Lack of hypophosphatemic effect on glucose uptake, lactate and pyruvate release by the normal rat perfused hind-limb.
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Biomedical subjects
Publications and source records attributed to F Peña.
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Captivity decreased tolerance to glucose and increased blood serotonin levels in 6 normal dogs investigated. Return to freedom brought normalization in the glucose tolerance test and reverted blood serotonin to control levels.
Pre-treatment with low doses of sulpiride, an atypical dopaminergic blocking agent, but not haloperidol, a classical dopaminergic blocking agent, decreased tolerance to glucose and increased blood serotonin levels in 6 normal humans and 6 normal dogs investigated.
Over five years, 105 patients with hepatic echinococcosis were studied. Plain radiographs of the hepatic area yielded the correct diagnosis in 35% of patients. Intravenous viscerograms were diagnostic in all but 14 of the patients (an accuracy of 83%). Computed tomography was performed in 19 cases and proved the most efficient of the techniques--it was diagnostic in all 19 cases. The radiological signs of this entity are discussed.
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Dihydroergotamine (dhe) (or phentolamine), an alpha-adrenergic blocking agent, induced important changes on the CCK-stimulated gallbladder emptying of 70 volunteer subjects. Two cholecystograms were performed with 10-day intervals in each subject. The first cholecystogram showed gallbladder emptying provoked by a test meal (35 subjects or by 0.5 U. CCK Kg. injected intravenously (35 subjects). During the second cholecystogram 1 mg. of DHE was injected intramuscularly 45 minutes befor the cholecystokinetic stimulus. The drug counteracted the gallbladder emptying induced by both endogenous and exogenous CCK. The effect was more pronounced when DHE was administered prior to the test meal stimulus than before CCK administration. This difference could be explained by a delayed gastric emptying induced by the alpha-adrenergic blockade. Our results suggest that the lack of gallbladder emptying could be due to the relaxation of this organ, in addition to a duodenal spasticity induced by DHE (or phentolamine).
Low doses of d-amphetamine plus propranolol rapidly improved the abdominal pain in 165 "spastic colon" patients. Concomitantly, these drugs reduced the sigmoidal hypertonicity and the rectal inhibition found in the manometric studies performed in some of those patients. The sigmoidal tone and phasic activity were also decreased by anticholinergic drugs. These results suggest that a cholinergic-serotonergic hyperactivity of the myenteric plexus may be responsible for the "spastic colon" syndrome.
Isolated perfused fed rat livers spontaneously liberated glucose and orthophosphate to the medium; 24-hr fasted rat livers did not exhibit these phenomena. In perfused fed rat livers, glucagon (2 mug) increased glucose output and promoted orthophosphate incorporation. In perfused fed rat livers, insulin (250 or 500 mU) inhibited the spontaneous liberation of glucose and orthophosphate. Comparable doses of insulin significantly reduced the glucagon (2 mug)-induced increase in glucose output from perfused fed rat liver, but did not affect orthophosphate uptake by the organ.
The present study was aimed at observing the effect on insulin secretion of serotonin (5-HT) administered intraportally to anesthetized adult dogs. The influence of 5-HT on insulin release was also studied in mouse pancreatic islets isolated by a collagenase method. In the in vivo studies, 6 mg of 5-HT rapidly injected in the portal vein of dogs induced hypoglycemia, and a significant increase of immunoreactive insulin plasma levels (IRI) in blood samples taken from the pancreatoduodenal vein. The phenomenon was registered throughout three consecutive 10 min periods after serotonin administration. With 3 mg of 5-HT the IRI increases were not observed. When serotonin was slowly infused at doses of 3 and 6 mg, no increases of IRI were recorded. In the in vitro studies, 5-HT at 100 mug/ml stimulated the output of insulin in the presence of a low concentration of glucose (0.6 mg/ml); when the islets were incubated with glucose at a higher concentration (3.0 mg/ml) there was a lower insulin release in the presence of serotonin (100 mug/ml) than that obtained with glucose alone at the same concentration (3.0 mug/ml). The results obtained suggest that serotonin stimulates insulin release under certain conditions in the intact dog and also in the isolated pancreatic islets of the mouse incubated in vitro.
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