Role of acute elevation of portal venous pressure by exogenous glucagon on gastric mucosal injury in rats with portal hypertension

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

doi:10.1016/s0024-3205(03)00413-2

Cited by 8 publications

(9 citation statements)

References 125 publications

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“…Gastric blood flow was assessed by the well-described reflectance spectrophotometry (RS) technique [15,16], and the laser Doppler flowmetry (LDF) technique [15,17,18] in separate groups of anesthetized rats.…”

Section: Methodsmentioning

confidence: 99%

Intragastric Nitroglycerin at a Vasodilatory Dose Attenuates Acidified Aspirin-Induced Gastric Mucosal Injury

Leung¹,

Chan

2007

Dig Dis Sci

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Clinical studies reveal that aspirin intake to prevent myocardial and cerebral ischemia is associated with a significant increase in upper gastrointestinal hemorrhage requiring hospitalization and that nitroglycerin or long-acting nitrates significantly lower this risk. Nitroglycerin can increase gastric blood flow and slow gastric emptying. We hypothesized that both features contribute to its gastroprotective property. Fasted anesthetized rats (Study 1) and conscious mice (Studies 2 to 4) received intragastric nitroglycerin or vehicle. The effects of these two treatments on various parameters were assessed in Study 1, on blood pressure and gastric blood flow; Study 2, on acidified aspirin-induced gastric mucosal lesions; and Study 3, on the weight of gastric content. In Study 4, the effect of nitroglycerin, vehicle, or vehicle plus saline, on acidified aspirin-induced gastric mucosal lesion was assessed. Compared with vehicle, nitroglycerin decreased blood pressure and produced a mild but significant increase in gastric vascular conductance, blood flow, and volume of gastric content. The number and length of gastric mucosal lesions induced by acidified aspirin were significantly attenuated by intragastric nitroglycerin in a vasodilatory dose. Exogenous saline in a volume equivalent to the increase produced by nitroglycerin, however, did not attenuate the lesions. These experimental data are consistent with the clinical observation that nitrates lower the risk of aspirin-induced gastrointestinal complications. Confirmation of the efficacy of nitroglycerin and nitrates in preventing such aspirin-induced complications in controlled trials is worthy of consideration by clinical investigators.

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Section: Methodsmentioning

confidence: 99%

Intragastric Nitroglycerin at a Vasodilatory Dose Attenuates Acidified Aspirin-Induced Gastric Mucosal Injury

Leung¹,

Chan

2007

Dig Dis Sci

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“…Geraghty et al [158] found a strong correlation between portal pressure and glucagon levels (r = 0.85). Tsui et al [160] reported that glucagon significantly increased portal pressure in rats with portal vein ligation, but did not alter portal pressure in sham-operated rats. The effect of glucagon occurred only in rats with preexisting portal hypertension.…”

Section: Angiogenesismentioning

confidence: 99%

“…The effect of glucagon occurred only in rats with preexisting portal hypertension. Exogenous glucagon rendered gastric mucosa more susceptible to injury from toxins, such as ethanol, which was attenuated by somatostatin [160] . For example, the lesion area was significantly higher at > 60% of gastric mucosa after glucagon administration, compared to somatostatin or glucagon and somatostatin administration (P < 0.05, ANOVA) [160] .…”

Section: Angiogenesismentioning

confidence: 99%

“…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%

“…the portal hypertensive and injury-promoting effects of glucagon [160] . Octreotide is a first-line treatment for acute bleeding from PHG.…”

Section: Pharmacotherapy For Phgmentioning

confidence: 99%

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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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Quercetin prevents oxidative stress and NF-κB activation in gastric mucosa of portal hypertensive rats

Moreira

Fraga

Alonso

et al. 2004

Biochemical Pharmacology

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Role of acute elevation of portal venous pressure by exogenous glucagon on gastric mucosal injury in rats with portal hypertension

Cited by 8 publications

References 125 publications

Intragastric Nitroglycerin at a Vasodilatory Dose Attenuates Acidified Aspirin-Induced Gastric Mucosal Injury

Intragastric Nitroglycerin at a Vasodilatory Dose Attenuates Acidified Aspirin-Induced Gastric Mucosal Injury

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

Quercetin prevents oxidative stress and NF-κB activation in gastric mucosa of portal hypertensive rats

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