Cytoprotection by Somatostatins

Usadel, K. H.; Kessler, Horst; Rohr, Gerhard; Kusterer, Klaus; Palitzsch, K. D.; Schwedes, U.

doi:10.1007/978-1-4684-5326-3_18

Cited by 10 publications

(10 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[38]; (4) the reduction of splanchnic blood flow, since changes in microcirculation or hemodynamic properties can lead to possible cyto-and organoprotective as well as stimulatory effect of somatostatin and its analogue on the RES further deterioration in the disease [21][22][23]. However, other authors found octreotide to protect against postis- [28][29][30][31][32][33][34][35][36][37][38][39][40][41], and (5) the continuation of pancreatic enzyme synthesis after the induction of the disease [35]. chemic reperfusion injuries [24].…”

mentioning

confidence: 99%

The Role of Octreotide and Somatostatin in Acute and Chronic Pancreatitis

et al. 1999

View full text Add to dashboard Cite

Acute pancreatitis may follow a mild or a severe course. Whereas mild or edematous pancreatitis is a self-limiting disease with a low complication rate and low death rate, morbidity and mortality in severe or necrotizing pancreatitis are still unacceptably high. The major problem is the lack of a specific drug, especially in the early phase of the disease, to interfere with the systemic inflammatory response syndrome and to limit or prevent complications of the disease. Although the initiating pathophysiological process is not known, the destruction of the gland (‘autodigestion’) by digestive enzymes may be responsible for disease progression. Inhibition of pancreatic activity, which reduces exocrine secretion and further prevents the release and activation of enzymes, was therefore suggested as a specific treatment concept. The results of clinical investigations using somatostatin or its analogue are controversial, since all these trials had low statistical power. In a recent multicenter randomized controlled study with a large number of patients (n = 302) (and an adequate level of disease severity), no benefit of octreotide on progression or outcome was found. Chronic pancreatitis is characterized by an irreversible destruction of the exocrine and endocrine pancreatic parenchyma leading to maldigestion and diabetes. Pain, which may be caused by increased ductal pressure, is one of the most dominant symptoms in chronic pancreatitis. However, no beneficial effects on pain with pancreatic exocrine secretion-inhibiting drugs have been demonstrated. Treatment of other complications of the disease (pseudocyst formation, fistula and pancreatic ascites), with somatostatin or octreotide has given conflicting results. However, in a prophylactic clinical setting (e.g. elective pancreatic surgery) the inhibition of exocrine pancreatic secretion reduces complications.

show abstract

mentioning

confidence: 99%

The Role of Octreotide and Somatostatin in Acute and Chronic Pancreatitis

et al. 1999

View full text Add to dashboard Cite

show abstract

“…A possible explanation is that as has been suggested [17], somatostatin may induce some cytoprotective mechanisms.…”

Section: Discussionmentioning

confidence: 89%

Treatment of secretory diarrhea in AIDS with the somatostatin analogue SMS 201-995

Füeßl¹,

Zoller²,

Kochen

et al. 1989

Klin Wochenschr

View full text Add to dashboard Cite

“…Our preliminary findings indicate that analogues of somatostatin reveal cytoprotective properties also under experimental in vivo conditions such as cerulein-or tauro-cholate-induced experimental pancreatitis, ethanolinduced gastric hemorrhagic erosions, and cysteamineinduced duodenal ulceration in rats [19]. These benefi cial effects were seen by the use of low doses of the ana logues.…”

mentioning

confidence: 78%

Hormonal and Nonhormonal Cytoprotective Effect by Somatostatins

Usadel¹

1988

Horm Res

View full text Add to dashboard Cite

Beside its known hormonal activity, somatostatin exerts cytoprotective action. Thus, its favorable effect on the course of experimental pancreatitis, liver and lung lesions, and gastric ulcerations cannot be explained solely on the basis of hormone-mediated mechanisms. Cytoprotection is only observed when somatostatin is administered prior to toxine exposure or tissue damage, and the structure/activity of the substance is important in determining this effect. Thus, the non-hormonal biological effects of somatostatin can be summarized as follows: (a) Natural somatostatin- 14 has been shown, in addition to its full endocrine effect, to block the uptake of toxic substances into liver cells, (b) Analogues with superactive cytoprotection may be devoid of endocrine activity. In turn, this effect is commonly found in the low-molecular derivatives, (c) Although the mechanism leading to tissue protection has not been clarified, stabilisation of cell membranes may play a role as well as changes in the aminoacid sequence.

show abstract

Cytoprotection by Somatostatins

Cited by 10 publications

References 21 publications

The Role of Octreotide and Somatostatin in Acute and Chronic Pancreatitis

The Role of Octreotide and Somatostatin in Acute and Chronic Pancreatitis

Treatment of secretory diarrhea in AIDS with the somatostatin analogue SMS 201-995

Hormonal and Nonhormonal Cytoprotective Effect by Somatostatins

Contact Info

Product

Resources

About