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

Due to an apparently selective vasoconstrictive effect on the splanchnic circulation, somatostatin (SRIF) has been advocated for the treatment of variceal hemorrhage. The present study was designed to compare and contrast the systemic and splanchnic hemodynamic effects of SRIF and two of its long-acting analogs (SMS 201,995 and L 363,568) with those of Pitressin. Anesthetized pigs were subjected to laparotomy for placement of an electromagnetic flowmeter on the main trunk of the superior mesenteric artery (SMA). Systemic hemodynamic parameters of arterial blood pressure and cardiac output were monitored with thermodilution catheters. Portal venous blood was collected for measurement of plasma levels of SMS 201,995 and L 363,568 and for determination of gastrin levels during infusion of the latter analog. Experimental drugs were administered via an aortic cannula in a range (5-10 mg/kg bolus and 5-10 mg/kg/min continuous infusion) of dosages. At the higher dosages, SRIF, SMS 201,995, and L 363,568 decreased SMA blood flow (mean% +/- SD) 5.6 +/- 2.2, 1.6 +/- 4.4, and 8.0 +/- 3.8 after 10 min. None of the values achieved significance when compared to variation in baseline determinations. Pitressin (0.25 units, intravenously) produced a consistent and highly significant (P less than 0.001) reduction-in SMA flow after 5 min. Pharmacologic levels of SMS 201,995 and L 363,568 were reliably achieved in portal blood and the latter produced significant reduction (P less than 0.05) in portal venous levels of gastrin. SRIF and its long-acting analogs produced no significant splanchnic nor systemic hemodynamic effects in this model.
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PMID:Somatostatin and analogs lack splanchnic vasoconstrictive effects in anesthetized pigs. 289 Jul 95

Somatostatin has been widely employed in studies of hepatic metabolism to suppress the endogenous secretion of the pancreatic hormones, insulin and glucagon. The possibility of somatostatin having hepatic effects has been considered before, but not decisively demonstrated. Eleven anesthetized dogs were used to assess the effect of somatostatin on hepatic insulin extraction (HIE) and hepatic glucose production (HGP). Insulin was infused by peripheral vein alone and during somatostatin (800 ng/kg/hr) in one series (I) of experiments and in the reverse sequence in another series (II). Portal vein and hepatic artery blood flow were measured electromagnetically, and blood samples were taken from the hepatic artery, portal vein, hepatic vein and a peripheral vein. HIE was increased in the presence of insulin plus somatostatin infusion. The combined results in Series I and II were 72.0 +/- 3.0% compared in insulin alone (64.0 +/- 4.0%, p less than 0.01). HGP was decreased in the presence of insulin and somatostatin infusion compared to insulin infusion alone both in Series I and II (1.71 +/- 0.25 to 3.72 +/- 4.0%, combined results, p less than 0.01). Whether this reduction in HGP indicates a direct effect of somatostatin on the liver, in addition to the inhibition of glucagon secretion, remains to be clarified. However, a decrease in hepatic glucose production is consistent with increased insulin extraction during somatostatin observed in the present study. We conclude that somatostatin increases the hepatic extraction of exogenous insulin. This effect of somatostatin is associated with decreased hepatic glucose production.
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PMID:Somatostatin increases hepatic insulin extraction. 290 90

The effects of a liquid diet low in amines on gastrin cell and somatostatin cell functions were studied in the rat. Significant decreases in portal gastrin levels (44% at 5 days) were noted in animals maintained on a liquid diet (Vivonex). Refeeding solid rat chow resulted in a significant, but transient, hypergastrinemia. Portal somatostatin levels were significantly increased during ingestion of the liquid diet. With refeeding, portal somatostatin promptly returned to baseline values. Gastrin cell density decreased progressively during liquid diet ingestion (37% decline by Day 5). Antral somatostatin cell numbers were increased during this time period (86% versus controls). With solid chow refeeding, both gastrin cell and somatostatin cell densities returned to baseline.
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PMID:Effects of low amine diet on gastric endocrine cell proliferation in the rat. 290 Mar 48

Tissue and serum somatostatin levels were measured in genetically lean and obese Zucker rats. Immunoreactive somatostatin content was decreased in three central nervous system regions (hypothalamus, septum and preoptic area and thalamus) of obese rats but was increased in cerebral cortex. No differences were observed in antral or colonic somatostatin content but obese animals had significantly elevated pancreatic levels. Portal vein somatostatin-like immunoreactivity in contrast was significantly lower in obese rats. The widespread alterations in tissue and serum somatostatin-like immunoreactivity suggest either a diffuse abnormality of somatostatin physiology or a response to a generalised feature of the obese hyperinsulinaemic state.
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PMID:Tissue and serum somatostatin-like immunoreactivity in lean and obese Zucker rats. 610 93

