylcholine receptors. Pupils contralateral to third nerve palsy, when tested on a separate occasion, also constricted by an amount approximately proportional to that of the clinically abnormal pupil. The possibilities that this may result in some way from reduction in total retinal illumination, or from retrograde changes in preganglionic pupilloconstrictor neurons affecting contralateral pupilloconstrictor neurons via central pathways, are discussed. It is concluded that supersensitivity to methacholine, tested carefully in the manner described, is a useful guide to the presence of parasympathetic denervation or decentralization, but that it is not reliable in distinguishing between the two sites.

Adie Syndrome↗
PubMed1982

Increased numbers of alpha receptors in sympathetic denervation supersensitivity in man.

Cardiovascular responses to intravenous administration of norepinephrine and the properties of alpha receptors on platelets were compared in normal human subjects and subjects with multiple system atrophy (MSA) and sympathetic degeneration. All the subjects with MSA had low plasma norepinephrine concentrations (in the supine position) (0.42 +/- 0.09 nM, normal 3.47 +/- 0.58 nM), which did not increase on tilt. The pressor sensitivity of subjects with MSA to norepinephrine infusion was increased 10- to 20-fold, demonstrating denervation supersensitivity to adrenergic agonists. Analysis of alpha receptors was by binding of [3H]dihydroergocryptine to platelets. Results are shown as mean +/- standard error of the mean. In the MSA subjects, the number of alpha receptors (1,712 +/- 699 fmol/10(8) platelets) was about sevenfold greater than in normal subjects (224 +/- 21 fmol/10(8) platelets), and the affinity, as measured by the equilibrium dissociation constant (Kd), was similar in both groups (MSA subjects, 9.6 +/- 4.3 nM; normal subjects, 4 +/- 0.5 nM). These observations suggest that an increase in alphaadrenergic receptor numbers may account for the denervation supersensitivity to infused norepinephrine in patients with sympathetic degeneration. All the subjects with MSA had low levels of the endogenous adrenergic transmitter norepinephrine: the simultaneous increase in alpha adrenergic receptors supports the theory of agonist regulation of receptor numbers.

Adult↗
PubMed1981

Generalised smooth-muscle disease with defective muscarinic-receptor function.

A patient with widespread smooth-muscle disease presented with chronic intestinal pseudo-obstruction but had in addition defects of the bladder, pupils, sweating, and cardiovascular function. There was no evidence of a primary neural lesion, and minor changes in the muscle did not resemble those of a myopathy. In each organ affected muscarinic cholinergic function was at fault, but instead of supersensitivity to cholinergic drugs, which occurs in postganglionic autonomic neuropathies, there was a lack of response to cholinergic drugs and anticholinesterases. It was therefore concluded that the patient had a new type of defect of muscarinic-receptor function. The cause was unknown, but it may have been an autoimmune disease resembling myasthenia, in which there is a postjunctional defect of muscarinic receptors. In similar cases binding of muscarinic agonists and antagonists should be tested. When antibodies to purified human muscarinic receptors become available different patterns of smooth-muscle defect may be identifiable, enabling the lesion to be defined more precisely.

Adult↗
PubMed1981

Laryngeal abductor paralysis in multiple system atrophy. A report on three necropsied cases, with observations on the laryngeal muscles and the nuclei ambigui.

Clinical and pathological findings are reported in three cases of Shy-Drager syndrome with laryngeal stridor severe enough to require tracheostomy. Indirect laryngoscopy in all three cases revealed a failure to abduct the vocal cords properly with a resulting narrowing of the glottic airway. Histological studies showed a marked atrophy of the posterior crico-arytenoid muscles and little atrophy of the other laryngeal muscles. The posterior crico-arytenoid muscles have the sole responsibility of abducting the vocal cords, so it is concluded that the patient's stridor was caused by the selective paralysis of these muscles. Histological studies of the posterior crico-arytenoid muscles were suggestive of denervation but despite this finding, no clear evidence of any motor cell loss in the nuclei ambigui was obtained. Other possible causes of the selective posterior crico-arytenoid atrophy are discussed.

