scholarly journals The use of vasoconstrictors in patients with liver cirrhosis: how, when, why

2012 ◽  
Vol 6 (3) ◽  
pp. 105-115
Author(s):  
Claudio Puoti
Keyword(s):  
Blood Flow ◽  
Liver Cirrhosis ◽  
Hepatorenal Syndrome ◽  
Portal Blood Flow ◽  
Decompensated Cirrhosis ◽  
Enos Activity ◽  
Enhanced Production ◽  
Massive Gastrointestinal Bleeding ◽  
No Release

Portal hypertension (PH) is a severe complication of liver cirrhosis. Patients with PH run the risk of developing gastro-esophageal varices and massive gastrointestinal bleeding, ascites, hepatorenal syndrome, and hepatic encephalopathy. Portal blood flow in its turn increases because of enhanced production of vasodilators, increased eNOS activity and NO release, systemic and splanchnic vasodilation, hyperkinetic circulation, and hyposensitivity to vasoconstrictors. Thus, it is now widely recognized that this hyperkinetic (hyperdynamic) circulation that characterizes liver cirrhosis is the main cause of the complications of the disease. This review is aimed at addressing the role of vasoconstrictor treatment in patients suffering from complications of decompensated cirrhosis, offering practical suggestions for the management of this treatment at bedside. In particular, the management of terlipressin in patients with cirrhosis, its side effects and the efficacy of this vasoconstrictor will be examined.

scholarly journals Update on Peripheral Arterial Vasodilation, Ascites and Hepatorenal Syndrome in Cirrhosis

2000 ◽  
Vol 14 (suppl d) ◽  
pp. 112D-121D ◽  
Author(s):  
Mladen Knotek ◽  
Boris Rogachev ◽  
Robert W Schrier
Keyword(s):  
Hepatorenal Syndrome ◽  
Decompensated Cirrhosis ◽  
Arterial Tree ◽  
Salt Diet ◽  
Bacterial Peritonitis ◽  
Low Salt ◽  
Intrahepatic Portosystemic Shunt ◽  
Peripheral Arterial ◽  
Orally Active

In cirrhosis of the liver, according to the peripheral arterial vasodilation hypothesis, relative underfilling of the arterial tree triggers a neurohumoral response (activation of renin-angiotensinaldosterone system, sympathetic nervous system, nonosmotic release of vasopressin) aimed at restoring circulatory integrity by promoting renal sodium and water retention. Evidence has accumulated for a major role of increased vascular production of nitric oxide as the primary cause of arterial vasodilation in cirrhosis. Ascites is a common complication in cirrhosis. Treatment of ascites consists of a low salt diet with diuretics, and paracentesis together with plasma volume expanders in diuretic-resistant patients. Progression of cirrhosis may result in hepatorenal syndrome, a state of functional renal failure that carries an ominous prognosis. Orthotopic liver transplantation has remained the only curative treatment for patients with advanced liver disease; other modalities such as transjugular intrahepatic portosystemic shunt or vasopressin analogues may serve as a bridge to transplantation. Another complication of decompensated cirrhosis is spontaneous bacterial peritonitis, the incidence of which can be reduced by primary or secondary antibiotic prophylaxis by using orally active antibiotics.

scholarly journals The Influence of Carbon Dioxide Pneumoperitoneum on Portal Blood Flow in Patients with Liver Cirrhosis.

2001 ◽  
Vol 34 (2) ◽  
pp. 75-82
Author(s):  
Sumito Takagi ◽  
Hironori Kaneko ◽  
Akira Tamura ◽  
Naoki Joubara ◽  
Toshio Katagiri ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Liver Cirrhosis ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Carbon Dioxide Pneumoperitoneum

scholarly journals TWO cases of liver cirrhosis with spontaneous reversal of portal blood flow demonstrated by percutaneous transhepatic portography

Kanzo ◽  
1980 ◽  
Vol 21 (11) ◽  
pp. 1558-1567
Author(s):  
Kenichi TAKAYASU ◽  
Motohide TAKASHI ◽  
Hirotaka MUSHA ◽  
Masao OMATA ◽  
Kunio OKUDA ◽  
...  
Keyword(s):  
Blood Flow ◽  
Liver Cirrhosis ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Spontaneous Reversal ◽  
Percutaneous Transhepatic Portography ◽  
Transhepatic Portography

Survival and quality of life after portal blood flow preserving procedures in patients with portal hypertension and liver cirrhosis

1994 ◽  
Vol 168 (1) ◽  
pp. 10-14 ◽  
Author(s):  
Hector Orozco ◽  
Miguel Angel Mercado ◽  
Takeshi Takahashi ◽  
Gilberto Rojas ◽  
Jorge Hernández ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Blood Flow ◽  
Liver Cirrhosis ◽  
Portal Hypertension ◽  
Portal Blood Flow ◽  
Portal Blood

New insights on the mechanism of the alcohol-induced increase in portal blood flow

1988 ◽  
Vol 66 (1) ◽  
pp. 1-9 ◽  
Author(s):  
H. Orrego ◽  
F. J. Carmichael ◽  
Y. Israel
Keyword(s):  
Blood Flow ◽  
Alcohol Dehydrogenase ◽  
Portal Blood Flow ◽  
Protective Role ◽  
Portal Blood ◽  
Acute Administration ◽  
Direct Role ◽  
Potent Vasodilator ◽  
Dose Dependent Increase

Acute administration of ethanol increases portal blood flow by 40–60%. This increase in blood flow compensates for the increase in O2 consumption that follows alcohol intake and may play a protective role against hypoxic hepatocellular necrosis. We have investigated the mechanism of this hemodynamic effect of ethanol in the rat using the labeled microsphere technique. We ruled out a direct role of systemic glucagon and of acetaldehyde in mediating the increase in portal flow. However, the increase in flow is maximal at a blood ethanol concentration of 3.5 mM, corresponding to that required to achieve the Vmax of alcohol dehydrogenase, and is suppressed by 4-methylpyrazole, an inhibitor of alcohol dehydrogenase. Alcohol ingestion results in zonal liver hypoxia and in increases in acetate, both of which have been shown to increase the levels of adenosine, a potent vasodilator, in blood and tissues. Ethanol produces a 400% increase in arterial adenosine. Adenosine infusion leads to a dose-dependent increase in portal blood flow of up to 100%, an effect that is suppressed by administration of 8-phenyltheophylline, an antagonist of adenosine at A1 and A2 receptors. Similarly, the ethanol-induced increase in portal blood flow is fully suppressed by 8-phenyltheophylline. In conclusion, adenosine appears to play an important role in the mechanism by which ethanol increases portal blood flow.

Effect of the Somatostatin Analogue Lanreotide on Meal-Stimulated Portal Blood Flow in Patients with Liver Cirrhosis

Digestion ◽  
2002 ◽  
Vol 65 (1) ◽  
pp. 56-60 ◽  
Author(s):  
Peter Schiedermaier ◽  
Phillip Harrison ◽  
Michael Arthur ◽  
Daniel Grandt ◽  
Robert Sutton ◽  
...  
Keyword(s):  
Blood Flow ◽  
Liver Cirrhosis ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Somatostatin Analogue
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