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Biomedical subjects

E Köhler

Publications and source records attributed to E Köhler.

At least 145 records · Page 8Linked to original sources
PubMed1975

Paradoxical glucagon response after stimulation with glucose and arginine in isolated pancreatic sand rat islets.

Isolated pancreatic islets of normoglycemic sand rats do not respond to 2.5 mM glucose with an enhanced glucagon secretion, which could be observed in normal Wistar rats. Arginine stimulates glucagon release in the presence of 2.5 mM glucose in Wistar rats as well as in sand rats. The secretion pattern is not caused by insulin deficiency since sand rat islets are characterized by an increased insulin secretion rate in vitro. This paradoxical glucagon secretion is not caused by a changed glucagon content but might be related to this species which is able to develop a diabetic syndrome spontaneously.

Animals↗
PubMed1975

[Animal experiments on the effect of triamterene and amiloride on heart and circulation and the toxicity of digoxin (author's transl)].

1. In anesthetized cats 2,4,7-triamino-6-phenyl-pteridine (triamterene) (5 mg/kg i.v.) causes a short-lasting increase in blood pressure, a decrease in heart rate, whereas the contractility (see article) remains unchanged. N-Amidino-3,5-diamino-6-chloropyrazinecarboxamide (amiloride) (5 mg/kg i.v.) causes a fall of blood pressure, an increase in heart rate, and an increase in contractility. 2. In cats the i.v. toxicity of digoxin is diminished by pretreatment with triamterene or amiloride; the arrhythmias and the cardiac arrest are significantly delayed in the course of an infusion of digoxin. In guinea-pigs a pretreatment with triamterene only delays the arrhythmias but not the lethal effect of digoxin or g-strophanthin. 3. In the isolated atria of the guinea-pig triamterene and amiloride (5 mug or 50 mug/ml) lowers the rate of contraction and prolongs the functional refractory period. The force of contraction is increased by triamterene and diminished by amiloride.

Amiloride↗
PubMed1975

Electronmicroscopy studies on the exocrine pancreas of Wistar-Rats following treatment with Streptozotocin.

In Wistar rats the intraveneous injection of streptozotocin (65 mg/kg body weight) caused a permanent hyperglycemia. After 5 days there were lesions in the exocrine parenchyme of the pancreas and its nerve fibers. Pathological changes were found in cytoplasm, cell membrane, nucleus and all other cell organelles, too. The zymogen granules remaining after extensive degranulation may disintegrate in two different ways: 1. Shrinking of the granules and formation of a hale between granule membrane and core, the electronic density of which is decreased; indistinct demonstrability of the granule membrane and finally its decomposition. 2. Shrinking of the granules, decrease of the electron density and either homogeneous or mainly peripheral arrangement of the disintegrated material of the granules; irregular shape of the granules and splitting of their membranes.

Animals↗
PubMed1975

[Streptozotocin diabetes in the rat with special reference to glucose utilization by the musculature].

The glucose utilization by different skeletal muscle tissues of short-term streptozotocin treated Wistar rats was studied both in vivo and in vitro. The findings permit the following statements: The reduced metabolic conversion of glucose is mainly the result of the diminished transport of glucose into the muscle cells. The utilization of the glucose taken up by the muscle cells for synthesis of glycogen is unchanged in the diabetic animals and can be stimulated by insulin correspondingly as in normal rats. The conversion of the glucose metabolized by the cells to lactate and the time course of the specific activity of glycogen and lactate lead to the conclusion that glycogenolysis in the muscles of streptozotocin diabetic rats during the incubation is enhanced.

Animals↗
PubMed1975

Insulin secretion of isolated islets of sand rats (Psammomys obesus) during adaptation on captivity.

In normoglycemic sand rats the insulin secretion of isolated islets was investigated dependent on the time of artificial nutrition in captivity. Whereas the islets of short-term adapted animals did not respond within 15 min with an enhanced insulin secretion after stimulation with 16.5 mM glucose or 10 mM arginine, prolongation of incubation time resulted in a significantly enhanced hormone release. An intraveneous glucose injection (1 g/kg body weight) 45 min prior to the excision of the pancreas caused an immediate insulin secretion of the isolated islets in response to glucose or arginine. Islets of sand rats adapted for more than 10 weeks to artificial nutrition responded immediately with an enhanced insulin release in contrast to the islets of short-term adapted animals. These differences could not be correlated to the insulin content, the A/B cell ratio, and ultrastructural alterations of the islets.

Adaptation, Physiological↗