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Biomedical subjects

R J Corrall

Publications and source records attributed to R J Corrall.

At least 91 records · Page 5Linked to original sources
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↗
PubMed1981

Autonomic neural control mechanisms of substrate and hormonal responses to acute hypoglycaemia in man.

The contributions of adrenergic and cholinergic mechanisms to recovery from acute hypoglycaemia induced by insulin (0.15 units/kg i.v.) were examined in eleven normal subjects, six subjects with a pre-ganglionic sympathectomy (adrenergic denervation) and six sympathectomized subjects given atropine (combined adrenergic denervation and cholinergic blockade). Blood glucose recovery was impaired only in the sympathectomized subjects given atropine. The blood lactate response was reduced and the rise in free fatty acids was delayed in both groups of sympathectomized subjects, in whom the normal rises of plasma cyclic AMP and noradrenaline were absent. The plasma pancreatic glucagon response was appropriate to the prevailing blood glucose concentrations in all three groups. The cortisol response was impaired and the pattern of ACTH secretion was abnormal in sympathectomized subjects given atropine. Growth hormone levels were higher in both sympathectomized groups. Blood glucose homeostasis was impaired during combined adrenergic denervation and cholinergic blockade. Glucagon secretion was activated independently of vagal control. In the sympathectomized group given atropine, the rise in plasma cortisol was blunted despite a greater degree of hypoglycaemia. A blockade of central cholinergic receptors producing impaired activation of ACTH secretion at hypothalamic level may explain, at least in part, this delayed restoration of normoglycaemia.

Adrenergic Fibers↗
PubMed1981

Hormonal and substrate responses during recovery from hypoglycaemia in man during beta 1-selective and non-selective beta-adrenergic blockade.

Recovery from acute hypoglycaemia induced by the injection of insulin has been examined in six human subjects under control conditions, under non-selective beta blockade (propranolol) and under selective beta 1 blockade (metoprolol). The normal blood glucose recovery was biphasic with an initial rapid and a slower subsequent phase of recovery. The early recovery mechanism was unaffected by either form of beta blockade, but with propranolol the late phase of recovery was significantly prolonged. Rises in blood lactate and plasma free fatty acids following hypoglycaemia were markedly reduced by propranolol but to a much lesser degree with metoprolol. The counterregulatory hormonal responses of glucagon, cortisol and growth hormone were augmented appropriately for the prolonged hypoglycaemia associated with propranolol. Non-selective beta adrenergic blockade with propranolol is associated with an impairment of the late phase of blood glucose recovery from hypoglycaemia. The possible mechanisms of this impairment are discussed.

Acetoacetates↗
PubMed1981

Syndrome of inappropriate ADH secretion concealed by hypokalaemia due to ectopic ACTH production.

A case is described of a patient with an oat cell carcinoma of the bronchus with moderately elevated levels of plasma corticotrophin (ACTH) and antidiuretic hormone (ADH). Ectopic secretion of ACTH induced severe hypokalaemia and concealed the effects of concomitant ADH secretion on renal function. Normal renal responsiveness was restored following correction of hypokalaemia. The hypokalaemia was associated with evidence of a marked increase in corticosteroid secretion but plasma ACTH concentrations did not show a proportionate elevation. Chromatographic studies on tumour extracts suggest that the presence of a large fraction of high molecular weight ACTH in plasma could explain this discrepancy.

Adrenocorticotropic Hormone↗
PubMed1980

Attenuation of the pancreatic beta cell response to a meal following hypoglycaemia in man.

The plasma concentration of C-peptide, insulin (IRI) and glucose was measured in 9 healthy subjects during insulin-induced hypoglycaemia followed by a meal. Identical observations were made in the same subjects after an equivalent period of fasting without hypolycaemia (control study). Endogenous secretion of insulin was suppressed following administration of exogenous insulin and this persisted long after the blood glucose concentration had returned to normal. After the meal the mean blood glucose rose to a peak of 8.4 +/- 0.3 mmol/l (mean +/- SEM) at 60 min and was still raised at 7.5 +/- 0.3 mmol/l at 120 min, compared with a peak value of only 5.1 +/- 0.2 mmol/l at 30 min after the meal in the control study. Following hypoglycaemia the mean plasma IRI rose from 8.3 +/- 1.3 mU/l to a delayed peak of 81.6 +/- 12.7 mU/l at 60 min and was 123.5 +/- 14 mU/l at 120 min post-prandially, compared with a peak of 72.4 +/- 0.5 mU/l at 30 min after the meal in the control study. Acute hypoglycaemia may thus induce in abnormal pattern of insulin secretion in response to a meal, with impaired carbohydrate tolerance in normal subjects.

Adult↗
PubMed1980

Increase in coagulation factor VIII activity in man following acute hypoglycaemia: mediation via an adrenergic mechanism.

Coagulation factor VIII activity has been assayed in nine normal volunteers before and after acute hypoglycaemia. In all subjects there was a rise in activity with a mean increment of 96%. Control studies using saline failed to demonstrate any change. In four subjects with pre-ganglionic sympathetctomy no increase in activity was observed. In the normal subjects the increase was blocked by propranolol but not by metoprolol, indicating mediation via beta2 receptors.

Acute Disease↗
PubMed1980

A simple low-magnesium diet.

Details are given of a semi-synthetic low-magnesium diet that provides adequate short-term nutrition. The diet is made up of proprietary foodstuffs and is suitable for short-term magnesium deprivation studies in man. After five days on the diet four subjects demonstrated a marked fall in urinary magnesium excretion.

Adult↗
PubMed1979

Familial pseudohyperkalaemia. A new syndrome.

Inherited pseudohyperkalaemia due to an abnormal red-blood-cell potassium leak was discovered in 16 of 28 relatives of a woman with pseudohyperkalaemia. Autosomal dominance seemed to account for inheritance of this abnormality. Affected subjects were not anaemic and had normal in-vivo plasma-potassium concentrations.

Adult↗
PubMed1979

Recovery mechanisms from acute hypoglycaemia in complete tetraplegia.

Acute hypoglycaemia has been achieved in tetraplegic subjects and in healthy controls using insulin. The recovery from hypoglycaemia has been followed by measuring appropriate substrate levels in blood. Abnormal responses of lactate and free fatty acid concentrations were observed; blood glucose recovery proceeded at a normal rate.

Adult↗
PubMed1978

Cardiac and respiratory standstill during sleep.

An obese man, with an attack of myocardial ischaemia, developed arrhythmias only when he was asleep. Episodes of sinus bradycardia occurred progressing to arterioventricular block and sinus arrest. These changes in the cardiac rhythm coincided with periods of sleep apnoea.

Apnea↗
PubMed1977

Stereospecificity of the hydrogen transfer catalyzed by human placental aldose reductase.

Placental aldose reductase (EC 1.1.1.21) was incubated with glucose in the presence of [4A-2H] NADPH prepared in the oxidation of [2-2H] isocitrate by isocitrate dehydrogenase (EC 1.1.1.42) or [4B-2H] NADPH prepared in the oxidation of [1-2H] glucose-6-phosphate dehydrogenase (EC 1.1.1.49). The sorbitol formed from [4A-2H] NADPH contained deuterium and from [4B-2H] NADPH it did not. Therefore, aldose reductase in an A-type enzyme.

Alcohol Oxidoreductases↗