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Biomedical subjects

K Hengst

Publications and source records attributed to K Hengst.

At least 37 records · Page 2Linked to original sources

[Massive natriuresis and polyuria after triple craniocervical subarachnoid hemorrhage: cerebral salt wasting syndrome?].

A thirty-year-old male patient suffered subarachnoidal haemorrhage from an angioma positioned in the cranio-cervical transition. After rebleeding twice the patient developed a hydrocephalus internus malresorptivus and excessive natriuresis and polyuria, accompanied by depressed renin activity and extremely low aldosterone plasma levels. Neither fluid restriction and sodium substitution, nor administration of hydro-chlorothiazide/indomethacin affected natriuresis and polyuria. It was only after treatment with fludrocortisone-acetate/hydrocortisone that hyponatraemia and polyuria were resolved. At the same time a ventriculo-peritoneal shunt was applied. Differential diagnosis excluded the syndromes of inadequate antidiuretic hormone secretion, renal and cerebral diabetes insipidus, osmotic receptor hypofunction, chronic renal dysfunction and tubular necrosis. Natriuresis and polyuria developed under dexamethasone therapy. Since patient history, physical examination and laboratory criteria could not explain the electrolyte and fluid imbalance, this might be attributed to the hydrocephalus. Similar disturbances have been reported from other patients with intracranial disorders. Mechanical pressure exercised on the hypothalamus might cause the disturbance of fluid and sodium balance. Assuming a cerebral salt wasting syndrome, a putative natriuretic factor coming from the brain or an imbalance in the cerebral renin-angiotensin-system, as described in rats and dogs, must be discussed.

Adult↗

[Determination of triiodothyronine in serum with a heterologous enzyme immunoassay: results of a group survey].

This paper summarises the results of the evaluation of a heterologous enzyme immunoassay in antibody coated tubes for the determination of triiodothyronine (T3) by a group of 11 laboratories. The assay procedure is analogous to an established heterologous thyroxine enzyme immunoassay. The evaluation demonstrated that 1. the specificity of the assay and its analytical range between 0.46 and 9.2 nmol/l meet diagnostic requirements, 2. the intra- and interassay precision was in accordance with that commonly found in radio immunoassays, 3. the recovery of added T3 was between 90 and 103%, 4. the results agreed well with those of self-established radio immunoassays and were comparable with commercial RIA kits, 5. there was no interference by hyperbilirubinaemia or by high concentrations of bile acids, but interference can occur in very haemolytic and lipaemic samples. The great advantage of T3 enzyme immunoassays lies in the absence of restrictions and any authorization needed for working with radioactive substances.

Evaluation Studies as Topic↗

Influence of somatostatin on carbohydrate absorption in human small intestine.

Oral carbohydrate tolerance tests with xylose, galactose and lactose were performed. After an interval of at least 24 h the same tests were repeated following an i.v. bolus and during infusion of somatostatin. Somatostatin does not influence xylose absorption. However, absorption of galactose and lactose is significantly reduced (p less than 0.01/0.008) during somatostatin infusion. On the other hand, serum levels of galactose remain unchanged despite administration of somatostatin, when galactose is given parenterally. The results support the assumption that the absorption process in small intestine is affected by somatostatin. Possible effects of somatostatin on hormones regulating the intestinal absorption and on energy-depending carrier mechanisms are discussed.

Adult↗

[On the influence of clanobutine on the formation of restraint ulcer in rats (author's transl)].

Prophylactic effect of 4-[(4-chlorobenzoyl)(4-methoxyphenyl)-amino]-butyric acid (clanobutine, Bykahepar) on restraint stress ulcer formation was studied in male albino rats. Number and size of ulcers were counted, pH value of gastric juice and plasma levels of corticoids, glucagon and blood sugar were measured. Rats treated with clanobutine had only the one-third of ulcers compared with the untreated animals. This effect was found to be dose-dependent. Clanobutine did not change plasma levels of corticoids, glucagon or blood sugar. Rise in pH value of gastric juice during stress exposition was found to be lower in clanobutine treated animals than in untreated controls. Blood flow in gastrointestinal tract was seen to be much better under the influence of clanobutine. The mechanism of action of clanobutine is discussed.

Animals↗

Leukocyte response to somatostatin in normals and patients with bacterial leukocytosis.

In normals and patients with acute bakterial leukocytosis synthetic somatostatin decreases cell count of stab neutrophils, neutrophils and eosinophils. After termination of somatostatin infusion a rebound phenomenon occurred. In healthy normals lymphocyte count increased during somatostatin infusion. This effect outlasts the end of infusion for more than 24 h. No significant effect could be demonstrated in patients with a bacterial leukocytosis.

Adult↗

Influence of somatostatin on peripheral leucocyte count and granulation tissue in man and rats.

Subcutaneous injection of synthetic protamin-zink-somatostatin completely prevents endotoxin-induced leucocytosis in normal rats. Piromen-induced elevated stab neutrophil, neutrophil and monocyte counts remain within the normal range during somatostatin administration. There is an inhibiting effect of synthetic protamin-zink-somatostatin on the wet weights of granulation tissue of cotton pellet granulomata, too. Incorporation of 35S-sulfate in sulfated mucopolysaccharides of granulation tissue in cotton pellet granulomata is not inhibited. Intravenous administration of synthetic linear somatostatin decreases stab neutrophil and neutrophil blood count in patients with acute bacterial leucocytosis. After the termination of somatostatin infusion a rebound phenomenon occurs. In healthy subjects lymphocyte count increases during somatostatin infusion. This effect can not be demonstrated in patients with bacterial leucocytosis.

Adult↗

Prophylactic effect of somatostatin on stress ulcer formation in rats.

The aim of the present study was to investigate the effect of somatostatin (growth-hormone release-inhibiting hormone) on ulcer formation during immobilisation stress. This was done in male Albino-rats to study the effect of somatostatin on number and size of ulcers, to calculate ulcer index, to measure pH-value of gastric juice as well as plasma levels of gastrointestinal hormones. Rats treated with somatostatin before and during stress exposition had only the third part of the ulcers compared with the untreated animals. Total ulceration area was less than the tenth of the untreated rats. Normal corticoid plasma levels during stress exposition were found in the lower range of normal values in somatostatin treated rats. Decrease of plasma gastrin during stress exposition exceeded the gastrin decrease of somatostatin treated rats. Rise of plasma glucagon was completely inhibited during somatostatin application. Results of serum glucose paralleled those seen in glucagon.

Animals↗

Inhibition of stress ulcer formation with somatostatin in rats.

Prophylactitc effect of somatostatin (Growth hormone inhibiting hormone) on restraint stress ulcer formation was studied in rats. Rats treated with somatostatin before and during stress had only the fifth part of the ulcers of the untreated animals after 9 hours of immobilisation. Pathophysiologic mechanism for stress ulcer production is as well discussed as the prohibiting effect of somatostatin on ulcer formation. Prophylactic clinical use has to be considered.

Animals↗

[Prolactin--a diagnostic aid in cerebral seizures].

Prolactin concentration was measured 20 minutes after each seizure in 8 patients with grand mal, 2 patients with complex partial seizures and 5 patients with petit mal seizures. In the group of grand mal and complex partial seizures serum prolactin showed markedly increased levels. After petit mal seizures there was no change in serum prolactin concentration. The possible causes for changes in serum prolactin after a seizure in children are discussed.

Adolescent↗