Somatostatin Attenuates the Hyperdynamic Circulatory State in the Gastric Mucosa of Rats with Portal Hypertension

Sung, Joseph J.Y.; Tsui, CP; Li, M. K. K.; Leung, Felix W.

doi:10.3109/00365529509101602

Cited by 6 publications

(6 citation statements)

References 17 publications

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“…No studies have analyzed the efficacy of carvedilol, another nonspecific β-adrenergic receptor antagonist, in controlling bleeding from PHG [227] . Somatostatin and octreotide: Somatostatin and octreotide, a synthetic somatostatin analogue, cause splanchnic vasoconstriction, reduce portal pressure, reduce portal blood flow, and decrease gastric perfusion in animal models and in patients with PHG [105,106,160,[228][229][230][231] . For example, Chan et al [228] found octreotide infusion, compared to placebo, significantly increased systemic vascular resistance [3.4 ± 0.2 (SD) mmHg/mL per minute per 100 g vs 2.7 ± 0.2 (SD) mmHg/mL per minute per 100 g, P < 0.05], and significantly decreased portal pressure [9.9 ± 0.5 (SD) mmHg vs 12.5 ± 1.2 (SD) mmHg, P < 0.05] in cirrhotic rats.…”

Section: Pharmacotherapy For Phgmentioning

confidence: 99%

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Gjeorgjievski¹

2016

WJH

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AIM:To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy (PHG) based on a systematic literature review. METHODS:Computerized search of the literature was performed via PubMed using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS:PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG. Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt and liver transplantation are highly successful ultimate therapies because they reduce the underlying portal hypertension. SYSTEMA...

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Section: Pharmacotherapy For Phgmentioning

confidence: 99%

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Gjeorgjievski¹

2016

WJH

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“…It has a half-life of 100 min compared to 2 or 3 min for somatostatin and can be administered both subcutaneously and intravenously. In animal models of portal hypertension, somatostatin has been shown to reduce GMBF [13]. Sung et al [13], using a rat model of portal hypertension, detected a significant decrease in mucosal hemoglobin saturation and hemoglobin concentration following the administration of somatostatin.…”

Section: Discussionmentioning

confidence: 98%

“…In animal models of portal hypertension, somatostatin has been shown to reduce GMBF [13]. Sung et al [13], using a rat model of portal hypertension, detected a significant decrease in mucosal hemoglobin saturation and hemoglobin concentration following the administration of somatostatin. They used reflectance spectrophotometry to measure gastric mucosal blood flow.…”

Section: Discussionmentioning

confidence: 98%

Octreotide lowers gastric mucosal blood flow in normal and portal hypertensive stomachs

2003

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“…Prehepatic portal hypertension was induced by a well-described standard technique. [1][2][3][4][5][6][7][8][9][10][11][12][13][14] An upper midline abdominal incision was made under aseptic conditions. The portal vein was isolated.…”

Section: Methodsmentioning

confidence: 99%

“…In rats with portal hypertension induced by partial portal vein ligation (PPVL), [1][2][3][4][5][6][7][8][9][10][11][12][13][14] there is an increase in splanchnic blood flow, 1,5,15 including gastric mucosal blood flow. 8,13,16 Reduction of the elevated portal pressure by ␤-adrenoceptor antagonists 1,10 in these rats is associated with a decrease in ethanol-induced gastric mucosal damage.…”

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confidence: 99%

Potassium channels participate in gastric mucosal protection in rats with partial portal vein ligation

Tsui

Sung

et al. 1998

Hepatology

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Glybenclamide, an adenosine triphosphate-dependent potassium (K ؉ ATP ) channel blocker, lowered portal pressure and attenuated the hyperdynamic splanchnic circulation in rats with partial portal vein ligation (PPVL). The purpose of this report was to confirm these observations and to test the hypothesis that glybenclamide could reduce acidified ethanol-induced gastric mucosal injury in rats with PPVL. Gastric mucosal blood flow (hydrogen gas clearance), systemic blood pressure, and portal pressure were monitored in rats with PPVL or sham operation (SO). Intravenous glybenclamide (20 mg/kg) or vehicle was administered, followed by intragastric acidified ethanol (0.15 N HCl and 15% ethanol). The area of gastric mucosal lesions was assessed by image analysis. In contrast to published findings, there was no significant elevation of portal pressure after glybenclamide administration in rats with PPVL. Glybenclamide did not alter the gastric mucosal hyperemia in these rats. Glybenclamide significantly increased mucosal injury. The data are consistent with the hypothesis that K ؉ ATP channels play a role in protecting the gastric mucosa in rats with PPVL. (HEPATOLOGY 1998;27:1530-1535.)In rats with portal hypertension induced by partial portal vein ligation (PPVL), [1][2][3][4][5][6][7][8][9][10][11][12][13][14] there is an increase in splanchnic blood flow, 1,5,15 including gastric mucosal blood flow. 8,13,16 Reduction of the elevated portal pressure by ␤-adrenoceptor antagonists 1,10 in these rats is associated with a decrease in ethanol-induced gastric mucosal damage. 10 The observation suggests that lowering of the elevated portal pressure may be a marker of decreased susceptibility of the gastric mucosa to noxious damage in rats with PPVL. One report described preliminary data that glybenclamide, an inhibitor of adenosine triphosphate-dependent potassium (K ϩ ATP ) channels, reduced portal pressure, portal tributary blood flow, and hepatic arterial blood flow, and increased portal territory and hepatic arterial vascular resistance in rats with PPVL. 5 The reproducibility of these observations has not been confirmed. If the increased gastric perfusion and elevated portal pressure in rats with PPVL play a role in modulating the susceptibility of the gastric mucosa to noxious damage, attenuation of such changes, as suggested by results of infusing ␤-adrenoceptor antagonist, 10 should lead to a change in the resistance of the mucosa to damage. We tested the hypothesis that glybenclamide, an inhibitor of K ϩ ATP channels, could attenuate gastric mucosal injury produced by intragastric acidified ethanol in rats with PPVL. MATERIALS AND METHODSAnimal Preparation. Male Sprague-Dawley rats weighing 220 to 300 g were kept in a room with controlled temperature of 23°C and humidity. They were fed laboratory rodent diet 5001 (Purina Mills Inc., St. Louis, MO) and tap water. After an overnight fast, rats of comparable weights were randomized to undergo PPVL or sham operation (SO). They were anesthetized with intraperitoneal pe...

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Somatostatin Attenuates the Hyperdynamic Circulatory State in the Gastric Mucosa of Rats with Portal Hypertension

Cited by 6 publications

References 17 publications

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Octreotide lowers gastric mucosal blood flow in normal and portal hypertensive stomachs

Potassium channels participate in gastric mucosal protection in rats with partial portal vein ligation

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