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Biomedical subjects

R L Himsworth

Publications and source records attributed to R L Himsworth.

70 records · Page 4Linked to original sources
PubMed1975

Effect of acute inhibition of adrenocorticotrophin secretion on plasma corticosteroids in the rhesus monkey (Macaca mulatta).

The half-life of plasma cortisol in the rhesus monkey (M. mulatta), determined by two methods, was about 130 min and longer than that in man; it was unaffected by administration of dexamethasone. Dexamethasone (5 mg, i.v.) immediately inhibited the secretion of ACTH from the monkey pituitary. The plasma half-life of NH2-terminal immunoreactive ACTH was found to be about 55 min which was much longer than the biological half-life. The adrenal synthesis of cortisol was inhibited by metyrapone which caused a prompt increase in the plasma concentration of ACTH and 11-deoxycortisol. The hypothalamic-pituitary-adrenal system of the rhesus monkey sedated with phencyclidine hydrochloride responded rapidly to alteration in the level of steroids in the circulation.

11-Hydroxycorticosteroids↗
PubMed1974

Cell-mediated immunity to intrinsic factor in autoimmune disorders.

Evidence of cell-mediated immunity to gastric intrinsic factor was present in 86% of patients with pernicious anaemia and in at least 13% of patients with hyperthyroidism, 21% of patients with atrophic gastritis, and four out of nine (46%) patients with hypogammaglobulinaemia. Controls gave negative results. The four patients with hypogammaglobulinaemia and cell-mediated immunity to intrinsic factor had evidence of impaired gastric function.

Agammaglobulinemia↗
PubMed1974

Hyperthyroidism induced by potassium iodide given in the course of 125I-fibrinogen test.

Hyperthyroidism developed in three patients during the administration of potassium iodide given for the purpose of blocking the thyroid uptake of radioactive iodine liberated in the course of the 125I-fibrinogen test. In a consecutive series of 31 geriatric patients, who received potassium iodide for the same reason, biochemical hyperthyroidism developed in three instances and significant depression of thyroid function was observed in 10. The performance and the interpretation of the 125I-fibrinogen test are unaffected if iodide is not administered to the patient. The possible hazards to some patients of either induced hyperthyroidism or faulty assessment of thyroid function may be greater than the risk of thyroid irradiation. It is suggested that for the performance of the 125I-fibrinogen test potassium iodide need not be given to the elderly and should be given in a dose of 30 mg daily for two weeks to younger patients. Under certain circumstances potassium perchlorate may be a preferable drug for preventing the accumulation of radioactive iodine by the thyroid.

Aged↗
PubMed1970

The location of the chemoreceptor controlling gastric acid secretion during hypoglycaemia.

1. The injection of 2-deoxy-D-glucose directly into the lateral hypothalamic area of rats, but not elsewhere, caused a prompt and sustained secretion of acid by the stomach at a rate comparable to that due to insulin hypoglycaemia.2. Acid secretion provoked by such injections, like that resulting from hypoglycaemia, could be stopped by raising the plasma glucose concentration by the intravenous infusion of glucose.3. Unilateral intrahypothalamic injection of 2-deoxy-D-glucose activated both vagi for, although cutting one vagus reduced the secretion, division of both was necessary to abolish it.4. Gastric acid secretion evoked by a systemic stimulus (insulin-induced hypoglycaemia or intravenous 3-O-methylglucose) could be prevented by inactivating the lateral hypothalamic area on each side with phenol or lignocaine.5. It is concluded that there exists in the lateral hypothalamic area a chemoreceptor, responsive to a lack of metabolizable glucose, which can initiate and sustain the vagally mediated secretion of acid by the stomach.

Animals↗
PubMed1970

Hypothalamic control of adrenaline secretion in response to insufficient glucose.

1. The rise of plasma glucose consequent upon the release of adrenaline following the systemic administration of 3-O-methylglucose is prevented by previous infiltration with lignocaine of the lateral hypothalamic area on both sides.2. The similarity between this effect and that of the same procedure in preventing the hypersecretion of gastric acid in response to the same stimulus, together with the known fact that hypoglycaemia or the systemic administration of some glucose analogues produce both gastric and adrenal medullary hypersecretion, provides strong presumptive evidence that there exists in the lateral hypothalamic area a chemoreceptor which controls the release of adrenaline. The cells of this receptor like those of the chemoreceptor controlling gastric acid secretion, are activated by an insufficiency of metabolizable glucose.

Adrenal Medulla↗
PubMed1969

The secretion of gastric acid in response to a lack of metabolizable glucose.

