The role of organic nitrates in portal hypertension and variceal haemorrhage

InPharma ◽  
1988 ◽  
Vol 647 (1) ◽  
pp. 2-3
Keyword(s):  
Portal Hypertension ◽  
Organic Nitrates ◽  
Variceal Haemorrhage

scholarly journals Role of cyclooxygenase isoforms in prostacyclin biosynthesis and murine prehepatic portal hypertension

2008 ◽  
Vol 295 (5) ◽  
pp. G953-G964 ◽  
Author(s):  
N. J. Skill ◽  
N. G. Theodorakis ◽  
Y. N. Wang ◽  
J. M. Wu ◽  
E. M. Redmond ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
The United States ◽  
Portal Vein Ligation ◽  
Wild Type ◽  
Sham Surgery ◽  
Cox 2 ◽  
Hemodynamic Measurements ◽  
Cyclooxygenase Isoforms ◽  
Cox 1

Portal hypertension (PHT) is a common complication of liver cirrhosis and significantly increases morbidity and mortality. Abrogation of PHT using NSAIDs has demonstrated that prostacyclin (PGI2), a direct downstream metabolic product of cyclooxygenase (COX) activity, is an important mediator in the development of experimental and clinical PHT. However, the role of COX isoforms in PGI2 biosynthesis and PHT is not fully understood. Prehepatic PHT was induced by portal vein ligation (PVL) in wild-type, COX-1−/−, and COX-2−/− mice treated with and without COX-2 (NS398) or COX-1 (SC560) inhibitors. Hemodynamic measurements and PGI2 biosynthesis were determined 1–7 days after PVL or sham surgery. Gene deletion or pharmacological inhibition of COX-1 or COX-2 attenuated but did not ameliorate PGI2 biosynthesis after PVL or prevent PHT. In contrast, treatment of COX-1−/− mice with NS398 or COX-2−/− mice with SC560 restricted PGI2 biosynthesis and abrogated the development of PHT following PVL. In conclusion, either COX-1 or COX-2 can mediate elevated PGI2 biosynthesis and the development of experimental prehepatic PHT. Consequently, PGI2 rather then COX-selective drugs are indicated in the treatment of PHT. Identification of additional target sites downstream of COX may benefit the >27,000 patients whom die annually from cirrhosis in the United States alone.

Diagnostic role of ASL-perfusion of liver in magnetic resonance imaging in assessing risk of developing portal hypertension in patients with viral hepatitis

2021 ◽  
pp. 38-43
Author(s):  
E. N. Simakina ◽  
T. G. Morozova
Keyword(s):  
Magnetic Resonance Imaging ◽  
Portal Hypertension ◽  
Magnetic Resonance ◽  
Viral Hepatitis ◽  
Prognostic Significance ◽  
Resonance Imaging ◽  
Diagnostic Role ◽  
Right Lobe ◽  
The Right

Objective. To establish the diagnostic role of ASL-perfusion of the liver in magnetic resonance imaging (MRI) in assessing the risk of portal hypertension in patients with viral hepatitis. Materials and methods. 109 patients with viral hepatitis were examined, including 69 (63.3 %) men and 40 (36.7 %) women, the average age of patients was 49.0 ± 2.3 years. All subjects (n = 109) underwent abdominal ultrasound with doppler vascular examination and clinical elastography, ASL-perfusion of the liver with MRI with an assessment of the volume of hepatic blood flow (HBF, ml/100 g/min).Results. The highest diagnostic and prognostic significance of ASL-perfusion for the liver is a targeted study of changes in the right lobe: for the right lobe, AUROC = 0.886 (95 % CI: 0.799–0.889); for the left, AUROC = 0.635 (95 % CI 0.627–0.641). The diagnostic and prognostic significance of ASLperfusion was evaluated in comparison with ultrasound with doppler vascular examination: AUROC = 0.991 (95 % CI: 0.880–0.993); AUROC = 0.801 (95 % CI: 0.776–0.804), respectively. The quantitative and qualitative characteristics of ASL – liver perfusion were evaluated.Conclusion. When performing ASL-perfusion of the liver, MRI should evaluate quantitative and qualitative criteria. Criteria for the prognosis of portal hypertension according to ASL- perfusion in MRI in patients with viral hepatitis: HBF 131–160 ml/100 g /min, red card – very high risk, HBF = 161–185 ml/100 g/min, red card – high, HBF = 40–130 ml/100 g/min, mixed card – medium; HBF = 131–160 ml/100 g/min, blue card-low risk (r = 0.883).

New Approaches to the Management of Portal Hypertension and Variceal Haemorrhage

1983 ◽  
pp. 268-280 ◽  
Author(s):  
D. Westaby ◽  
B. Macdougall ◽  
R. Williams
Keyword(s):  
Portal Hypertension ◽  
Variceal Haemorrhage ◽  
New Approaches

The Role of Liver Transplantation in Portal Hypertension

2011 ◽  
pp. 310-313
Author(s):  
Nancy L. Ascher ◽  
John P. Roberts
Keyword(s):  
Liver Transplantation ◽  
Portal Hypertension

scholarly journals Short-Term Western Diet Aggravates Non-Alcoholic Fatty Liver Disease (NAFLD) With Portal Hypertension in TGR(mREN2)27 Rats

2020 ◽  
Vol 21 (9) ◽  
pp. 3308 ◽  
Author(s):  
Carla Cremonese ◽  
Robert Schierwagen ◽  
Frank Erhard Uschner ◽  
Sandra Torres ◽  
Olaf Tyc ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Liver Fibrosis ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Western Diet ◽  
Suitable Model ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is gaining in importance and is linked to obesity. Especially, the development of fibrosis and portal hypertension in NAFLD patients requires treatment. Transgenic TGR(mREN2)27 rats overexpressing mouse renin spontaneously develop NAFLD with portal hypertension but without obesity. This study investigated the additional role of obesity in this model on the development of portal hypertension and fibrosis. Obesity was induced in twelve-week old TGR(mREN2)27 rats after receiving Western diet (WD) for two or four weeks. Liver fibrosis was assessed using standard techniques. Hepatic expression of transforming growth factor-β1 (TGF-β1), collagen type Iα1, α-smooth muscle actin, and the macrophage markers Emr1, as well as the chemoattractant Ccl2, interleukin-1β (IL1β) and tumor necrosis factor-α (TNFα) were analyzed. Assessment of portal and systemic hemodynamics was performed using the colored microsphere technique. As expected, WD induced obesity and liver fibrosis as confirmed by Sirius Red and Oil Red O staining. The expression of the monocyte-macrophage markers, Emr1, Ccl2, IL1β and TNFα were increased during feeding of WD, indicating infiltration of macrophages into the liver, even though this increase was statistically not significant for the EGF module-containing mucin-like receptor (Emr1) mRNA expression levels. Of note, portal pressure increased with the duration of WD compared to animals that received a normal chow. Besides obesity, WD feeding increased systemic vascular resistance reflecting systemic endothelial and splanchnic vascular dysfunction. We conclude that transgenic TGR(mREN2)27 rats are a suitable model to investigate NAFLD development with liver fibrosis and portal hypertension. Tendency towards elevated expression of Emr1 is associated with macrophage activity point to a significant role of macrophages in NAFLD pathogenesis, probably due to a shift of the renin–angiotensin system towards a higher activation of the classical pathway. The hepatic injury induced by WD in TGR(mREN2)27 rats is suitable to evaluate different stages of fibrosis and portal hypertension in NAFLD with obesity.

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