Autonomic Nervous System Diseases↗
PubMed1981

Pathology of the intrinsic muscles of the larynx.

The intrinsic muscles of the larynx were exposed in each of 54 normal larynges derived from the autopsy series of a general hospital and submitted to microscopic examination. Muscle fibre alterations were found in all the posterior cricocarytenoid muscles in patients from 13 years of age on wards. In about half of the patients these changes included necrosis of segments of muscle fibres and secondary cellular reactions to this. In two cases of chronic autonomic failure with multiple system atrophy the intrinsic laryngeal muscles were similarly examined. Both cases showed a marked gross and microscopic atrophy of the posterior cricoarytenoid muscles; there were also microscopic changes similar to those found in the normal population. The significance of the changes in the routine post-mortem larynges, the changes in the cases of chronic autonomic failure with multiple system atrophy and the relationship between the two are discussed.

Adolescent↗
PubMed1981

beta-Receptor numbers and thermodynamics in denervation supersensitivity.

1. Denervation supersensitivity to adrenergic agonists occurs after degeneration of the sympathetic nervous system in the disease called multiple system atrophy (MSA) or the Shy Drager Syndrome.2. Supersensitivity to the chronotropic effect of i.v. isoprenaline on the heart was demonstrated in eight subjects with sympathetic nervous system degeneration and MSA.3. There was an increased number of beta-receptors present in MSA as measured by [H(3)]dihydroalprenolol ([H(3)]DHA) binding to beta-receptors on lymphocytes isolated from venous blood taken from the MSA subjects compared with [H(3)]DHA binding to lymphocytes from seven normal subjects. There was no difference in the affinity of lymphocyte beta-receptors for [H(3)]DHA in MSA.4. [H(3)]DHA binding to lymphocytes from MSA subjects was decreased at lower temperatures but was unaffected by lower temperatures in lymphocytes from normal subjects.5. Equilibrium constants for [H(3)]DHA binding to normal and MSA lymphocytes were similar, indicating that the affinity of the beta-receptors was similar in both groups. The equilibrium constants were little affected by cooling from 37 to 4 degrees C suggesting that the heat of reaction (enthalpy) for [H(3)]DHA binding was low. The Gibbs free energy change on binding was negative and similar in quantity for both normal and MSA lymphocytes. There was a similar, large, increase in entropy on binding of [H(3)]DHA to both normal and MSA lymphocytes, showing that the binding reaction was entropy driven.6. If lymphocyte beta-receptors reflect the status of cardiac beta-receptors, increased numbers of cardiac beta-receptors may contribute to the denervation supersensitivity to isoprenaline in MSA with sympathetic degeneration.

Adult↗
PubMed1981

Laryngeal electromyography in multiple system atrophy with autonomic failure.

In five patients with multiple system atrophy, electromyographic studies using a new surface electrode technique, showed unequivocal evidence of denervation of the posterior crico-arytenoid muscle, and in three of them, of the interarytenoid muscle or crico-pharyngeal sphincter. By comparison, only minor electromyographic abnormalities were found in one-third of patients with other extra-pyramidal syndromes, though in two cases, the abnormalities were of a different kind from those found in multiple system atrophy.

Aged↗
PubMed1981

The use of lisuride in the treatment of multiple system atrophy with autonomic failure (Shy-Drager syndrome).

In a controlled trial lisuride, an ergolene derivative with dopamine receptor agonist properties was given maximum tolerated doses (2.4 mg/day) to seven patients with multiple system atrophy with autonomic failure (Shy-Drager syndrome). Improvement in Parkinsonian features occurred in only one patient and another patient who had been deriving marked benefit from levodopa treatment before the study began failed to respond to large doses of lisuride. Psychiatric side effects (including nightmares, isolated visual hallucinations and toxic confusional states) were the dose-limiting factor in six patients. A modest reduction in orthostatic hypotension occurred in two patients, one of whom had experienced an aggravation of this disturbance on levodopa and bromocriptine. Destruction of post-synaptic dopamine receptors and damage to central noradrenergic systems may offer an explanation for the lack of therapeutic effect of lisuride.

Adult↗