Portal and systemic haemodynamic action of N-acetylcysteine in patients with stable cirrhosis.

Jones, Alison L; Bangash, I.H.; Bouchier, I. A. D.; Hayes, Peter

doi:10.1136/gut.35.9.1290

Cited by 27 publications

(20 citation statements)

References 22 publications

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“…2,10,11 Both groups were comparable before treatment, especially with regard to hemodynamics and tissue oxygenation parameters. No difference could be observed after reperfusion when comparing patients administered NAC and the control patients.…”

Section: Discussionmentioning

confidence: 95%

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Does N-acetylcysteine improve hemodynamics and graft function in liver transplantation?

et al. 1998

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The release of toxic oxidative free radicals induced by ischemia and reperfusion may jeopardize liver graft function. N-acetylcysteine (NAC) has shown protective effects on hypothermic and warm ischemia reperfusion liver injury in animals. NAC improves hemodynamics and survival rates in patients with fulminant hepatic failure. The aim of this study was to investigate whether intraoperative treatment with NAC would improve hemodynamics and postoperative graft function in liver transplantation. Sixty patients with chronic endstage liver disease were included in a prospective randomized placebo-controlled study. NAC or the same volume of 5% glucose was started during the anhepatic phase. Hemodynamic data and calculated tissue oxygenation parameters were compared throughout the procedure. Postoperative graft function was assessed by measurements of aminotransferases, prothrombin time, and monoethylglycinexylidide test over the 3 first postoperative days. Patient demographics were similar before the infusion of NAC or glucose. Hemodynamic parameters, oxygen consumption, oxygen delivery, oxygen extraction ratio, and lactates were not different throughout the procedure. One hour after the revascularization of the hepatic artery, the oxygen extraction ratio by the liver was similar (17% ؎ 7.6% v 17% ؎ 6.2%) in both groups. Postoperative graft function was comparable within the 3 first postoperative days. This study failed to show any beneficial effect of the intraoperative administration of NAC on hemodynamics and graft function in liver transplantation in patients with chronic liver disease.

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Section: Discussionmentioning

confidence: 95%

“…Jones et al have studied portal and systemic hemodynamic action of NAC in 11 patients with stable cirrhosis. 11 They reported a slight increase in CI, resulting in better oxygen delivery, however, without an increase in OER or oxygen consumption. Liver blood flow, estimated by infusion of indocyanine green, did not change significantly.…”

Section: Discussionmentioning

confidence: 98%

Does N-acetylcysteine improve hemodynamics and graft function in liver transplantation?

et al. 1998

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“…30 Acute infusion of NAC leads to improved tissue oxygen delivery and extraction in acute liver failure 1 ; however, in the context of cirrhotic liver disease, it confers no hemodynamic advantage. 2 Chronic administration of NAC has recently been shown to cause histopathological protection to livers following bile duct ligation, 3 and a modest reduction of portal pressure, but full hemodynamic evaluation was not performed. There are no studies evaluating chronic administration in patients with cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

N-acetylcysteine prevents development of the hyperdynamic circulation in the portal hypertensive rat

et al. 1998

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Partial portal vein ligation (PPVL) leads to the development of a hyperdynamic circulation. It is associated with elevated levels of tumor necrosis factor (TNF-␣) and nitric oxide (NO) production, both of which can result in oxidant injury. In this study, we have investigated whether PPVL is associated with the development of oxidative stress, by measuring urinary F 2 -isoprostanes. In addition, we have examined whether N-acetylcysteine (NAC) can ameliorate oxidant injury and prevent the development of the hyperdynamic circulation. Urinary excretion of F 2 -isoprostanes increased sixfold following PPVL together with a significant increase in plasma nitrite and nitrate. Treatment with NAC inhibited the formation of F 2 -isoprostanes as well as the increase in plasma nitrite and nitrate. Hemodynamic studies in anesthetized rats showed that following PPVL, cardiac output and portal pressure increased, and systemic vascular resistance decreased, consistent with the development of a hyperdynamic circulation. These changes were prevented by chronic administration of NAC. We conclude that NAC prevents the development of the hyperdynamic circulation and that the formation of reactive oxygen species may be important in the pathogenesis of these hemodynamic changes. (HEPATOLOGY 1998;28:689-694.)

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“…1,[23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39] In these studies, ICG was used and the hepatic extraction was measured and taken into account in the calculations. The median (of the reported mean HBF in the individual studies) was 1.18 L/min (range 0.93-1.90).…”

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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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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Portal and systemic haemodynamic action of N-acetylcysteine in patients with stable cirrhosis.

Abstract: The effects of intravenous N-acetylcysteine on hepatic and systemic haemodynamics were investigated in 11

Cited by 27 publications

References 22 publications

Does N-acetylcysteine improve hemodynamics and graft function in liver transplantation?

Does N-acetylcysteine improve hemodynamics and graft function in liver transplantation?

N-acetylcysteine prevents development of the hyperdynamic circulation in the portal hypertensive rat

Hepatic blood flow and splanchnic oxygen consumption in patients with liver failure. Effect of high-volume plasmapheresis

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