The effects of serum estrogen levels on hypoxemia and blood nitric oxide levels in experimental hepatopulmonary syndrome

Yol, Serdar; Erikoğlu, Mehmet; Toprak, Şükrü Salih; Tavlı, Şakir; Tavlı, Lema

doi:10.1016/j.hepres.2005.04.007

Cited by 4 publications

(6 citation statements)

References 27 publications

(28 reference statements)

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“…Previous studies have suggested that an increased estradiol level in CBDL rats may contribute to pulmonary vasodilatation via an excessive formation of the potent vasodilator NO [9,11,17]. The present findings are in agreement with those previous ones, i.e.…”

Section: Discussionsupporting

confidence: 94%

“…The mechanisms involved in generalized vasodilatation and the hyperdynamic syndrome are incompletely understood, but several lines of evidence support a role for an increased formation of nitric oxide ( NO) [1][2][3][4][5][6][7][8]. Moreover, from clinical and animal studies it has been suggested that an increased level of estradiol may be implicated most likely through an increased NO formation [9][10][11]. The generalized vasodilatation leads to complications and especially to a hepatopulmonary syndrome (HPS).…”

Section: Introductionmentioning

confidence: 99%

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Effect of the oestrogen receptor antagonist fulvestrant on the cirrhotic rat lung

Oswald‐Mammosser

Rashid

Boehm

et al. 2015

Fundamemntal Clinical Pharma

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It has been postulated that cirrhosis-related lung vasodilatation and the subsequent hepatopulmonary syndrome are partly explained by an increased estradiol level through an enhanced endothelial formation of nitric oxide (NO). In this study, we assessed whether the oestrogen receptor antagonist fulvestrant (F) improves cirrhosis-related lung abnormalities. Cirrhosis was induced in rats by chronic bile duct ligation (CBDL). Four groups were studied: CBDL, CBDL+F, sham, and sham+F. Histological, immunohistochemical, and Western blot analyses were performed on lung samples. In the lung, the endothelial NO synthase and the nitrotyrosine protein expressions were increased in CBDL as compared to sham rats. Both parameters were significantly reduced by fulvestrant in the CBDL rats. Surprisingly, the level of pVASP (an indirect marker of NO formation and action) was decreased in CBDL rats, and fulvestrant had no effect on this parameter. The level of the vascular endothelial growth factor, the diameter of small lung vessels, and the number of macrophages were increased in CBDL lungs in comparison with sham lungs, and these parameters were unaffected by fulvestrant treatment. In conclusion, fulvestrant may not be relevant to improve lung abnormalities in cirrhosis because NO may not be biologically active and because key events contributing to the lung abnormalities are not affected by fulvestrant.

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Effect of the oestrogen receptor antagonist fulvestrant on the cirrhotic rat lung

Oswald‐Mammosser

Rashid

Boehm

et al. 2015

Fundamemntal Clinical Pharma

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“…NO may cause pulmonary vasodilatation in HPS [23,24]. Ligation and excision of the CBD in the rat induce an extrahepatic cholestasis with histologic features of biliary cirrhosis, intrapulmonary vascular dilatation, and hypoxemia 5 weeks later [25], as was confirmed in our study.…”

Section: Discussionsupporting

confidence: 87%

Effects of Caffeic Acid Phenethyl Ester (CAPE) on Hepatopulmonary Syndrome

et al. 2010

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The aim of this study was to investigate the effects of caffeic acid phenethyl ester (CAPE) on inflammatory and related histopathological changes in the lung and liver in experimental hepatopulmonary syndrome (HPS) model. Forty Sprague Dawley rats were used in this study. The animals were divided into four groups of ten rats each. Group 1 and 2 was subjected the common bile duct (CBD) but not ligated, Group 3; (cirrhosis + saline): the CBD was ligated and was given intraperitoneal saline infusion treatment during 5 weeks. Group 4; (cirrhosis + CAPE): the CBD was ligated and was given intraperitoneal CAPE infusion treatment during 5 weeks. A 5-week waiting period was observed for the development of cirrhosis and the rats' lungs and liver were taken for histopathological examination. The induction of HPS resulted in a significant increase in serum bilurubin, AST, ALT, and NO levels, and decrease PO2 and O2 saturation. The use of CAPE significant decrease these parameters. Histopathological examination revealed less congestion, portal inflammation, and nodular formations of the liver, and less congestion, emphysematous and inflammatory changes and smallest perialviolar vascular diameters, in the lung in the cirrhosis + CAPE groups than in the other groups. CAPE treatment may be a potential approach for the treatment of hepatopulmonary syndrome in the future.

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“…Early experimental and human studies implicated pulmonary microvascular dilation, in part related to excess nitric oxide production and altered estrogen signaling in disease pathogenesis 6–8. Although impaired vasomotor tone contributes to the pathophysiology of HPS, incomplete response to pharmacologic blockade of these pathways implies additional mechanisms 9,10.…”

mentioning

confidence: 99%

Genetic Risk Factors for Hepatopulmonary Syndrome in Patients With Advanced Liver Disease

et al. 2010

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The effects of serum estrogen levels on hypoxemia and blood nitric oxide levels in experimental hepatopulmonary syndrome

Cited by 4 publications

References 27 publications

Effect of the oestrogen receptor antagonist fulvestrant on the cirrhotic rat lung

Effect of the oestrogen receptor antagonist fulvestrant on the cirrhotic rat lung

Effects of Caffeic Acid Phenethyl Ester (CAPE) on Hepatopulmonary Syndrome

Genetic Risk Factors for Hepatopulmonary Syndrome in Patients With Advanced Liver Disease

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