Effect of oxygen inhalation on systemic, central, and splanchnic haemodynamics in cirrhosis

Möller, Sören; Becker, Ulrik; Schifter, Søren; Abrahamsen, Jan; Henriksen, Jens H.

doi:10.1016/s0168-8278(96)80118-8

Cited by 34 publications

(33 citation statements)

References 46 publications

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“…VO 2,sp is around 2.0-3.0 mmol/ min in healthy controls [43][44][45] as well as in patients with cirrhosis. 37,38,46 In the present study, liver failure was associated with increased VO 2,sp (Fig. 1).…”

Section: Discussionsupporting

confidence: 65%

“…The median (of the reported mean HBF in the individual studies) was 1.18 L/min (range 0.93-1.90). In seven studies (with ICG and similar methodology) comprising 60 healthy controls or patients without evidence of liver disease 1,[38][39][40][41][42][43] , nϭ11), ALF (nϭ12), cirrhosis without hepatic encephalopathy (nϭ18), and AOCLD (nϭ9). NS, not significant (P ϭ .053); * P Ͻ .05; ** P Ͻ .01; *** P Ͻ .005; **** P Ͻ .001. with these studies.…”

Section: Discussionmentioning

confidence: 99%

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Hepatic Blood Flow and Splanchnic Oxygen Consumption in Patients With Liver Failure. Effect of High–Volume Plasmapheresis

Clemmesen

Gerbes²,

Gülberg³

et al. 1999

Hepatology

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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 F .01) and (2.3 ؎ 0.7 mmol/min, P F .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 F .005; and 2.0 ؎ 0.6 mmol/min, P F .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 F .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 F .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 F .01) more blood was directed to the splanchnic region. In all liver failure patients treated with HVP (n‫,)81؍‬ DO 2,sp increased by 15% (P F .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 F .005) and VO 2,sp (P F .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 F .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.(HEPATOLOGY 1999;29: 347-355.)A basic requirement for organ function is adequate blood flow and oxygen delivery. Hepatic blood flow (HBF) and splanchnic oxygenation in patients with liver failure (in the present study, defined as having developed hepatic encephalopathy [HE] grade II or more) have not been assessed because a method to estimate HBF in such patients has not been available until recently. 1,2 Knowledge in this field, therefore, rests on indirect evidence and animal experiments. The observation that whole-body (systemic) oxygen consumpti...

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Hepatic Blood Flow and Splanchnic Oxygen Consumption in Patients With Liver Failure. Effect of High–Volume Plasmapheresis

Clemmesen

Gerbes²,

Gülberg³

et al. 1999

Hepatology

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“…17 Plasma concentrations of norepinephrine were determined by high-performance liquid chromatography, as described elsewhere. 18 The intra-assay and interassay coefficients of variation were 8% and 9%, respectively. The plasma renin concentration was determined with a commercially available 2-site immunoradiometric assay (DGR International, Inc., Hamburg, Germany).…”

Section: Methodsmentioning

confidence: 94%

Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome

et al. 2007

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Patients with advanced cirrhosis and ascites are characterized by circulatory dysfunction with splanchnic vasodilatation and renal vasoconstriction, which often lead to ascites. The vasoconstrictor terlipressin improves renal function in hepatorenal syndrome (HRS). The aim of this study was to evaluate if terlipressin also improves renal function in patients with ascites without HRS. Twenty-three patients with cirrhosis participated; 15 with nonrefractory ascites were randomized to either terlipressin (N group, n ‫؍‬ 11) or a placebo (P group, n ‫؍‬ 4), and 8 had refractory ascites and received terlipressin (R group). The glomerular filtration rate (GFR), sodium clearance (C Na ), lithium clearance (C Li ), osmolal clearance (C Osm ), and urine sodium concentration (U Na ) were assessed before and after the injection of 2 mg of terlipressin or the placebo. GFR increased in the N group (69 ؎ 19 versus 92 ؎ 25 mL/min, P < 0.005) and in the R group (31 ؎ 19 versus 41 ؎ 31 mL/min, P < 0.05) after terlipressin. In the N group, terlipressin induced an increase in C Na (0.89 ؎ 0.21 versus 1.52 ؎ 1.45 mL/min, P < 0.05), C Li (17.3 ؎ 8.9 versus 21.5 ؎ 11.6 mL/min, P < 0.05), and C Osm (2.10 ؎ 0.81 versus 3.06 ؎ 2.0 mL/min, P < 0.05). In the R group, terlipressin induced an increase in C Na (0.11 ؎ 0.18 versus 0.35 ؎ 0.40 mL/min, P < 0.05) and C Li (5.5 ؎ 4.2 versus 9.5 ؎ 8.55 mL/min, P < 0.05). U Na increased in both groups after terlipressin (P < 0.005). Plasma norepinephrine (P < 0.05) and renin (P < 0.05) decreased after terlipressin. All parameters remained unchanged after the placebo. A scites is a serious complication of cirrhosis, occurring in about 50% of patients within 10 years after diagnosis, and it is associated with 50% mortality in 2 years. 1,2 Patients with ascites have hyperdynamic circulation, which is characterized by peripheral and splanchnic arterial vasodilatation and reduced arterial blood pressure and systemic vascular resistance. 3 Portal hypertension and splanchnic vasodilatation are major factors in the development of ascites. 4,5 Secondary to vasodilatation, vasoactive hormones, such as the reninangiotensin-aldosterone system and the sympathetic nervous system, are activated. This leads to renal vasoconstriction and reduced renal perfusion and filtration pressure. The current standard treatment of ascites involves diuretics and paracentesis, which are not designed to improve the underlying pathophysiology. The changes in the renal handling of water and salt seem to develop stepwise from a stage that can be controlled by diuretics to a stage refractory to diuretics and finally to full-blown renal failure, which is known as hepatorenal syndrome (HRS) type 1. 6 Several clinical studies have evaluated the efficacy of the long-term administration of terlipressin [a vasopressin 1 (V1) receptor agonist] in patients with HRS, [7][8][9][10][11][12][13] and there is evidence that terlipressin may improve renal

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“…Haemodynamics and portal pressure were quantified in all patients before treatment with propranolol [25,26]. Biopsy verified the diagnosis in all except three patients with tense ascites and coagulopathy.…”

Section: Patientsmentioning

confidence: 90%

Acute non-selective β-adrenergic blockade reduces prolonged frequency-adjusted Q–T interval (QTc) in patients with cirrhosis

Henriksen

Bendtsen

Hansen

et al. 2004

Journal of Hepatology

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115

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Effect of oxygen inhalation on systemic, central, and splanchnic haemodynamics in cirrhosis

Cited by 34 publications

References 46 publications

Hepatic Blood Flow and Splanchnic Oxygen Consumption in Patients With Liver Failure. Effect of High–Volume Plasmapheresis

Hepatic Blood Flow and Splanchnic Oxygen Consumption in Patients With Liver Failure. Effect of High–Volume Plasmapheresis

Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome

Acute non-selective β-adrenergic blockade reduces prolonged frequency-adjusted Q–T interval (QTc) in patients with cirrhosis

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