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)

The effect of somatostatin on splanchnic haemodynamics in patients with liver cirrhosis is not clearly defined, as some Authors reported a decrease in portal pressure and in liver blood flow during i.v. administration of this hormone, while others did not. In 19 subjects with liver cirrhosis and portal hypertension the following parameters were measured before and during i.v. infusion of somatostatin (7.5 micrograms/min): porto-hepatic gradient, effective hepatic plasma flow, specific splenic blood flow, cardiac output. Moreover the gastrin-G-17 plasma levels, those of insulin and growth hormone were measured. Effective hepatic plasma flow decreased significantly during somatostatin infusion (P less than 0.05), averaging a 15% decrease. Porto-hepatic gradient, specific splenic blood flow, cardiac output did not vary significantly. Gastrin, insulin and growth hormone plasma levels decreased significantly (P less than 0.02, 0.01, 0.05). These data indicate that somatostatin infused at the dose of 7.5 micrograms/min provokes endocrine effects, but as far as the splanchnic circulation is concerned, it induces a slight decrease in liver blood flow without affecting portal hypertension.
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PMID:[Effect of somatostatin on splanchnic hemodynamics in liver cirrhosis]. 615 Nov 51

The task of pharmacotherapy in acute haemorrhage from oesophageal varices in patients with cirrhosis of the liver and portal hypertension is to arrest bleeding by reducing the blood pressure and blood flow in the oesophageal varices. The mechanism of action of the majority of drugs used is vasoconstriction of the arterioles in the splanchnic region. Somatostatin seems to be more effective and in particular safer than vasopressin, terlipressin or their combination with the vasodilatator nitroglycerin. Initial pharmacotherapy for rapid control of haemorrhage is simple and effective treatment, however, it cannot be considered an alternative of sclerotherapy, which remains the method of choice in acute haemorrhage from oesophageal varices and is effective in 90-95%. Pharmacotherapy is useful also in the prevention of relapsing haemorrhage from oesophageal varices. A combination of sclerotherapy with somatostatin or nitrates to reduce early relapses of haemorrhage is particularly effective. The effectiveness of beta-blockers to reduce the risk of relapsing haemorrhage is less clear. Prophylactic treatment for the prevention of the first haemorrhage from oesophageal varices (pharmacological, but also endoscopic or surgical) is justified only in strictly selected patients with a high risk of haemorrhage.
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PMID:[Pharmacotherapy of portal hypertension]. 776 77

Numerous conditions lead to portal hypertension with the development of esophageal varices. Treatment for acute variceal hemorrhage should progress in a logical, stepwise fashion. Therapy after fluid resuscitation includes vasopressin, somatostatin, or a Sengstaken-Blakemore tube. This is followed by treatment with sclerotherapy, variceal ligation, or a combination of both. Continued bleeding is managed by more invasive measures that include radiologic embolization or shunting, esophageal transection, distal splenorenal shunt, or liver transplantation. Beta-blockade may be useful to prevent recurrent bleeding in compliant patients without medical conditions that would preclude use of beta-blockade. Once control of the bleeding has been achieved, sclerotherapy or ligation should be used to obliterate the varices, but prophylactic use of sclerosant is not particularly beneficial.
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PMID:Esophageal varices. 781 45

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

Numerous conditions lead to portal hypertension and the development of esophageal or gastric varices, or both. Treatment of patients with acute bleeding should progress in a logical, stepwise fashion. Initial therapy includes vasopressin, somatostatin, or balloon tamponade with a Sengstaken-Blakemore tube. The next step is treatment with sclerotherapy, variceal ligation, or a combination of both. Continued bleeding is managed by more invasive measures, which may include radiologic embolization or shunting, esophageal transection, distal splenorenal shunt, or liver transplantation.
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PMID:Gastroesophageal varices: pathogenesis and therapy of acute bleeding. 790 63

Continued haemorrhage from oesophageal varices despite adequate injection sclerotherapy and tamponade has a high mortality rate. Such patients are usually referred for surgery. Over a 10-year period, 30 patients (21 men and nine women of median age 52 (range 21-70) years) with acute variceal haemorrhage uncontrolled by initial treatment underwent early emergency oesophageal transection. Portal hypertension was caused by alcoholic cirrhosis in 22 patients; other forms of cirrhosis were present in seven and portal vein thrombosis in one. Hepatic function immediately before operation was Pugh grade A in two patients, B in six and C in 22. Deterioration between admission and transection from grade A to B occurred in one patient and from B to C in five. Oesophageal transection stopped variceal haemorrhage in 29 of the 30 patients. Rebleeding from gastric varices within 35 days of surgery occurred in five patients. Postoperative haemorrhage also occurred from perioesophageal vessels (two patients), a gastrotomy (one) and oesophageal ulceration (two). Hepatic failure developed in seven patients, renal failure in five and both hepatic and renal failure in four. Mortality at 30 days occurred in neither of the two patients with liver function of grade A, in one of six of grade B and in 18 of 22 of grade C. The overall 30-day mortality rate was thus 63 per cent. Mortality was related to the preoperative Pugh grade (hazard ratio 3.95 per grade; P = 0.013) and preoperative blood transfusion (hazard ratio 1.37 per unit; P = 0.035). Four of six patients with grade B liver function died within 3 months and 21 of 22 with grade C disease within 1 year. Oesophageal transection is effective at stopping variceal bleeding but does not modify the underlying disease. Caution is urged for patients with grade C hepatocellular impairment proceeding to acute oesophageal transection after initial sclerotherapy. Such patients may benefit more from treatment with somatostatin or an intrahepatic porta-systemic stent shunt while awaiting definitive therapy.
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PMID:Emergency oesophageal transection for uncontrolled variceal haemorrhage. 792 95

