Aminoguanidine corrects hyperdynamic circulation without ameliorating portal hypertension and portal hypertensive gastropathy in anesthetized portal hypertensive rats

Lee, Fa Yauh; Suh-Sang, Wang; Tsai, Yang‐Te; Hwai-Jeng, Lin; H, Lin; Chu, Chi‐Jen; Wu, Shwu-Ling; Chung-Ching, Tai; Lee, Shou‐Dong

doi:10.1016/s0168-8278(97)80436-9

Cited by 34 publications

(27 citation statements)

References 26 publications

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“…Nitrous oxide may underlie the gastric vascular dilation [152] , and hyperdynamic circulation in PHG [148] . However, Lee et al [155] reported administration of aminoguanidine, an iNOS inhibitor, successfully corrected the hyperdynamic circulation without affecting PHG, suggesting that iNOS and NO are important in the hyperdynamic circulation in portal hypertension, but play a limited role in PHG development. They argued that PHG should be treated by reducing portal pressure rather than reversing the hyperdynamic circulation [155,156] .…”

Section: Angiogenesismentioning

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: Angiogenesismentioning

confidence: 99%

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

Gjeorgjievski¹

2016

WJH

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“…Continuous recordings of mean arterial pressure and heart rate were performed on a multi-channel recorder (model RS 3400, Gould Inc., Cupertino, CA, USA). The external zero reference was placed at the level of the mid-portion of the rat [17,18].…”

Section: Measurement Of Systemic Hemodynamicsmentioning

confidence: 99%

Chronic inhibition of nitric oxide increases the collateral vascular responsiveness to vasopressin in portal hypertensive rats

Huang

Wang

Chan

et al. 2004

Journal of Hepatology

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“…The external zero reference was at the level of the midportion of the rat. Continuous recordings of mean arterial pressure, heart rate and portal pressure were performed on a multichannel recorder (model RS 3400, Gould Inc., Cupertino, Calif., USA) [21,22]. …”

Section: Animals and Methodsmentioning

confidence: 99%

The Roles of Angiotensin II Receptors in the Portosystemic Collaterals of Portal Hypertensive and Cirrhotic Rats

Chang¹,

Wang

Lee

et al. 2012

J Vasc Res

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Background/Aims:In liver cirrhosis/portal hypertension, collaterals as varices may bleed and are influenced by vasoresponsiveness. An angiotensin blockade ameliorates portal hypertension but the influence on collaterals is unknown. Methods:Portal hypertension and cirrhosis were induced by portal vein (PVL) and common bile duct ligation (BDL). Hemodynamics, real-time PCR of angiotensin II receptors (AT₁R, AT₂R) in the left adrenal vein (LAV, sham) and splenorenal shunt derived from LAV (PVL, BDL) were performed. With an in situcollateral perfusion model, angiotensin II vasoresponsiveness with different preincubations was evaluated: (1) vehicle; (2) AT₁R blocker losartan; (3) losartan plus nonselective nitric oxide synthase (NOS) inhibitor (N^ω-nitro-L-arginine); (4) AT₂R blocker PD123319; (5) PD123319 plus N^ω-nitro-L-arginine; (6) N^ω-nitro-L-arginine, and (7) losartan plus inducible NOS inhibitor aminoguanidine. Results: LAV AT₁R and AT₂R expression decreased in PVL and BDL rats. Losartan attenuated angiotensin II-elicited vasoconstriction but PD123319 had no effect. N^ω-nitro-L-arginine but not aminoguanidine reversed the losartan effect. Conclusions:Angiotensin receptors are downregulated in the collateral vessel of portal hypertensive and cirrhotic rats. The AT₁R blockade attenuates the angiotensin II vasoconstrictive effect, suggesting AT₁R mediates collateral vasoconstriction and the influence of AT₂R is negligible. The lack of aminoguanidine influence indicates that endothelial NOS participates in the losartan effect.

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Aminoguanidine corrects hyperdynamic circulation without ameliorating portal hypertension and portal hypertensive gastropathy in anesthetized portal hypertensive rats

Cited by 34 publications

References 26 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

Chronic inhibition of nitric oxide increases the collateral vascular responsiveness to vasopressin in portal hypertensive rats

The Roles of Angiotensin II Receptors in the Portosystemic Collaterals of Portal Hypertensive and Cirrhotic Rats

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