To determine the effectiveness of glucagon suppression in improving glucose homeostasis in diabetes, tracer-determined glucose kinetics were measured during a 6-h somatostatin infusion in six alloxan-diabetic dogs (moderately severe diabetes) and five depancreatized dogs deprived of insulin treatment for 3 days (prolonged severe diabetes). Plasma immunoreactive glucagon (IRG) decreased 70 +/- 9% in the alloxan-diabetic and 80 +/- 4% in the depancreatized dogs. Portal vein levels of plasma immunoreactive insulin (IRI) fell (17.0 +/- 2.3 to 4 micro.5 +/- 0.4 microU/ml) as did peripheral vein IRI levels (6.7 +/- 0.9 to 4.7 +/- 0.5 microU/ml) in the alloxan-diabetic dogs. In the depancreatized dogs plasma IRI levels were undetectable. Plasma glucose concentrations fell (278 +/- 17 to 169 +/- 12 mg/dl) during IRG suppression in the alloxan-diabetic dogs due to a rapid and sustained decrease in glucose production (Ra) (6.0 + 0.9 to 3.6 + 0.3 mg X kg-1 X min-1). Glucose disappearance (Rd) decreased gradually (5.9 + 0.6 to 3.9 + 0.2 mg X kg-1 X min-1). In contrast, in the depancreatized dogs, IRG suppression did not alter glucose concentrations or kinetics. Thus, glucagon suppression decreased glycemia by decreasing Ra only in moderately severe diabetes. However, this was associated with decreased rather than improved glucose utilization. The ineffectiveness of glucagon suppression during prolonged severe diabetes could relate to the degree and duration of the metabolic derangement and/or indicate that the continuous presence of some insulin is necessary for glucagon suppression to improve glucose homeostasis.
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PMID:Glucagon suppression improves glucoregulation in moderate but not chronic severe diabetes. 613 57

Portal plasma immunoreactive secretin (IRS) concentrations, pancreatic juice flow, and amylase output were simultaneously measured in response to intraduodenal infusion of 1-phenyl-1-hydroxy-n-pentane (PHP), as well as infusion of hydrochloric acid (HCl). These data were compared with those obtained from intravenous bolus injections of synthetic porcine secretin in anesthetized rats. The intraduodenal infusion of PHP or HCl at a rate of 2 ml/min for 2 min produced a dose-related increase in portal plasma secretin concentrations, pancreatic juice flow, and amylase output. However, the mechanism of secretin release by PHP seems to differ from that of HCl. The secretin response to 0.1 N HCl infused at a rate of 0.1 ml/min for 30 min was complete after 10 min, despite continued infusion, while PHP stimulated a secretin release which persisted for 10 min after cessation of infusion. The pH in the second portion of the duodenum, following PHP infusion, remained consistently greater than 6.3. PHP-stimulated pancreatic exocrine secretions were only partially suppressed by somatostatin, while secretin release was almost completely inhibited. However, intraduodenal PHP may stimulate the release of secretin along with other gastrointestinal hormones, and the endogenous release of these hormones may not be inhibited by somatostatin.
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PMID:Pancreatic exocrine secretion and immunoreactive secretin release after intraduodenal instillation of 1-phenyl-1-hydroxy-n-pentane and HCl in rats. 616 34

In order to assess the interrelationships between stomach and pancreas regarding the secretions of somatostatin-like immunoreactivity (SLI), glucagon (IRG), and insulin (IRI), concentrations of the three hormones were assayed in portal plasma and portal blood flow was measured in enterectomized rats before and after the selective removal of stomach or pancreas. Portal plasma SLI, IRG, and IRI concentrations were significantly increased by i.v. arginine in control rats (pancreas + stomach present). After gastrectomy, SLI, IRG, and IRI concentrations were, respectively, 52 +/- 13% (N = 15; P less than 0.005), 234 +/- 40% (P less than 0.001), and 119 +/- 15% (NS) of the pregastrectomy values. A decreased SLI secretion, an increased IRG release, and an unmodified basal IRI release were estimated by portal flow measurement. The A- and B-cell responses to arginine in the gastrectomized rats were significantly higher than in the control rats, while the D-cell response was no longer detectable. After pancreatectomy, by contrast, SLI concentrations were 360 +/- 75% of the prepancreatectomy values (N = 12; P less than 0.001). This reflected an actual increment of SLI release, taking into account the concomitant measurement of portal blood flow. The concentrations of IRG declined by 51 +/- 5% (P less than 0.001) and IRI was no longer measurable. A- and B-cell responses to arginine also were no longer detectable. These results suggest that in these experimental conditions (1) the stomach restrained pancreatic A- and B-cell responses to arginine, perhaps through the SLI released from the stomach and (2) the pancreas restrained gastric SLI secretion, perhaps through insulin.
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PMID:Reciprocal gastropancreatic modulations for the release of somatostatin-like immunoreactivity, glucagon, and insulin in the rat. 634 73

