Search PubMed⌕ Search

Biomedical subjects

B M Frier

Publications and source records attributed to B M Frier.

At least 199 records · Page 11Linked to original sources
PubMed1984

Autonomic neural control mechanisms and the release of adrenal steroids after hypoglycaemia in man.

The changes in blood glucose, plasma potassium, plasma renin activity, aldosterone, cortisol, corticosterone and ACTH were measured in 11 normal subjects, 6 tetraplegic subjects (pre-ganglionic sympathectomy) and 6 tetraplegic subjects given atropine (sympathectomy with cholinergic blockade), in response to acute insulin-induced hypoglycaemia. After hypoglycaemia, blood glucose recovery was impaired only in the tetraplegic group given atropine in whom ACTH secretion was delayed and the peak cortisol and corticosterone concentrations were lower compared with the other groups. Plasma renin activity rose both in the normal and the tetraplegic subjects; the aldosterone rise and the fall in potassium were similar in all three groups. Aldosterone release after hypoglycaemia appears to occur independently of stimulation of the sympatho-adrenal system and cholinergic blockade, and may result from activation of the renin-angiotensin system, rather than from ACTH stimulation. Activation of ACTH secretion in response to hypoglycaemia may involve a cholinergic mechanism at the hypothalamic level, with a consequent reduction in the increments of plasma cortisol and corticosterone after atropine administration.

Adrenal Cortex Hormones↗
PubMed1984

The influence of adrenergic denervation on the response to feeding of the gastroenteropancreatic system in man.

The effect of adrenergic denervation on the metabolic and hormonal response to a standard meal was studied in six tetraplegic subjects (pre-ganglionic sympathectomy) and compared with six normal subjects. Gastric emptying, estimated by isotope scintiscanning, was similar in both groups. Following the meal the mean blood glucose and plasma insulin rose in both groups, but were higher and remained elevated for longer in the tetraplegic subjects. There were no significant differences in the secretion of pancreatic glucagon, enteroglucagon, gastric inhibitory peptide (GIP) and neurotensin between the two groups. The mean basal and post-prandial levels of pancreatic polypeptide and motilin were significantly higher in the tetraplegic group. This study confirms the presence of mild glucose intolerance in tetraplegic subjects which is not explicable on the basis of abnormal insulin or pancreatic glucagon secretion or abnormal gastric emptying. In addition the results provide evidence for a sympathetic inhibitory influence on the secretion of pancreatic polypeptide and motilin in man, which is probably adrenergically-mediated.

Adult↗
PubMed1984

Diabetes and insurance: a survey of patient experience.

A survey of 186 diabetic patients examined their collective experience of life and motor insurance. Some form of life insurance policy had been obtained by 150 patients, with a combined total of 204 policies, 107 of which had been agreed before the diagnosis of diabetes. Most patients had declared diabetes to the insurer but 12 patients had been refused acceptance. Only 15 patients sought alternative quotations. The premium had been loaded by 10-40% for 36 patients because of diabetes, and 48 required a medical report. Of 147 diabetic drivers, 95 (65%) had declared diabetes either to the Licensing authority, or to the motor insurer, but only 62 (42%) had informed both. Fourteen patients had been refused motor insurance cover by individual companies, and 36 patients were aware of having had their premium increased, but only 16 patients had sought alternative quotations. Major differences in attitude with regard to diabetes as a risk factor for insurance are evident, and patients should be advised to approach several companies when seeking insurance cover.

Accidents, Traffic↗
PubMed1984

Pharmacokinetics of human insulin zinc suspension (recombinant DNA) in normal man: a comparison with porcine insulin zinc suspension.

A single dose crossover study in 10 fasting, non-diabetic men compared the 24-hour profiles of blood glucose, plasma insulin, and C-peptide following a single subcutaneous injection of either human insulin zinc suspension crystalline (recombinant DNA), or highly purified porcine insulin zinc suspension (mixed), in a standard dose of 0.2 U/kg. Both insulins produced moderate hypoglycaemia within 3 hours which persisted for 24 hours after administration. The rate of fall of blood glucose was similar from 0-3 hours but was significantly lower after the porcine insulin at 4 and 7 hours (p less than 0.05). Mean plasma insulin values were higher after porcine insulin between 2 and 6 hours (p less than 0.05) and a biphasic pattern was observed following injection of both insulins. Plasma C-peptide declined after each insulin was administered, and was significantly lower between 2 and 7 hours after porcine insulin. The duration of the hypoglycaemic action of human crystalline insulin (recombinant DNA), assessed by blood glucose measurements and C-peptide suppression, was equivalent to porcine insulin zinc suspension (mixed) (Monotard MC, Novo) over 24 hours.

Adult↗
PubMed1983

Cholinergic manifestations of the acute autonomic reaction to hypoglycaemia in man.

1. The effects of insulin-induced hypoglycaemia on pupil size, parotid salivary secretion and sweating were studied in seven normal volunteers. 2. Hypoglycaemia was associated with an acute stimulation of parotid salivary secretion and of sweating, synchronous in onset with the rise in heart rate. There was no clear evidence of concurrent pupillary constriction.

Acute Disease↗
PubMed1983

Peripheral blood cell changes in response to acute hypoglycaemia in man.

