[An attempt at estimating the incidence of deaths in tonsillectomies].
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Biomedical subjects
Publications and source records attributed to J Marchand.
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The interrelationships between glucose and calcium in glucagon release were investigated using the dynamic system of the in vitro perfused rat pancreas. When calcium deprivation was induced in the presence of fixed concentrations of glucose prevailing throughout the experiments (3.3, 5.5, 8.3 and 16.6 mM), an enhancement of glucagon release invariably occurred, the shape and amplitude of such response differing in relation to the environmental glucose concentration. Such enhancement of glucagon release was readily reversible upon restoration of normal calcium levels. By contrast, during the period of calcium deprivation itself, glucagon release was little influenced by either raised (from 3.3 to 16.6 mM) or decreased (from 16.6 to 3.3 mM) glucose concentrations. These results clearly indicate that calcium plays, at least, a dual role - both inhibitory and permissive - in glucagon secretion, but the intimate mechanisms by which calcium exerts such a dual action are at present unknown.
The interrelationship between arginine and calcium in glucagon release was studied using the in vitro perfused rat pancreas. In the presence of a normal 2 mM calcium concentration, 10 mM arginine provoked biphasic glucagon release, the amplitude of such a response being inversely related to the glucose concentration of the perfusate. At the lowest 3.3 mM glucose concentration, and after prolonged (40 min) as well as short (10 min) periods of calcium deprivation, arginine-induced glucagon release was inhibited. These results clearly indicate that calcium is necessary for either the recognition or effectiveness of arginine as a stimulus to the alpha-cell. Taking into account this, as well as other data presently available in the literature, it is suggested that calcium plays a versatile role - permissive, inhibitory and stimulatory - in glucagon secretion. The intimate mechanisms by which calcium exerts such versatile actions in the alpha-cell remain to be elucidated.
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During calsium deprivation, the rate of glucagon release by the isolated perfused rat pancreas is positively related to the glucose concentration of the perfusion medium. It is suggested that such a paradoxical behavior, which is reminiscent of the abnormality of glucagon secretion recently disclosed in diabetic subjects, results from a perturbation in the normal structural and functional bridging between pancreatic alpha and beta cells.
A combined radioimmunoassay for glucagon and insulin in biological fluids is presented. It is based on the use of 131I-glucagon and 125I-insulin tracers and a charcoal-dextran separation procedure. Standard curves, sample determinations and recovery studies gave comparable results whether in the combined or individual assay for glucagon and insulin. The combined assay, especially if supported by a decoding and calculating computer program, offers the advantages that it requires a smaller volume of the material to be sampled, is more economical and less time-consuming.
Parathormone (0.15 U/ml) failed to affect the rate of glucagon and insulin release by the perfused rat pancreas exposed to glucose in either low (3.3 mM) or high (8.3 mM) concentration. Parathormone also failed to interfere with the suppressive effect of glucose (16.6mM) upon glucagon release and its stimulatory action upon insulin secretion. Likewise, the biphasic release of both glucagon and insulin evoked by arginine (10.0 mM) in the presence of glucose (8.3 mM) was unaffected by parathormone. These findings suggest that the endocrine pancreas may not be a target organ for any direct and immediate action of parathormone.
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