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Biomedical subjects

R Bannister

Publications and source records attributed to R Bannister.

At least 73 records · Page 4Linked to original sources
PubMed1981

Adrenergic innervation in autonomic failure.

In 10 patients with chronic autonomic failure, the sympathetic perivascular nerve plexuses from quadriceps muscle biopsies were studied by catecholamine fluorescence and electronmicroscopy. There was almost complete absence of catecholamine fluorescence and fewer than normal numbers of small granular (noradrenergic) vesicles in all nerves studied. The most marked depletion of noradrenergic vesicles was seen in two of the patients with pure autonomic failure, but more studies are needed for a full quantitative comparison of pure autonomic failure and autonomic failure with multiple system atrophy (Shy-Drager syndrome).

Aged↗
PubMed1980

Neural and hormonal peptides in rectal biopsy specimens from patients with Chagas' disease and chronic autonomic failure.

The neural and hormonal peptide content of rectal biopsy specimens from 10 patients with chronic autonomic failure, 10 patients with chronic gastrointestinal Chagas' disease, and 13 controls was studied with radioimmunoassay and immunocytochemistry. In the patients with Chagas' disease the mean concentrations of rectal vasoactive intestinal polypeptide, enteroglucagon, substance P, and somatostatin were all less than half of those in controls and in patients with chronic autonomic failure. Immunocytochemistry revealed a considerable reduction in the number and immunostaining of the peptide-containing cells and nerves. Concentrations of regulatory peptides in the rectum are thus reduced in association with intrinsic but not extrinsic autonomic neuropathy.

Autonomic Nervous System↗
PubMed1980

Preservation of autoregulation of cerebral blood flow in autonomic failure.

Cerebral blood flow (CBF) measurements have been made at systolic pressures between 40 and 170 mm Hg in 8 patients with chronic autonomic failure and widespread sympathetic efferent defects. Hypotension was produced by head up tilt. Cerebral autoregulation was preserved over a wide range and only failed at a systolic pressure close to 60 mm Hg, which is below the level at which it fails in normal subjects. Therefore, although autoregulation is probably mediated largely by local myogenic factors, its lower limit appears to be reduced by defective sympathetic function. These findings help to explain the remarkable tolerance of severe postural hypotension in autonomic failure.

Adult↗
PubMed1980

The pressor actions of noradrenaline and angiotension II in chronic autonomic failure treated with indomethacin.

1 Indomethacin treatment of postural hypotension in four patients with chronic autonomic failure increased their pressor supersensitivity to intravenous noradrenaline without causing fluid retention. 2 All patients were supersensitive to angiotensin II in spite of normal levels of plasma renin activity in the supine position and therefore (by inference) of angiotensin II. This suggests that in autonomic failure, the degree of angiotensin receptor occupancy by endogenous angiotensin II is not important in determining pressor sensitivity to exogenous angiotensin II. Indomethacin increased the pressor supersensitivity to angiotensin II in all patients. 3 Indomethacin treatment decreased supine plasma renin activity to 50% of the level present before indomethacin treatment. 4 Indomethacin increased the lying but not the standing blood pressure. The failure to raise the standing pressure may be the result of the additional postural stress overcoming any vasoconstriction resulting from the increased sensitivity of vascular receptors to noradrenaline. The decrease in plasma renin activity could also contribute to the failure of indomethacin to prevent a fall in blood pressure on standing. 5 In our patients the excretion of the main urinary metabolite (PGFM) of prostaglandin F2 alpha was higher than recorded previously in normal controls. During treatment with indomethacin, plasma indomethacin levels were in the range at which inhibition of prostaglandin synthesis occurs and the excretion of PGFM was decreased. 6 Indomethacin was not effective in the treatment of postural hypotension in these patients with autonomic failure.

Adult↗
PubMed1980

Mucociliary clearance in patients with chronic autonomic failure.

Mucociliary clearance was measured in four patients with chronic autonomic failure and normal ventilatory function using a method of scanning the clearance of inhaled polystyrene particles tagged with 99mTc. Previous surgical and experimental evidence has suggested that autonomic denervation might be expected to impair clearance. However, the four patients in this study showed no significant difference in clearance rate compared to groups of sex-matched control subjects. A fifth patient was found to have impaired mucociliary clearance. However she had the symptoms and ventilatory function of smoking-related chronic obstructive bronchitis, a condition which has previously been shown to impair mucociliary clearance.

Adult↗
PubMed1979

Alterations in [3H]spiperone binding in human caudate nucleus, substantia nigra and frontal cortex in the Shy-Drager syndrome and Parkinson's disease.