Peripheral white and red blood cell changes were studied in response to acute insulin-induced hypoglycaemia in six normal, six splenectomized and five sympathectomized (tetraplegic) subjects. The normal subjects were restudied during beta (propranolol) and beta 1-selective (metoprolol) adrenergic blockade. In the normal subjects a lymphocytosis immediately followed the acute hypoglycaemic reaction (R) with a neutrophilia 2 h later. The early lymphocytosis was absent in sympathectomized subjects (P less than 0.001) and reduced under beta blockade (P less than 0.02) in normal subjects, indicating mediation via an adrenergic mechanism. The later neutrophilia from R + 60 min was not abolished by adrenergic blockade or preceding sympathectomy; the enhanced response with propranolol was associated with an elevated plasma cortisol. Haemoglobin, packed cell volume and total erythrocyte count rose maximally at R in all groups except the sympathectomized subjects in whom all parameters declined progressively from basal values. These peripheral erythrocytes changes appear to be mediated via an adrenergic mechanism which is unaffected by beta adrenergic blockade and which does not involve splenic contraction.

Acute Disease↗
PubMed1982

Is testicular endocrine function abnormal in young men with spinal cord injuries?

Plasma concentrations of FSH, LH, testosterone and prolactin have been studied in seventeen men, aged 19 to 38 years, with traumatic paraplegia. Plasma testosterone, FSH and LH values were normal in all patients. The median LH concentration in patients was significantly higher (P less than 0.05) than in controls but there was no difference for FSH or testosterone. Plasma prolactin was high in five patients and the median prolactin concentration in patients was significantly greater (P less than 0.001) than in controls. It is concluded that there is no evidence of primary testicular failure in young paraplegics but it is possible that testicular hypofunction in some paraplegics may be related to increased prolactin production.

Adult↗
PubMed1982

The effect of adrenergic and cholinergic mechanisms on the secretion of pancreatic polypeptide and gastrin following hypoglycaemia in man.

The changes of plasma pancreatic polypeptide (PP) and plasma gastrin following acute insulin-induced hypoglycaemia (0 . 15 U/kg) were examined in six normal subjects, six tetraplegic subjects (preganglionic sympathectomy) and six tetraplegic subjects given atropine (combined adrenergic denervation and cholinergic blockade). Adequate hypoglycaemia was achieved in all three groups. The normal rise of plasma PP following hypoglycaemia was present in the tetraplegic group without atropine but was abolished in the tetraplegic subjects given atropine. There was no significant rise in plasma gastrin following hypoglycaemia except in the tetraplegic group given atropine. These results confirm that the secretion of PP in response to acute hypoglycaemia is mediated via cholinergic activity, while gastrin secretion appears to be inhibited in normal subjects by a vagal cholinergic mechanism.

Adult↗
PubMed1981

Why palpate the radial artery?

The palpability of the radial-artery wall was assessed before death in 43 patients and compared with the histology of the artery at necropsy. There was no relationship between the degree of palpability and the histological changes of atheroma or of Mönckeberg's sclerosis, or the presence of clinical vascular disease. It is suggested that palpation of the wall of the radial artery provides no useful clinical information.

Aged↗
PubMed1981

Acute hypoglycemia in man: neural control of pancreatic islet cell function.

Acute hypoglycemia is associated with stimulation of the pancreatic alpha cells and a concurrent, prolonged suppression of insulin secretion by the beta cells. The islets receive a rich autonomic innervation and may therefore be subject to control by adrenergic and cholinergic mechanisms. The role of such neuroregulation of pancreatic islets in response to hypoglycemia has been examined in normal subjects, in subjects with a preganglionic sympathectomy due to traumatic tetraplegia, and in tetraplegic subjects given atropine to induce effective dual autonomic denervation. The normal rise of plasma norepinephrine following hypoglycemia was absent in both groups of tetraplegic subjects, providing evidence of a complete sympathectomy. Blood glucose recovery was significantly impaired only in the group of tetraplegic patients given atropine. Changes in plasma C-terminal glucagon-like immunoreactivity (C-GLI) and C-peptide immunoreactivity (CPR) following hypoglycemia were commensurate with blood glucose levels and were not significantly influenced by islet denervation. These observations suggest that neuroregulation of human islet cell function in response to hypoglycemia may be of limited importance and that stimulation of glucagon secretion may occur independent of cholinergic vagal control.

Acute Disease↗
PubMed1981

Changes in plasma renin activity after hypoglycaemia in sympathectomized man.

1. The changes in blood glucose, plasma noradrenaline and plasma renin activity were measured in 11 normal subjects and in six tetraplegic subjects with a transection of the cervical spinal cord (preganglionic sympathectomy), in response to acute insulin-induced hypoglycaemia (0.15 unit/kg). 2. After hypoglycaemia, a pronounced rise in plasma noradrenaline was observed in the normal subjects but was absent in the tetraplegic group; plasma renin activity increased markedly in both groups. 3. It is concluded that the stimulation of renin release in response to hypoglycaemia can occur independently of any activation of the sympathoadrenal system.

Adult↗
PubMed1981

The mechanism of abnormal pancreatic beta cell response to food following acute hypoglycaemia in man.

Following acute insulin-induced hypoglycaemia, an abnormal pattern of insulin secretion in response to a meal has been demonstrated in six healthy volunteers. This is characterized by an initial impairment in insulin secretion and late hyperinsulinaemia. Postprandial gastrointestinal hormone levels were normal following hypoglycaemia in these subjects. In four other subjects, the administration of intravenous glucose prior to the meal partially reversed the abnormal pattern of secretion. In two patients with a total pre-ganglionic sympathectomy, the pattern of blood glucose, plasma insulin and C-peptide was similar to that observed following hypoglycaemia in normal subjects. It is unlikely that an abnormal entero-insular axis or an elevation of plasma catecholamine levels are primarily responsible for this phenomenon. This effect of hypoglycaemia on postprandial insulin secretion may be caused by glucopenia of the pancreatic beta cells.

Blood Glucose↗