1. The onset of the secretion of acid from the stomach of rats during insulin-induced hypoglycaemia has been found to correspond to a mean plasma glucose concentration of 72 mg/100 ml. (equivalent to a blood glucose concentration of 44 mg/100 ml.).2. Infusions of the non-metabolizable sugar, 3-O-methylglucose, into rats with denervated adrenal glands caused a large and sustained rise in the gastric acid output. This gastric acid secretion could be prevented by prior vagotomy or stopped, when previously established, by cutting the vagi or by the administration of glucose.3. A consistent relationship was demonstrated between the plasma concentration of glucose and the total concentration of glucoses (glucose plus 3-O-methylglucose) in the plasma at the onset of gastric acid secretion during the infusion of 3-O-methylglucose into these rats. The theoretical basis for this relationship is discussed.4. 3-O-methylglucose did not cause the release of gastric acid when infused into rats with intact sympathetic nervous systems owing to the effects of the secretion of adrenaline provoked by this agent.5. The qualitative and quantitative similarities between the factors governing both the secretion of gastric acid and the release of adrenaline in the absence of a sufficiency of metabolizable glucose are discussed. It is suggested that the reactions of both these systems under such circumstances are determined by chemoreceptors which possess identical characteristics.

Adrenal Glands↗
PubMed1969

Factors which determine the gastric secretory response to 2-deoxy-D-glucose.

The physiological factors which determine the penetration of the brain by 2-deoxy-D-glucose have been studied and the practical importance of the blood-brain barrier has been demonstrated. The evaluation of the gastric secretory response to 2-deoxy-D-glucose has been shown to depend upon the plasma glucose concentration. It is concluded that because of the hazards and uncertainties in the use of 2-deoxy-D-glucose in man its use is to be deprecated.

Animals↗
PubMed1968

Compensatory reactions to a lack of metabolizable glucose.

1. Following the injection of adrenaline into rats pre-treated with thyroxine, there is a pronounced and prolonged increase in their oxygen consumption. On this basis a method is described for following increases in the rate of secretion of adrenaline in response to physiological stimuli in rats.2. Using this method the onset and the cessation of the increased rate of secretion of adrenaline during insulin induced hypoglycaemia has been found to correspond to a blood glucose concentration of approximately 40 mg/100 ml.3. 3-Methylglucose (3-O-methyl-D-glucopyranose) is shown to cause a marked and sustained increase in the blood glucose concentration.4. This action of 3-methylglucose can be accounted for by an increase in the rate of secretion of adrenaline, as it is accompanied by a rise in oxygen consumption in thyroid treated rats and is prevented by interruption of the central nervous connexions of the adrenal medulla.5. These findings can be explained by 3-methylglucose's acting upon the receptor which reacts to insulin hypoglycaemia by bringing about the secretion of adrenaline. It is shown that the effective stimulus to this receptor is not a low blood glucose concentration. The stimulus is possibly a depressed rate of utilization of glucose by the receptor tissue.

Animals↗
PubMed1968

Interference with the metabolism of glucose by a non-metabolizable hexose (3-methylglucose).

1. It having previously been shown that the injection of the non-metabolizable sugar, 3-methylglucose, into normal rats provokes the release of adrenaline with consequent hyperglycaemia, the effect of 3-methylglucose upon the metabolism of glucose was investigated. In rats, whose adrenal glands had been denervated by transplantation, 3-methylglucose reduced the oxidation of glucose by 46%. A reduction of this magnitude cannot be accounted for unless the oxidation of glucose by the brain is depressed.2. The lowering of the blood glucose concentration of adrenalectomized rats by insulin was prevented by the prior administration of 3-methylglucose.3. 3-Methylglucose retarded the movement of a glucose load from the blood into the tissues.4. The results of these experiments are consistent with competition between glucose and 3-methylglucose for the glucose transfer system at cell surfaces.5. The similarity between the effects upon cerebral metabolism of hypoglycaemia and the interference by a non-metabolizable sugar with glucose transport into the brain, is discussed.

Adrenal Glands↗
PubMedDate not supplied

Studies on the antigenicity of human thyroglobulin.

Human iodothyronine-binding auto-antisera were used to define a thyroxyl containing antigenic site on thyroglobulin. The peptide sequences flanking the thyroxyl residue are important antigenic determinants of this region and only one such thyroxyl seems to be exposed on the thyroglobulin molecule. Apparent specificity for binding of free thyroxine or triiodothyronine by these auto-antibodies does not necessarily imply the presence of either one or the other in the immunogen.

Antigens↗