Sequence of morphological and hemodynamic changes of gastric microvessels in portal hypertension

Albillos, Agustı́n; Colombato, Luis; Enriquez, Rosa E.; Ng, Oi Cheng; Sikuler, Emanuel; Groszmann, Roberto J.

doi:10.1016/0016-5085(92)90333-t

Cited by 57 publications

(32 citation statements)

References 10 publications

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“…26 A review of the literature 1-14 shows a range of portal pressures that varied with the time after PPVL, and generally higher than those found in the present study. The reasons for the variations from laboratory to laboratory have not been defined.…”

Section: Discussioncontrasting

confidence: 54%

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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Section: Discussioncontrasting

confidence: 54%

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

Tsui

Sung

et al. 1998

Hepatology

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“…Decreased gastric mucosal perfusion may explain the increased rate of erosions, ulcers, and bleeding in PHG [118] . Abnormal regulation of the gastric microcirculation in PHG may render gastric mucosa more vulnerable to hypoxia [112,122] , and more susceptible to noxious gastric factors, such as aspirin and ethanol [123][124][125] . Misra et al [126] showed that gastric mucosal capillaries, obtained by endoscopic mucosal biopsies, have a much thicker wall in patients with cirrhosis than in healthy volunteers.…”

Section: Pathogenesismentioning

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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“…In the present study of an experimental model, marked dilatation of lymphatic vessels and submucosal edema were observed in the gallbladder tissues along with thick ening of the mucosa and dilatation of blood vessels, as seen in the stomach in patients with liver cirrhosis with portal hypertension [23,24], Therefore, it is suggested that gallbladder wall thickening in liver cirrhosis is associ ated with dilatation of blood vessels and lymphatic vessels in the gallbladder wall as well as submucosal edema. Fur thermore, we observed a positive correlation between the area of vessels in the gallbladder wall and the degree of portal hypertension in the cirrhosis group.…”

Section: Discussionmentioning

confidence: 94%

Reduced Contractility and Histological Changes in the Gallbladder due to Portal Hypertension in a Hamster Cirrhosis Model

Sakata

Ueno²,

Torimura³

et al. 1997

Digestion

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Background/Aims: Little is known about the relationship of portal venous pressure to contractility and histological changes in the gallbladder. In this study, we investigated the relationship between portal hypertension and contractility and histological changes in the gallbladder in a hamster cirrhosis model. Methods: Liver cirrhosis was induced in the hamsters (n = 20) by thioacetamide (TAA). Portal venous pressure was directly measured using a pressure-measuring instrument. The contractility of the gallbladder was appraised by the diameter before and after caerulein treatment. Gallbladder wall thickness and vessel areas in tissues were evaluated in relation to the portal venous pressure. Results: The portal venous pressure, gallbladder wall thickness with submucosal edema and area of vessels in the gallbladder wall in the cirrhosis group were significantly increased compared with those in the control group (n = 20, receiving saline instead of TAA). The gallbladder contraction rate in the cirrhosis group was significantly decreased compared with that in the control group. In the cirrhosis group, there were positive correlations between the portal venous pressure and the gallbladder contraction rate, gallbladder wall thickness, and area of vessels. Conclusions: In the gallbladders of experimental cirrhotic hamsters, portal hypertension caused dilatation of the vessels as well as submucosal edema, and was an important factor in the increased thickness and reduced contractility of the gallbladder wall.

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Sequence of morphological and hemodynamic changes of gastric microvessels in portal hypertension

Cited by 57 publications

References 10 publications

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

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

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

Reduced Contractility and Histological Changes in the Gallbladder due to Portal Hypertension in a Hamster Cirrhosis Model

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