Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 21 female Beagle dogs an experimental pancreatitis was induced by injection of bile into the pancreatic duct system. Beside controls, dogs received 62.5 micrograms/h cyclic somatostatin (SRIF) a continuous i.v. infusion starting with a bolus of 250 micrograms 15 minutes before or 2 hours after bile injection. Following blood parameters were determined: lipase, amylase, blood count, minerals, glucose, insulin, gastrin, secretin and CCK. Two controls died within 24 hours, the others were sacrificed after 48 hours. All pancreata were examined morephologically. The controls developed all clinical signs of acute hemorrhagic pancreatitis, whereas all SRIF-treated dogs were in much better general condition. Lipase and amylase increased in all groups. In the controls insulin, gastrin and secretin remained unchanged and CCK rose slightly. SRIF-treatment diminished insulin, CCK and the test meal-induced increase of secretin. At autopsy the pancreata of the controls were nearly entirely apoplectic. The SRIF-treated dogs showed less damage of the pancreas and no severe hemorrhagic necrosis was noted. The beneficial effect of SRIF cannot only be due to an interaction with intestinal hormones. An additional direct protective effect on the exocrine parenchyma is proposed to exist.
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PMID:Effect of somatostatin on bile-induced acute hemorrhagic pancreatitis in the dog. 39 59

Because somatostatin (SRIF) reduces exocrine pancreatic secretion, its effect on acute pancreatitis was investigated in rats. Linear SRIF reduced serum amylase and lipase but had no effect on pancreatic necrosis, oedema, leucocyte infiltration, and enzyme content. The mortality rate was not reduced. These results do not recommend the use of SRIF in the treatment of acute pancreatitis.
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PMID:Somatostatin therapy of acute experimental pancreatitis. 60 91

Somatostatin 28 (S-28), originating in gastrointestinal cells, is secreted into the circulation and increases in humans after ingestion of a mixed meal. To evaluate the possibility that the increased levels of S-28 post cibum might modulate the release of enzymes and bicarbonate from the exocrine pancreas, S-28 was infused intravenously into healthy volunteers to levels seen after food intake. During S-28 infusion, the output of lipase, trypsin, amylase, and bicarbonate stimulated by either exogenous cholecystokinin octapeptide or endogenous signals from intraduodenal administration of tryptophan or a mixture of amino acids was significantly reduced. It is concluded that S-28 released from the gut during food intake modulates pancreatic exocrine function in humans.
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PMID:Evidence for hormonal inhibition of exocrine pancreatic function by somatostatin 28 in humans. 135 58

The effects of somatostatin and alpha 1-adrenergic receptor agonists on cytosolic Ca2+ in striatal astrocytes from the embryonic mouse in primary culture have been investigated by microfluorimetry. Methoxamine or somatostatin induced a transitory increase in cytosolic Ca2+, but their combined addition led to a sustained increase in cytosolic Ca2+ which seems to be due to a Ca2+ influx since it was not observed in the absence of external Ca2+. Voltage-independent Ca2+ channels contribute to this process. Indeed, voltage-operated calcium channels are not involved since neither dihydropyridines nor La3+ were effective in suppressing the sustained cytosolic Ca2+ elevation. Moreover, depolarization by 50 mM KCl, which was ineffective alone, suppressed the effect of somatostatin observed in the presence of the alpha 1 agonist, methoxamine. The implication of arachidonic acid in the observed potentiation is suggested by the following observations: 1) arachidonic acid induced a sustained elevation of cytosolic Ca2+ similar to that evoked by the co-application of methoxamine and somatostatin; 2) the addition of ETYA, an inactive and non-metabolizable analogue of arachidonic acid suppressed the calcium plateau produced by the agonists. In addition, direct activation of PKC by an exogeneous diacylglycerol analogue allowed somatostatin alone to evoke a sustained elevation of cytosolic Ca2+. Therefore, methoxamine through the successive activation of PLC and PKC could allow a lipase, probably PLA2, to be stimulated by somatostatin. Since arachidonic acid has already been shown to trigger the opening of K+ channels and the formation of inositol phosphates, somatostatin, through the arachidonic acid-mediated hyperpolarization could increase the Ca2+ driving force and thus improve Ca2+ influx through the inositol phosphate gated channels.
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PMID:Synergistic regulation of cytosolic Ca2+ concentration by somatostatin and alpha 1-adrenergic agonists in mouse astrocytes. 136 95

The prophylactic effect of perioperative use of somatostatin on postoperative increase of pancreatic digestive enzymes was investigated in this double blind, randomized study. Thirty three patients undergoing pancreatic surgery because of chronic pancreatitis were divided randomly into two groups. Fifteen patients received somatostatin- (dose 125 micrograms/hour), 18 placebo-infusion, pre- and postoperatively for a total time of 48 hours. The level of serum amylase, lipase, gammaGT, calcium, creatinine and blood glucose was determined every 12 hours. In the placebo group the serum lipase and amylase increased significantly (p less than 0.001), while the calcium decreased. In the somatostatin treated patients only the lipase level increased significantly (p less than 0.01), while the amylase and calcium showed no significant changes compared to their initial values. The postoperative increase in serum enzyme levels is interpreted as being an indicator of pancreatic injury. These results suggest that the perioperative use of somatostatin has beneficial effect for the prevention of pancreatic enzymes increases, associated with pancreatic surgery or its complications in patients with chronic pancreatitis.
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PMID:[Somatostatin in the prevention of postoperative increase of pancreatic enzyme after pancreatic surgery]. 137 31

