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Isolation of Neonatal Extrahepatic Cholangiocytes
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Cirrhosis regression: extrahepatic angiogenesis and liver hyperarterialization persist
Audrey Payancé1,2, Pierre-Emmanuel Rautou3,2,4
1DHU Unity, Pôle des Maladies de l'Appareil Digestif, Service d'Hépatologie, Centre de Référence des Maladies Vasculaires du Foie, Hôpital Beaujon, AP-HP, Clichy, France.
Clinical Science (London, England : 1979)
|June 30, 2018
Summary
Cirrhosis regression improves portal hypertension and normalizes systemic hemodynamics in rats. However, some splanchnic hemodynamic changes, like liver hyperarterialization, persist, suggesting ongoing mechanisms.
Area of Science:
- Hepatology
- Cardiovascular Physiology
- Gastroenterology
Background:
- Limited data exists on cirrhosis regression's impact on portal hypertension and hemodynamics.
- Previous studies focused on hepatic venous pressure gradient, not comprehensive hemodynamic changes.
Purpose of the Study:
- To analyze the effects of cirrhosis regression on splanchnic and systemic hemodynamics.
- To investigate persistent hemodynamic alterations despite liver disease reversal.
Main Methods:
- Utilized rat models of cirrhosis induced by thioacetamide and bile duct ligation.
- Comprehensive analysis of splanchnic and systemic hemodynamic parameters.
Main Results:
- Cirrhosis regression significantly reduced portal pressure and intrahepatic vascular resistance.
- Systemic hemodynamics normalized, but extrahepatic vascular structures and liver hyperarterialization showed marginal changes.
- Portosystemic collaterals persisted but were unperfused.
Conclusions:
- Cirrhosis regression normalizes systemic hemodynamics and portal pressure.
- Persistent splanchnic hemodynamic changes, including liver hyperarterialization, suggest autonomous mechanisms.
- Microbiota alterations and bacterial translocation may contribute to persistent effects.
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