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Hepatic arterial vasodilation is independent of portal hypertension in early stages of cirrhosis.

Moeller M, Thonig A, Pohl S, Ripoll C, Zipprich A - PLoS ONE (2015)

Bottom Line: The compensatory increase in hepatic arterial flow with a decrease in portal venous flow is known as the hepatic arterial buffer response.HAR in both groups of cirrhotic animals (8W and 12W) were lower compared to controls.Nitric oxide is the main vasodilator.

View Article: PubMed Central - PubMed

Affiliation: First Department of Internal Medicine, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.

ABSTRACT

Introduction: The compensatory increase in hepatic arterial flow with a decrease in portal venous flow is known as the hepatic arterial buffer response. In cirrhosis with elevated portal pressure, the vascular resistance of the hepatic artery is decreased. Whether this lower resistance of the hepatic artery is a consequence of portal hypertension or not remains unknown.

Study aim: The aim of the study was to investigate the hepatic arterial resistance and response to vasoconstriction in cirrhosis without portal hypertension (normal portal resistance).

Methods: Cirrhosis was induced by CCl4-inhalation for 8 weeks (8W, normal portal resistance) and for 12-14 weeks (12W, elevated portal resistance). Bivascular liver perfusion was performed at 8W or 12W and dose response curves of methoxamine were obtained in the presence or absence of LNMMA (nitric oxide synthase blocker). Vascular resistances of the hepatic artery (HAR), portal vein (PVR) and sinusoids (SVR) were measured. Western Blot (WB) and Immunohistochemistry (IHC) were done to measure eNOS and HIF 1a expression.

Results: HAR in both groups of cirrhotic animals (8W and 12W) were lower compared to controls. Dose response curves to methoxamine revealed lower HAR in both cirrhotic models (8W and 12W) regardless the magnitude of portal resistance. LNMMA corrected the dose response curves in cirrhosis (8W and 12W) to control. WB and IHC show increased protein expression of eNOS and HIF1a in 8W and 12W.

Conclusion: Hepatic arterial resistance is decreased in cirrhosis independent of portal resistance. Vasodilation of the hepatic artery in cirrhosis seems to be influenced by hypoxia rather than increase in portal resistance. Nitric oxide is the main vasodilator.

No MeSH data available.


Related in: MedlinePlus

Immunhistochemistry showing the higher expression of phospho-eNOS in hepatic arteries and HIF 1 alpha in livers of cirrhotic rats without or with elevated portal resistance compared to normal animals.
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pone.0121229.g005: Immunhistochemistry showing the higher expression of phospho-eNOS in hepatic arteries and HIF 1 alpha in livers of cirrhotic rats without or with elevated portal resistance compared to normal animals.

Mentions: Western Blot and immunhistochemistry showed a higher expression of eNOS in hepatic arteries from cirrhotic rats compared to normals. This difference was observed in rats normal portal resistance (p = 0.03) as well as in rats with elevated portal resistance (p = 0.023, Fig. 4) compared to normal animals. Immunhistochemistry revealed higher expression of phospho-eNOS in the hepatic arteries of cirrhotic livers in animals with normal and elevated portal resistance (Fig. 5) compared to normal rats. Interestingly, HIF-1 alpha expression was higher in cirrhotic livers of rats with elevated portal resistance compared to normal (p<0.05). Cirrhotic rats with normal portal resistance had a higher expression of HIF-1 alpha than normal rats and equal to rats with elevated portal resistance (Fig. 4 and Fig. 5; p<0.001 vs. normal; p = 0.555 vs. cirrhosis with elevated portal resistance).


Hepatic arterial vasodilation is independent of portal hypertension in early stages of cirrhosis.

Moeller M, Thonig A, Pohl S, Ripoll C, Zipprich A - PLoS ONE (2015)

Immunhistochemistry showing the higher expression of phospho-eNOS in hepatic arteries and HIF 1 alpha in livers of cirrhotic rats without or with elevated portal resistance compared to normal animals.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4368541&req=5

pone.0121229.g005: Immunhistochemistry showing the higher expression of phospho-eNOS in hepatic arteries and HIF 1 alpha in livers of cirrhotic rats without or with elevated portal resistance compared to normal animals.
Mentions: Western Blot and immunhistochemistry showed a higher expression of eNOS in hepatic arteries from cirrhotic rats compared to normals. This difference was observed in rats normal portal resistance (p = 0.03) as well as in rats with elevated portal resistance (p = 0.023, Fig. 4) compared to normal animals. Immunhistochemistry revealed higher expression of phospho-eNOS in the hepatic arteries of cirrhotic livers in animals with normal and elevated portal resistance (Fig. 5) compared to normal rats. Interestingly, HIF-1 alpha expression was higher in cirrhotic livers of rats with elevated portal resistance compared to normal (p<0.05). Cirrhotic rats with normal portal resistance had a higher expression of HIF-1 alpha than normal rats and equal to rats with elevated portal resistance (Fig. 4 and Fig. 5; p<0.001 vs. normal; p = 0.555 vs. cirrhosis with elevated portal resistance).

Bottom Line: The compensatory increase in hepatic arterial flow with a decrease in portal venous flow is known as the hepatic arterial buffer response.HAR in both groups of cirrhotic animals (8W and 12W) were lower compared to controls.Nitric oxide is the main vasodilator.

View Article: PubMed Central - PubMed

Affiliation: First Department of Internal Medicine, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.

ABSTRACT

Introduction: The compensatory increase in hepatic arterial flow with a decrease in portal venous flow is known as the hepatic arterial buffer response. In cirrhosis with elevated portal pressure, the vascular resistance of the hepatic artery is decreased. Whether this lower resistance of the hepatic artery is a consequence of portal hypertension or not remains unknown.

Study aim: The aim of the study was to investigate the hepatic arterial resistance and response to vasoconstriction in cirrhosis without portal hypertension (normal portal resistance).

Methods: Cirrhosis was induced by CCl4-inhalation for 8 weeks (8W, normal portal resistance) and for 12-14 weeks (12W, elevated portal resistance). Bivascular liver perfusion was performed at 8W or 12W and dose response curves of methoxamine were obtained in the presence or absence of LNMMA (nitric oxide synthase blocker). Vascular resistances of the hepatic artery (HAR), portal vein (PVR) and sinusoids (SVR) were measured. Western Blot (WB) and Immunohistochemistry (IHC) were done to measure eNOS and HIF 1a expression.

Results: HAR in both groups of cirrhotic animals (8W and 12W) were lower compared to controls. Dose response curves to methoxamine revealed lower HAR in both cirrhotic models (8W and 12W) regardless the magnitude of portal resistance. LNMMA corrected the dose response curves in cirrhosis (8W and 12W) to control. WB and IHC show increased protein expression of eNOS and HIF1a in 8W and 12W.

Conclusion: Hepatic arterial resistance is decreased in cirrhosis independent of portal resistance. Vasodilation of the hepatic artery in cirrhosis seems to be influenced by hypoxia rather than increase in portal resistance. Nitric oxide is the main vasodilator.

No MeSH data available.


Related in: MedlinePlus