The effects of acute stress on growth hormone (GH) secretion and the mechanisms involved in its changes have been investigated in sheep. An acute isolation-restraint stress induced a rapid and significant increase in jugular GH levels in 12 out of 14 rams. GH-releasing hormone (GHRH) and somatostatin secretion during the same stress were studied in 5 animals prepared for hypophysial portal blood collection. A 3.5-fold increase in portal GHRH levels was observed concomitantly with a slight elevation in portal somatostatin. Portal corticotropin-releasing hormone (CRH) and jugular cortisol plasma levels increased during the same stress. Our data suggest that an isolation-restraint stress stimulates GH secretion in the sheep and that GHRH may be responsible for GH response.
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PMID:Acute stress stimulates secretion of GHRH and somatostatin into hypophysial portal blood of conscious sheep. 781 15

This study was designed to investigate the effect of octreotide (Sandostatin, Sandoz), an analogue of somatostatin, on the hemodynamics and glucagon level in portal hypertension. Sixteen portal hypertensive rabbits produced by partial ligation of the portal vein two weeks earlier received an intravenous infusion of octreotide at a dose of 30 micrograms/h. After infusion of octreotide, a significant reduction in portal venous pressure from 16.2 +/- 3.9 mmHg (mean +/- SD) to 13.3 +/- 4.3 mmHg at 21 minutes and 12.0 +/- 4.5 mmHg 42 minutes was noted. A persistent decrease in portal pressure to 11.0 +/- 4.5 mmHg 21 minutes after stopping infusion of octreotide was also observed. Portal venous blood flow was decreased significantly from 60.9 +/- 13.1 mL/min to 46.9 +/- 15.0 ml/min at 21 minutes and to 45.8 +/- 12.8 ml/min at 42 minutes. A slight elevation of portal blood flow to 49.0 +/- 14.1 ml/min was noted 21 minutes after cessation of octreotide infusion. Portal venous resistance was slightly elevated during infusion of octreotide (before infusion: 2.2 +/- 1.4 dyne.s.cm-5, 21 minutes after infusion: 2.4 +/- 1.4 dyne.s.cm-5 and 42 minutes after infusion: 2.3 +/- 1.3 dyne.s.cm-5), and decreased (1.9 +/- 1.0 dyne.s.cm-5, p < 0.1) with a forward significance after stopping infusion. There were no significant changes in systemic arterial pressure during this experiment. A significant decrease (p < 0.05) in glucagon level from 323 +/- 93 pg/dl to 267 +/- 62 pg/dl at 21 minutes and to 298 +/- 88 pg/dl at 42 minutes in the portal vein was noted during the infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of octreotide on hemodynamics and glucagon levels in portal hypertensive rabbits. 785 49

The authors investigated whether combined treatment with the somatostatin analogue, SMS 201-995, and low-dose isosorbide dinitrate enhanced the hemodynamic effects of the individual agents on rats with thioacetamide-induced cirrhosis. Four groups of cirrhotic rats received SMS 201-995 (0.1 microgram.min-1.kg-1), isosorbide dinitrate (10 micrograms.min-1.kg-1), both agents, or placebo, respectively. Hemodynamics were measured serially in conscious rats, using a radioactive microsphere method. SMS 201-995 reduced portal venous inflow 21 +/- 4% and portal pressure 17 +/- 3%. Isosorbide dinitrate decreased portal venous inflow 20 +/- 4%, by inducing splanchnic vasoconstriction mediated by low pressure baroreflexes, and this agent also decreased portal pressure, by 14 +/- 2%. Portal venous resistance rose 7.6 +/- 3% with isosorbide dinitrate alone, but decreased 18 +/- 4% with combination therapy. This effect may have been induced by the pronounced vasodilatory effect of isosorbide dinitrate on the venous vasculature, since the reflex splanchnic vasoconstriction that occurs with low-dose isosorbide dinitrate disappears when this agent is combined with SMS 201-995. The decrease in portal pressure was more marked (22 +/- 4%) and changes in systemic hemodynamics were milder with the combined treatment. It was concluded that combination therapy with SMS 201-995 and low-dose isosorbide dinitrate may be beneficial for portal hypertension in liver cirrhosis.
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PMID:Hemodynamic effects of combined treatment with somatostatin analogue (SMS 201-995) and low-dose isosorbide dinitrate on portal hypertension in conscious cirrhotic rats. 795 57


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