Effect of Acute Portal Hypertension on Hepatosplanchnic Hemodynamics and Liver Function

Jensen, Lone Susanne; Krarup, Niels; Larsen, Jørgen Falck; Juhl, C. O.; Nielsen, Torsten Holm

doi:10.3109/00365528609003101

Cited by 9 publications

(9 citation statements)

References 12 publications

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“…However, post-PVE pressure and increased portal pressure were not correlated with changes of functional volume in the present study. Jensen et al reported that acute portal hypertension did not induce severe hypoxic damage in the functional part of the liver [37] Revised-May 5-Nanashima et al, Page 15 and, therefore, hepatic function could be preserved by an immediate increase of portal pressure from PVE. This increase of pressure may be correlated with the extent of the vascular bed in the embolized or remnant liver.…”

Section: Discussionmentioning

confidence: 99%

Relationship of Hepatic Functional Parameters with Changes of Functional Liver Volume Using Technetium-99m Galactosyl Serum Albumin Scintigraphy in Patients Undergoing Preoperative Portal Vein Embolization: A Follow-Up Report

Nanashima¹,

Tobinaga²,

Abo³

et al. 2010

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 99%

Relationship of Hepatic Functional Parameters with Changes of Functional Liver Volume Using Technetium-99m Galactosyl Serum Albumin Scintigraphy in Patients Undergoing Preoperative Portal Vein Embolization: A Follow-Up Report

Nanashima¹,

Tobinaga²,

Abo³

et al. 2010

Journal of Surgical Research

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“…3,6 Therefore, in the diseased liver, hepatic blood flow (HBF)-dependent oxygen supply may become limiting for the metabolic capacity of the liver. 1,[7][8][9] Interestingly, in a large proportion of patients with liver cirrhosis, resting energy expenditure is increased, reflected by increased whole-body VO 2 . 10,11 Hypermetabolism has been described as an independent risk factor for the prognosis of patients with liver cirrhosis and also as a predictor for survival after orthotopic liver transplantation (OLT).…”

mentioning

confidence: 99%

Decreased splanchnic oxygen uptake and increased systemic oxygen uptake in cirrhosis are normalized after liver transplantation

Tietge¹

2001

Liver Transplantation

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The aim of this study is to (1) characterize the impact of orthotopic liver transplantation (OLT) on splanchnic and systemic oxygen uptake (VO 2 ) in patients with liver cirrhosis, and (2) investigate possible influencing factors, as well as metabolic consequences, of reduced splanchnic VO 2 in patients with cirrhosis. Therefore, we measured systemic VO 2 (indirect calorimetry), portal pressure (hepatic venous pressure gradient), hepatic blood flow (HBF; primed continuous infusion of indocyanine green), and hepatic turnover (arteriohepatic venous concentration differences multiplied by HBF) of oxygen, glucose, free fatty acids (FFAs), and aromatic amino acids (AAAs) in 52 patients with advanced cirrhosis and 16 patients with a clinically stable long-term course after OLT. Systemic VO 2 was significantly increased in patients with cirrhosis (261 ؎ 7 mL/min) and normalized after OLT (216 ؎ 8 mL/min; P < .001). Arterial and hepatic venous oxygen saturation and splanchnic oxygen extraction (in percent) were not different between patients with cirrhosis and after OLT. Splanchnic VO 2 was decreased in patients with cirrhosis (41 ؎ 3 mL/min, representing 16% ؎ 1% of systemic VO 2 ) and normalized after OLT (69 ؎ 6 mL/min; P < .001, representing 32% ؎ 3% of systemic VO 2 ; P < .001). In patients with cirrhosis, a decrease in HBF was associated with decreased splanchnic VO 2 (r ‫؍‬ 0.74; P < .001). Conversely, decreased splanchnic VO 2 reflected a decrease in hepatic glucose production (r ‫؍‬ 0.34; P ‫؍‬ .01) and hepatic extraction of FFAs (r ‫؍‬ 0.40; P < .01) and AAAs (r ‫؍‬ 0.30; P < .05). These results show that (1) splanchnic and systemic VO 2 normalize after OLT, indicating correction of hepatic and extrahepatic metabolic derangements; (2) in cirrhosis, HBF becomes limiting for hepatic oxygen supply; and (3) T he high metabolic activity of the liver demands a sufficient oxygen supply. In healthy controls at rest in the postabsorptive state, hepatic oxygen uptake (VO 2 ) was determined to be approximately 55 mL/min, representing approximately 25% of whole-body VO 2 , whereas splanchnic VO 2 was approximately 70 mL/min. 1,2 A normal organ takes up oxygen in approximately equal parts from the portal vein and hepatic artery; the special anatomy of the normal liver does not represent a major diffusion barrier for oxygen. 1 Under normal conditions, hepatic oxygen extraction is less than 40% of supply. Importantly, in healthy controls, there is no dependence of liver blood flow on an increased hepatic oxygen requirement; an increased hepatic need for oxygen is met by increasing the extraction percentage from blood. 1,3 In cirrhosis, hepatic and splanchnic VO 2 are decreased. 4,5 The cirrhotic liver cannot meet an increased oxygen need by increasing oxygen extraction from the blood. 3,6 Therefore, in the diseased liver, hepatic blood flow (HBF)-dependent oxygen supply may become limiting for the metabolic capacity of the liver. 1,[7][8][9] Interestingly, in a large proportion of patients with liver cirrhosis, resting ener...

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“…22 In contrast to the increase in portal blood flow associated with chronic development of portal hypertension, 23,24 it was concluded that acute prehepatic portal hypertension is accompanied by a decrease in splanchnic blood flow. 22 In contrast to the increase in portal blood flow associated with chronic development of portal hypertension, 23,24 it was concluded that acute prehepatic portal hypertension is accompanied by a decrease in splanchnic blood flow.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of splanchnic oxygen extraction ratio as an index of portal vein pressure in dogs

MacPhail¹,

Monnet²,

Gaynor³

2002

ajvr

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An increase in splanchnic oxygen extraction ratio is evident with partial attenuation of the portal vein and the concurrent decrease in portal vein blood flow. Correlation of oxygen extraction ratio with portal vein blood flow may be a more important indicator for determination of an endpoint to prevent congestion and ischemia of the gastrointestinal tract and pancreas during ligation of portosystemic shunts.

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Effect of Acute Portal Hypertension on Hepatosplanchnic Hemodynamics and Liver Function

Cited by 9 publications

References 12 publications

Relationship of Hepatic Functional Parameters with Changes of Functional Liver Volume Using Technetium-99m Galactosyl Serum Albumin Scintigraphy in Patients Undergoing Preoperative Portal Vein Embolization: A Follow-Up Report

Relationship of Hepatic Functional Parameters with Changes of Functional Liver Volume Using Technetium-99m Galactosyl Serum Albumin Scintigraphy in Patients Undergoing Preoperative Portal Vein Embolization: A Follow-Up Report

Decreased splanchnic oxygen uptake and increased systemic oxygen uptake in cirrhosis are normalized after liver transplantation

Evaluation of splanchnic oxygen extraction ratio as an index of portal vein pressure in dogs

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