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

Pharmacological prophylaxis and the therapy of complications of portal hypertension have recently been attracting more attention. This especially holds true for gastroesophageal variceal bleeding. Vasoconstrictors such as vasopressin, somatostatin, and beta-blockers, as well as vasodilators such as organic nitrates, alpha 2-adrenergic agonists and serotonin-antagonists, are currently used in clinical settings. The aim of this article is to delineate the present pathophysiological concepts accounting for the hemodynamic changes in animal models and patients with portal hypertension, and to summarize the mechanisms of action of the most frequently used pharmacological agents.
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PMID:[Pathophysiological and pharmacotherapeutic aspects of portal hypertension]. 809 46

Somatostatin has been used to effectively control acute variceal haemorrhage, with conjectured mechanisms on portal hypertension. We, therefore, evaluated the effects of somatostatin on hepatic and systemic haemodynamics in 15 patients with hepatitis B-related cirrhosis and portal hypertension. All patients received an intravenous, continuous infusion of somatostatin 250 micrograms/h, following a bolus injection of 250 micrograms. In systemic haemodynamics, the mean arterial pressure (MAP) increased (P < 0.05), associated with a reflex bradycardia within 3 min following bolus injections, compared with basal values. The right atrial pressure, pulmonary capillary wedge pressure, inferior vena cava pressure, cardiac index, and systemic vascular resistance remained unaffected after drug infusion. In hepatic haemodynamics, the wedge hepatic vein pressure remained unchanged after drug administration. However, there was an increase in free hepatic vein pressure (FHVP; P < 0.05), and a trend toward a decrease in the hepatic vein pressure gradient (HVPG; P = 0.063), within 3 min after bolus injection. Furthermore, the hepatic blood flow decreased significantly at 10 and 30 min after somatostatin infusion (P < 0.05). The effective sinusoidal perfusion assessed by indocyanine green infusion also decreased progressively at 10 min (P = 0.057) and 30 min (P < 0.05). We concluded that somatostatin, at the dose used in this study, caused a transient and bolus-related vasoconstrictive effect, resulting in increases in MAP and FHVP, a decrease in heart rate, and a trend toward lower HVPG. In addition, somatostatin reduced the hepatic blood flow and effective sinusoidal perfusion which may be hazardous to cirrhotic patients during variceal haemorrhage.
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PMID:Changes of hepatic and systemic haemodynamics following somatostatin administration in patients with hepatitis B-related cirrhosis. 809 83

We retrospectively studied 22 patients with hepatopulmonary syndrome (HPS) evaluated at the Mayo Medical Center from 1984 to 1991. All patients had hepatic cirrhosis with clinical evidence of portal hypertension; 13 (59 percent) had severe hypoxemia while breathing room air in the supine position (PaO2 < 60 mm Hg), and 14 of 16 (88 percent) had orthodeoxia breathing room air. On the basis of angiographic observations, we defined type 1 and type 2 patterns of pulmonary vascular abnormalities in HPS. Response to 100 percent oxygen and therapeutic regimens may differ in the angiographic patterns. Substantial deterioration in PaO2 associated with clinically stable hepatic dysfunction was documented in five of seven patients studied with sequential arterial blood gas testing; four subsequently died within 48 months. Overall mortality was 41 percent, occurring a mean of 2.5 years after diagnosis. In 7 of the 22 patients, we prospectively studied the effect of somatostatin analogue given subcutaneously for 4 consecutive days. No significant improvement in PaO2 was documented while breathing room air or 100 percent oxygen (p < 0.05). We conclude that in selected patients with clinically stable hepatic dysfunction and deteriorating oxygenation, the prognosis is poor. Our data in combination with recent surgical reports suggest that liver transplantation may be the treatment of choice in patients with HPS and worsening oxygenation.
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PMID:Hepatopulmonary syndrome. Clinical observations and lack of therapeutic response to somatostatin analogue. 810 97


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