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Hepatic blood flow and splanchnic oxygen consumption in patients with liver failure. Effect of high‐volume plasmapheresis
Author(s) -
Clemmesen Jens Otto,
Gerbes Alexander L.,
Gülberg Veit,
Hansen Bent Adel,
Larsen Fin Stolze,
Skak Claus,
Tygstrup Niels,
Ott Peter
Publication year - 1999
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510290206
Subject(s) - splanchnic , hepatic encephalopathy , medicine , cirrhosis , plasmapheresis , pathophysiology , gastroenterology , perfusion , blood flow , oxygenation , liver disease , immunology , antibody
Liver failure represents a major therapeutic challenge, and yet basic pathophysiological questions about hepatic perfusion and oxygenation in this condition have been poorly investigated. In this study, hepatic blood flow (HBF) and splanchnic oxygen delivery (DO 2,sp ) and oxygen consumption (VO 2,sp ) were assessed in patients with liver failure defined as hepatic encephalopathy grade II or more. Measurements were repeated after high‐volume plasmapheresis (HVP) with exchange of 8 to 10 L of plasma. HBF was estimated by use of constant infusion of D‐sorbitol and calculated according to Fick's principle from peripheral artery and hepatic vein concentrations. In 14 patients with acute liver failure (ALF), HBF (1.78 ± 0.78 L/min) and VO 2,sp (3.9 ± 0.9 mmol/min) were higher than in 11 patients without liver disease (1.07 ± 0.19 L/min, P < .01) and (2.3 ± 0.7 mmol/min, P < .001). In 9 patients with acute on chronic liver disease (AOCLD), HBF (1.96 ± 1.19 L/min) and VO 2,sp (3.9 ± 2.3 mmol/min) were higher than in 18 patients with stable cirrhosis (1.00 ± 0.36 L/min, P < .005; and 2.0 ± 0.6 mmol/min, P < .005). During HVP, HBF increased from 1.67 ± 0.72 to 2.07 ± 1.11 L/min (n=11) in ALF, and from 1.89 ± 1.32 to 2.34 ± 1.54 L/min (n=7) in AOCLD, P < .05 in both cases. In patients with ALF, cardiac output (thermodilution) was unchanged (6.7 ± 2.5 vs. 6.6 ± 2.2 L/min, NS) during HVP. Blood flow was redirected to the liver as the systemic vascular resistance index increased (1,587 ± 650 vs. 2,020 ± 806 Dyne · s · cm −5 · m 2 , P < .01) whereas splanchnic vascular resistance was unchanged. In AOCLD, neither systemic nor splanchnic vascular resistance was affected by HVP, but as cardiac output increased from 9.1 ± 2.8 to 10.1 ± 2.9 L/min ( P < .01) more blood was directed to the splanchnic region. In all liver failure patients treated with HVP (n=18), DO 2,sp increased by 15% ( P < .05) whereas VO 2,sp was unchanged. Endothelin‐1 (ET‐1) and ET‐3 were determined before and after HVP. Changes of ET‐1 were positively correlated with changes in HBF ( P < .005) and VO 2,sp ( P < .05), indicating a role for ET‐1 in splanchnic circulation and oxygenation. ET‐3 was negatively correlated with systemic vascular resistance index before HVP ( P < .05) but changes during HVP did not correlate. Our data suggest that liver failure is associated with increased HBF and VO 2,sp . HVP further increased HBF and DO 2,sp but VO 2,sp was unchanged, indicating that splanchnic hypoxia was not present.