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Biomedical subjects

R A Chieri

Publications and source records attributed to R A Chieri.

17 recordsLinked to original sources

Studies on the dynamics and mechanism of glibenclamide-induced insulin secretion.

Sustained, 60-minute perfusion of glibenclamide (0.5, 1.5 and 10 mug/ml) elicits a one-phase insulin release profile, formed by a rapid secretion peak followed by a second peak with lower insulin levels than the former. Basal insulin secretion values are observed during the period comprised between 13 and 60 minutes of perfusion. Concurrent stimulation with glucose (100, 150, 200 and 300 mg%) plus glibenclamide (1 mug/ml) causes a marked rise in both phases of insulin secretion. The addition of glibenclamide does not modify the biphasic secretion pattern caused by maximal glucose concentration (400 mg%). The maximal values of both phases of secretion in the dose-response curve elicited by different glucose concentrations shift to the left when glibenclamide is added to the perfusate. The increase in insulin secretion caused by glibenclamide is not inhibited by puromycin. Both theophylline and phentolamine modify and increase the glibenclamide-induced insulin release pattern. Propranolol and imidazole inhibit glibenclamide-induced insulin release. Our results suggest that: 1. Glibenclamide increases beta cell sensitivity to glucose stimulation. 2. Glibenclamide and glucose induce secretion of insulin originating in the same compartment. 3. Modification of alpha and beta adrenergic receptors may modify glibodulate the beta cell response to glibenclamide.

Adrenergic alpha-Antagonists

Evidence for a hypophyseal factor that stimulates insulin secretion by the pancreas (insulotrophine?)

The continuous infusion of glucose (1 mg/kg/min) via the carotid artery in anesthetized dogs produced a biphasic pattern of insulin secretion. The first peak reached a maximum 3 min after glucose infusion and decreased to basal level at 7 min. As long as glucose infusion persisted a slow and maintained increase in insulin level in the pancreatico-duodenal vein was observed. The same amount of glucose infused in to the carotid arteries of hypophysectomized dogs, failed to induce any change in plasma insulin level. Plasma sample obtained from the jugular vein of dogs receiving glucose via the carotid arteries were infused into a second dog via the pancreatico-duodenal artery. One minute after the onset of infusion a rise in insulin was observed in the pancreatico-duodenal vein. The stimulating effect was not due to the high blood glucose level present in the jugular vein of dogs undergoing the cephalic glucose infusion. Infusion through the pancreatico-duodenal artery of a glucose solution at a concentration equal to the highest blood glucose level observed in the jugular vein did not evoke insulin secretion. Plasma samples obtained from the jugular vein of dogs receiving saline via the carotid arteries did not evoke insulin secretion when receiving into the pancreatico-duodenal arteries of dogs. Pancreatic infusion of plasma obtained from the jugular vein of hypophysectomized dogs infused glucose through the carotid arteries did not evoke any pancreatic response. These findings are demonstrative of the presence of a hypophyseal humoral insulin stimulating factor in the jugular vein of dogs receiving a cephalic glucose load.

Animals

[Animal experimental study on spasmolytic and analgesic activities of pramiverine, metamizole and their combination (author's transl)].

In two pharmacological in vivo tests a comparative study was performed on the spasmolytic and analgesic effects of 4,4-diphenyl-N-isopropyl-cyclohexylamine-hydrochloride (pramiverine, Sistalgin), metamizole and a combination of both active principles in equal dose ratio (1 : 1000). The results demonstrated that pramiverine showed a potent spasmolytic effect which was potentiated by the combination with metamizole, and that the positive analgesic effect of metamizole was fully displayed in the combination with pramiverine, but that for pramiverine alone no analgesic effect was detected.

Aminopyrine

Effect of cephalic glucose infusion on insulin secretion.

The continuous infusion of glucose (1 mg/kg/min) via the carotid artery in anesthetized dogs produces a biphasic pattern of insulin secretion. The first peak reaches a maximum 3 min after glucose infusion and drops to basal level at 7 min. As long as the glucose infusion persists a slow and mantained increase in insulin level in the pancreaticoduodenal vein can be observed. The same amount of glucose infused in the general circulation via the jugular vein provoked a different pattern of insulin secretion. Cerebral glucose infusion to vagotomized dogs also produced a two phase response to insulin secretion, but the levels reached in the first phase were lower that those observed in the normal dogs. The infusion of glucose, via the jugular vein, in vagotomized dogs, failed to induce any change in plasma insulin levels. Our data suggest that a glucose load to the brain induces pancreatic insulin secretion mediated partially by the vagus nerves. These results are also compatible with the hypothesis that a humoral factor could be involved in the pancreatic response.

Animals