The effects of a long-acting somatostatin analog (SMS 201-995) were studied in an established model of acute necrotizing pancreatitis in rats. SMS 201-995, when given prior to induction of pancreatitis, decreased the mortality rate from 100% to 40% (P = 0.0001). When treatment was given after induction of pancreatitis, the mortality rate was 75% (P = 0.2). Administration of SMS 201-995 did not influence the serum concentrations of amylase markedly, but the lipase levels were significantly lowered (P less than 0.05). The low levels of serum insulin and the glucose level in whole blood were not influenced. The volume of ascitic fluid was reduced (P less than 0.01). Moreover, less peritoneal fat necrosis was seen, suggesting a reduction in toxic factors in the ascitic fluid. Treatment with SMS 201-995 prior to induction of pancreatitis caused a significant increase in the levels of circulating 6-keto-PGF1 alpha, the stable metabolite of prostaglandin I2 (P less than 0.01). The levels of thromboxane B2 and prostaglandin E2 did not change significantly. The present data support the hypothesis that SMS 201-995 is an activator of prostaglandin I2, thereby modifying the course of the disease.
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PMID:Effects of long-acting somatostatin analog (SMS 201-995) on eicosanoid synthesis and survival in rats with acute necrotizing pancreatitis. 138 Apr 26

In a double-blind randomized study, 30 patients received somatostatin infusion during ERCP and 30 patients placebo with the aim of evaluating whether somatostatin can reduce the incidence of injection pancreatitis. S-amylase, U-amylase and S-lipase were evaluated before, during and after (up to 48 hours) ERCP. C-peptide was also determined as a marker of the function of the endocrine pancreas. While no statistically significant effect of somatostatin in terms of amylase and lipase was to be found, somatostatin did significantly decrease c-peptide levels in plasma, indicating that the peptide inhibited beta-cell secretion. About 40% of patients in the somatostatin group and about 50% in the placebo group showed signs of injection pancreatitis (elevated levels of enzymes) and in both groups there are patients with clinically apparent pancreatitis.
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PMID:Can somatostatin prevent injection pancreatitis after ERCP? 138 Apr 75

This study evaluates the effect of the long acting somatostatin analogue octreotide on biochemical and clinical parameters of endoscopic retrograde cholangiopancreatography (ERCP) induced pancreatitis. Altogether 245 patients were randomised to receive either octreotide or isotonic saline. Octreotide (100 micrograms) was administered intravenously five minutes before ERCP and subcutaneously 45 minutes after ERCP. There were no significant differences in the median serum amylase and lipase activities at baseline, eight, and 24 hours after ERCP. Five patients (2%) developed clinical pancreatitis--three in the octreotide and two in the placebo groups. Excluding patients who developed pancreatitis, 43 (18%) developed abdominal pain after ERCP--21 in the octreotide and 23 in the placebo groups. There were no significant differences in the median serum amylase and lipase values between the treatment groups. None of the 52 patients who had therapeutic interventions developed pancreatitis. This study suggests that octreotide may not protect against ERCP induced pancreatitis.
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PMID:Does the somatostatin analogue octreotide protect against ERCP induced pancreatitis? 138 99

In a prospective trial 30 patients underwent pancreaticoduodenectomy (Whipple operation) for cancer. They were randomly assigned to receive Somatostatin (SST) (n = 15) or not (n = 15). SST was started at laparotomy with 250 micrograms/h and given over a period of 5 days. A small catheter, which was placed into the duct of the pancreatic remnant, gave access to the pancreatic juice. Volume, amylase, lipase and protein as well as bicarbonate outputs were analyzed. As regards endocrine function, insulin and glucagon plasma levels were measured. The nitrogen balance was calculated. A stimulation test was done on the fifth postoperative day. Six patients (3/3) were assessed as drop-outs. A significant reduction was found for volume, amylase, lipase, protein and bicarbonate with SST, this effect lasting for two days. Lipase however was reduced significantly for 5 days. Pancreatic exocrine function was reduced as well after stimulation, if SST was given. Insulin and glucagon were inhibited with SST, the latter more effectively. We found a positive nitrogen-balance as early as on the second postoperative day in the SST-group, whereas without SST this did not occur before the fourth postoperative day. This findings were significant on the third and fourth postoperative day. The inhibitoric effects of SST, which are demonstrated by our laboratory investigations, conform very well with a more favorable clinical course and a reduction of perioperative morbidity and mortality.
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PMID:[Effect of somatostatin on basal and stimulated exocrine pancreatic secretion after partial duodenopancreatectomy. A clinical experimental study]. 167 16

The effect of the long-acting somatostatin analogue, octreotide acetate (Sandostatin) on enzyme elevation after endoscopic pancreatography was studied in a prospective, randomized, double-blind trial. Sixty-three consecutive patients undergoing ERCP were randomly allocated to two group. In the control group, 34 patients received isotonic sodium-chloride, and in the treated group 29 patients received 0.1 mg of octreotide acetate subcutaneously before the pancreatography. After the endoscopy, amylase levels increased to pathological range in 15 of the controls and in 3 of the treated patients, whereas lipase levels showed a pathological rise in 17 of the controls and in 5 of the treated patients. A significant difference (p less than 0.01) was observed in the amylase and lipase changes between the two groups at 90 and 180 min after pancreatography. The enzyme levels showed at 90 min, mean +/- SD amylase: controls 540 +/- 185 units/liter, treated patients 261 +/- 108 units/liter; lipase: controls 304 +/- 98 units/liter, treated patients 198 +/- 88 units/liter. These findings suggest that the use of long-acting somatostatin analogue ameliorates the enzyme increases in the serum after endoscopic pancreatography.
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PMID:The effect of long-acting somatostatin analogue on enzyme changes after endoscopic pancreatography. 170 82


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