Somatostatin therapy of acute experimental pancreatitis.

Lankisch, P. G.; Koop, H.; Winckler, K.; Fölsch, Ulrich R.; Creutzfeldt, W.

doi:10.1136/gut.18.9.713

Cited by 77 publications

(26 citation statements)

References 16 publications

(20 reference statements)

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“…Simultaneous with the induc tion of pancreatitis, a bolus of somatostatin was given intravenously (15 pg/kg) and an infusion (15 pg/kg/h) was given for 5 h, until the last microsphercs had been injected. This dose is approximately 4 times higher than the normal clinical dose and almost similar to the dose used by Lankisch et al [13].…”

Section: Treatmentmentioning

confidence: 80%

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Microcirculatory Effects of Somatostatin in Acute Pancreatitis

Schröder¹,

Millard

Nakajima

et al. 1988

Eur Surg Res

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Somatostatin, a 28-amino-acid inhibitory polypeptide has been advocated for the treatment of upper gastrointestinal bleeding and acute pancreatitis. This study examines the effect of somatostatin in acute hemorrhagic pancreatitis in piglets (n = 12), weighing 8–12 kg. Six animals served as controls, and received only fluid resuscitation (0.9%, NaCl, 20 ml/kg/h). Six animals received somatostatin treatment consisting of a 15 µg/kg bolus i.v. given simultaneously with the induction of pancreatitis, and treatment continued with an intravenous infusion (15 µg/kg/h) for 5 h. Cardiac output, heart rate, blood pressure, arterial pO₂ hematocrit and serum amylase were recorded before and each hour during the experiment. Regional blood flow in the gastrointestinal area was measured using the microsphere method. The microspheres labelled with three different isotopes were administered before the experiment and at 2 and 5 h, respectively. There was a significant decrease in the cardiac output (p < 0.05) and an increase in systemic blood pressure in the somatostatin-treated group (p < 0.025). Pancreatic blood flow decreased by 43 % following somatostatin infusion. The decreases at 2 and 5 h were highly significant (p < 0.005). Blood flow to the mucosal but not muscular region of the stomach was decreased by somatostatin. This study suggests that somatostatin might be harmful in acute pancreatitis due to its adverse effects on pancreatic blood flow and cardiac output. However, somatostatin may be effective in reducing gastrointestinal bleeding. If the drug is used clinically, careful monitoring of the cardiac output is necessary.

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Section: Treatmentmentioning

confidence: 80%

“…Some report that so matostatin is beneficial whilst others show no effect of the drug [5,12,13,18]. No con trolled clinical studies have been performed using somatostatin in acute pancreatitis.…”

Section: Introductionmentioning

confidence: 99%

Microcirculatory Effects of Somatostatin in Acute Pancreatitis

Schröder¹,

Millard

Nakajima

et al. 1988

Eur Surg Res

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“…The main pancreatic duct was cannulated transduodenally with a flexible catheter (Intracath, P50, Becton-Dickinson, Parsippany, NJ) and 0.5 ml of 5% sodium taurocholate in saline was infused at a constant rate. In order to direct the solution to the pancreatic duct a clamp was applied to the proximal part of the hepatic duct during injection (8,9). Sham-operated groups were submitted to the same surgical steps as the experimental group except for the induction of acute pancreatitis and the animals were sacrificed 2, 4, 12, 24 and 48 h after the surgical procedure.…”

Section: Methodsmentioning

confidence: 99%

Hepatic damage during acute pancreatitis in the rat

Coelho

Machado

Sampietre

et al. 1997

Braz J Med Biol Res

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We studied the alterations in the metabolism of liver mitochondria in rats with acute pancreatitis. Male Wistar rats were allocated to a control group (group I) and to five other groups corresponding to 2, 4, 12, 24 and 48 h after the induction of acute pancreatitis by the injection of 5% sodium taurocholate into the pancreatic duct. Sham-operated animals were submitted to the same surgical steps except for the induction of acute pancreatitis. Mitochondrial oxidation and phosphorylation were measured polarographically by determining oxygen consumption without ADP (basal respiration, state 4) and in the presence of ADP (activated respiration, state 3). Serum amylase, transaminases (ALT and AST) and protein were also determined. Ascitic fluid, contents of amylase, trypsin and total protein were also determined and arterial blood pressure was measured in all groups. In ascitic fluid, trypsin and amylase increased reaching a maximum at 2 and 4h, respectively. Serum amylase increased at 2 h reaching a maximum at 4 h. Serum transaminase levels increased at 12 and 24 h. After 2 h (and also 4 h) there was an increase in state 4 respiration (45.65 ± 1.79 vs 28.96 ± 1.50) and a decrease in respiration control rate (3.53 ± 0.09 vs 4.45 ± 0.08) and in the ADP/O ratio (1.77 ± 0.02 vs 1.91 ± 0.01) compared to controls (P<0.05). These results indicate a disruption of mitochondrial function, which recovered after 12 h. In the 48-h groups there was mitochondrial damage similar to that occurring in ischemic lesion. Beat-to-beat analysis (30 min) showed that arterial blood pressure remained normal up to 24 h (111 ± 3 mmHg) while a significant decrease occurred in the 48-h group (91 ± 4 mmHg). These data suggest biphasic damage in mitochondrial function in acute pancreatitis: an initial uncoupled phase, possibly secondary to enzyme activity, followed by a temporary recovery and then a late and final dysfunction, associated with arterial hypotension, possibly related to ischemic damage.

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“…Initially, the effects in acute pancreatitis of intravenous administration of the native hormone, somatostatin, were investigated, and the results were inconclusive [27, 28, 29, 30, 31, 32, 33, 34, 35]. In some of the subsequent clinical trials with the synthetic analogue, the drug was administered subcutaneously [10, 11, 12].…”

Section: Discussionmentioning

confidence: 99%

Continuous Intravenous Octreotide Treatment for Acute Experimental Pancreatitis

Greenberg

Haddad²,

Kashtan³

et al. 1999

Digestion

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Background: The efficacy of octreotide, the synthetic analogue of the hormone somatostatin, for the treatment of acute pancreatitis is controversial. Octreotide has been commonly administered in subcutaneous bolus injections; however, continuous intravenous infusion may be advantageous for acute conditions. Methods: Acute experimental pancreatitis was induced in rats by intraparenchymal injections of 1 ml 10% sodium taurocholate, and octreotide (1 µg/kg/h, dissolved in physiological solution, intravenously was started 4 h later and continuously infused for 48 h. Physiological solution infusions, in identical volumes, were used in the controls. The following parameters were examined: mortality; macroscopic and histological damage; hematocrit; plasma pH; acid-base balance; serum glucose; calcium, and amylase. Results: Octreotide treatment had a striking effect on mortality: 8.3 versus 91.6% in the treatment and control groups, respectively (p < 0.001). Octreotide also ameliorated pancreatic edema and intestinal dilatation, and had significant beneficial effects on histopathological damage and the biochemical alterations which are associated with acute pancreatitis. Conclusions: Continuous intravenous octreotide infusion is a potentially efficacious therapeutic method for acute pancreatitis.

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Somatostatin therapy of acute experimental pancreatitis.

Cited by 77 publications

References 16 publications

Microcirculatory Effects of Somatostatin in Acute Pancreatitis

Microcirculatory Effects of Somatostatin in Acute Pancreatitis

Hepatic damage during acute pancreatitis in the rat

Continuous Intravenous Octreotide Treatment for Acute Experimental Pancreatitis

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