Untersuchungen zum kurativen Effekt von Somatostatin bei der akuten Pankreatitis

Usadel, K. H.; Schwedes, U.; Wdowinski, J. M.; Althoff, P. H.; Seiffert, U. B.; Raptis, Sotirios A.; Klempa, I; Strohm, W. D.; Leuschner, U.

doi:10.1007/978-3-642-85454-5_110

Cited by 3 publications

(2 citation statements)

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“…Prophylactic infusion of somatostatin before the Start of an Operation on the pancreas reduced the postoperative complications (147). Also, two studies have shown an impressive recovery from acute pancreatitis after treatment with somatostatin (148,149). For further investigation on somatostatin treatment in acute pancreatitis, a multicentre double-blind trial was started in 1980.…”

Section: Clinical Somatostatin Treatmentmentioning

confidence: 99%

Somatostatin — A Regulatory Peptide of Clinical Importance

Bethge¹,

Diel²,

Kh³

1982

CCLM

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Somatostatin was first discovered in the hypothalmus and has since been located in many parts of the central and periphefal nervous System, äs well äs in the pancreas and the gastrointestinal tract. Its main biological activity is to inhibit the action of somatotropin (growth hormone, STH, GH) and a number of other hormones. The therapeutic value of somatostatin has been demonstrated in the treatment of both acute bleeding gastric ulcers and acute pancreatitis. In additioii, the measurement of somatostatin in the blood is a useful method for the screening of somatostatin-produeing tumours. This paper reviews the location, action, clinical significance and measurement of somatostatin. Somatostatin-Ein Regulatorpeptid mit klinischer Bedeutung Zusammenfassung: Somatostatin, zuerst im Hypothalamus entdeckt, ist in vielen Teilen des zentralen und peripheren Nervensystems, im Pankreas und im Gästrointestinaltrakt lokalisiert. Seine biologische Hauptwirkung ist die Hemmung von Somatotropin (GH, STH) und einer Vielzahl anderer Hormone. Der therapeutische Wert von Somatostatin konnte bei der Behandlung von akuten Magenulkusblutungen und akuter Pankreatitis gezeigt werden. Die Somatostatin-Bestimmuiig im Blut stellt eine wertvolle Methode bei der Suche nach einem somatostatinproduzierenden Tumor dar. Die Lokalisation, Wirkung, klinische Bedeutung und Bestimmung von Somatostatin wird dargestellt. hormones control ädenohypophysis hormone secretion Schally (2); Luliberin (luteinizing-hormone-releasing (fig. 2). Certain of these hormones affect more than hormone, LHRH), isolated in 1971 by Schally (3); and one pitüitary hormone: e.g., thyroliberin causes the somatostatin, reported by Guillemiii in 1973 (4) and by release of thyrotropin (thyrotropic hormone, TSH) Schally in 1976 (5). Figure l shows the chemical struc-(l, 2) and prolactin (6); luliberin releases lutropin tures of these three hormones. (luteinizing hormone, LH) and follitropin (follicle-The tuberohypophyseal neurons are believed to syn-stimulating hormone, FSH) (3,7), and somatostatin thesize, transport, and release the hypothalamic hör-inhibits the secretion of somatotropin (4) and thyromones into perivascular spaces in the median eminence tropin (8).

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Section: Clinical Somatostatin Treatmentmentioning

confidence: 99%

Somatostatin — A Regulatory Peptide of Clinical Importance

Bethge¹,

Diel²,

Kh³

1982

CCLM

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“…Somatostatin has a beneficial effect on experimentally induced ulcers [5], pancreatitis [7,[9][10][11], and adrenal and lung lesions [6]. Very recently we found that somatostatin exerts a beneficial effect on the survival rate after alpha-amanitin intoxication in the rat [14] though no differences in DNA synthesis and liver enzymes were obvious.…”

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Beneficial effect of somatostatin in phalloidin-intoxicated rats

et al. 1981

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The effect of somatostatin in phalloidin-intoxicated rats was studied. Animals were given phalloidin i.p. 1.2 mg/kg (LD 90-100). Somatostatin, 250 microgram/animal, was administered i.p. in saline 5 min prior and s.c. in protamine-sulphate/ZnCl2 suspension 30 min prior and 30 min after intoxication, unless stated otherwise. In vivo and in vitro uptake studies of the toxin were performed. Liver enzymes (GPT, GLDH) and kallikrein-like activities were determined in blood obtained by orbital venipuncture. Light and electron microscopy was carried out. Somatostatin treatment led to an increase in survival rate. Of the 20 treated rats six died whereas of the 20 untreated animals 18 died. A dose dependency was proven effective when half of the initial dose of somatostatin was given. In vivo and in vitro uptake studies of the toxin demonstrate that somatostatin does not alter uptake rate by rat livers. Liver enzymes remained elevated in treated and control rats. Kallikrein-like activities showed a 61% decline in treated animals whereas they rose up to 120% in controls as compared to pretreatment conditions. Light and electron microscopy reveals less severe lesions in somatostatin-treated animals. A possible interaction of somatostatin in shock development is discussed, phalloidin seems to be a suitable tool for further investigations concerning cell protection by somatostatin.

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