[3H]Spiperone binding was investigated in the caudate nucleus, substantia nigra (s. nigra) and frontal cortex of control subjects and of patients with Parkinson's disease and the Shy-Drager syndrome. Binding sites for [3H]spiperone were interpreted as dopamine receptors in caudate and s. nigra, and as 5-hydroxytryptamine (5-HT) receptors in frontal cortex. Scatchard analysis showed that the Bmax (maximal number of binding sites) in caudate was similar in the 3 groups, whereas in s. nigra the Bmax was reduced by approximately 60% in both Parkinsons disease and Shy-Drager syndrome. The dissociation constant (Kd) for [3H]spiperone binding in s. nigra was similar in the 3 groups. In caudate nucleus, the Kd was similar in control and Parkinson groups; however, there was a significant increase in the dissociation constant in the caudate nucleus from cases of Shy-Drager syndrome. No differences in binding characteristics were observed in the frontal cortex. These results are taken to reflect a loss of dopamine receptor sites in the s. nigra in both Parkinson's disease and Shy-Drager syndrome, and a reduced affinity of dopamine receptor sites in the caudate nucleus in Shy-Drager syndrome.

Binding Sites↗
PubMed1979

Multiple system atrophy with autonomic failure: clinical, histological and neurochemical observations on four cases.

Four cases of progressive autonomic failure are described, in all of which there were additional non-autonomic neurological abnormalities, including pyramidal, extra-pyramidal and cerebellar features. Histological examination revealed cell degeneration in the substantia nigra, putamen and intermediolateral columns of the spinal cord as a common pathological finding. In addition, 3 cases showed loss of Purkinje cells in the cerebellum and degeneration of pontine nuclei and inferior olivary nuclei. In one case there was cell loss from the locus coeruleus, caudate nucleus, vestibular nuclei and dorsal vagal nuclei. These were, therefore, cases of multiple system atrophy. Neurochemically, a common feature was a profound depletion in dopamine and noradrenaline from brain regions which are normally rich in these catecholamines. Central cholinergic systems appeared to be involved also, but to a variable degree.

Aged↗
PubMed1979

Defective cardiovascular reflexes and supersensitivity to sympathomimetic drugs in autonomic failure.

In 10 patients with chronic autonomic failure the clinical features and cardiovascular reflexes were correlated with the pressor responses to intravenous noradrenaline and tyramine. In all patients there was an exaggerated response to noradrenaline but a normal or only mildly exaggerated response to tyramine. Patients with lack of sinus arrhythmia and by implication baroreceptor reflex loss had greater responsiveness to pressor drugs than patients with preservation of this reflex. The responses to tyramine infusions imply that there must be sufficient noradrenaline released at defective sympathetic endings for a pressor response to occur. However, the lack of rise of plasma noradrenaline following tyramine, except in the patients with pure autonomic failure, clearly separates these responses from those of normal subjects. These results can be explained by the presence of lesions of both central and peripheral sympathetic pathways in patients with chronic autonomic failure and multiple system atrophy or Parkinsonism. The peripheral lesion, which is incomplete, may consist of replication of the receptors so causing supersensitivity with a duration of response that is little prolonged. The peripheral defect in the two patients with pure autonomic failure was found to be more complex and the prolonged response in one of these patients suggests the possibility of defective re-uptake or metabolism of noradrenaline. Clearly further study of the defects of sympathetic endings is required, including the use of other techniques such as catecholamine fluorescence. The extreme supersensitive responses underline the need for blood pressure monitoring during pressor drug studies prior to treatment, if the hazards of recumbent hypertension are to be avoided.

Adult↗
PubMed1978

Pressor amines and monoamine-oxidase inhibitors for treatment of postural hypotension in autonomic failure. Limitations and hazards.

The short-term effects of pressor amines were investigated in four patients with postural hypotension caused by autonomic failure. In supine patients p-tyramine alone or with a monoamine-oxidase inhibitor produced pronounced supine hypertension without abolishing the symptoms associated with a postural fall in blood-pressure. Phenylephrine or ephedrine maintained a normal blood-pressure on standing but caused supine hypertension. Thus the effects of p-tyramine with or without a monoamine-oxidase inhibitor were unpredictable and did not include relief of postural hypotension. Phenylephrine or ephedrine had some beneficial effect, but since all these drugs influence standing pressure only at the expense of pronounced supine hypertension, alternative therapy must be sought.

Aged↗