Continuous prazosin administration in cirrhotic patients: Effects on portal hemodynamics and on liver and renal function
Department of Gastroenterology, Clínica Puerta de Hierro, Madrid, Spain. Gastroenterology
(Impact Factor: 16.72).
10/1995; 109(4):1257-65. DOI: 10.1016/0016-5085(95)90586-3
Hepatic vascular resistance is influenced by alpha-adrenergic tone. The aim of this study was to investigate the effects of continuous blockade of alpha-adrenoceptors with prazosin on hemodynamics, liver function, and renal function and whether the association of propranolol or furosemide enhances the portal pressure lowering effect of prazosin.
Cirrhotic patients with portal hypertension were studied at baseline and after a 3-month course of prazosin (n = 18) or placebo (n = 10).
No changes were observed in the placebo group. Prazosin decreased the hepatic venous pressure gradient (HVPG) while increasing hepatic blood flow. Liver function improved as shown by an increase in hepatic and intrinsic hepatic clearances of indocyanine green and galactose elimination capacity. A significant reduction in mean arterial pressure and systemic vascular resistance was associated with increases in plasma renin activity and aldosterone concentration and a decrease in glomerular filtration rate. The plasma volume increased significantly, and 6 patients developed edema. The association of propranolol (n = 8) but not furosemide (n = 7) to prazosin increased the reduction in HVPG and attenuated the increase in plasma renin activity.
In cirrhotic patients, continuous prazosin administration reduces portal pressure and improves liver perfusion and function but favors sodium and water retention. The association of propranolol enhances the decrease in portal pressure, suggesting a potential benefit from this combined therapy.
Available from: Jordi Colmenero
- "Nevertheless, it is possible that the renal ability to excrete sodium in some patients with compensated cirrhosis may be just in the limit of sodium intake. In these patients the formation of ascites might be precipitated by increasing the intake of sodium or by impairing renal sodium excretion, for example, after the administration of vasodilators such as nitrates   or prazosin  "
Journal of Hepatology 02/2003; 38 Suppl 1(1):S69-89. DOI:10.1016/S0168-8278(03)00007-2 · 11.34 Impact Factor
Available from: Andrew K Burroughs
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ABSTRACT: Pharmacological treatment of portal hypertension has played an increasing clinical role in the past 20 years. In the setting of acute variceal bleeding, drug therapy should be considered the initial treatment of choice and can be administered as soon as possible; even during the transfer of the patient to hospital. Several recent trials have reported similar efficacy to emergency sclerotherapy, therefore drug treatment should no longer be considered as a "stop gap" therapy until definitive endoscopic therapy is performed but continued for several days. Antibiotic prophylaxis is an integral part of therapy as it reduces mortality and should be instituted from admission. Non selective b-blockers are the treatment of first choice for secondary and primary prevention. If they are contraindicated or non tolerated banding ligation can be used. There is less evidence for the benefit of ligation for primary prophylaxis. The use of haemodynamic targets for reduction in hepatic venous pressure gradient response need further study, and surrogate markers of pressure response need evaluation
Annals of hepatology: official journal of the Mexican Association of Hepatology 1(3):102-20. · 2.07 Impact Factor
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ABSTRACT: L’hypertension portale est due à une augmentation de la résistance à l’écoulement du sang dans la veine porte. L’élévation
de la pression porte est secondairement entretenue par l’augmentation du débit sanguin porte (hypercinésie circulatoire splanchnique).
L’hypercinésie circulatoire peut être en relation avec un excès de substances vasorelaxantes dans ou au contact de la paroi
des vaisseaux. Ces substances sont: le monoxyde d’azote, la prostacycline, l’hyperactivité nerveuse sympathique, les agonistes
des récepteurs β2-adrénergiques, les neuropeptides (calcitonin gene related-peptide, vasoactive intestinal peptide, substance P), le glucagon,
les produits de l’hypoxie tissulaire. Par ailleurs, l’hypercinésie circulatoire peut être en relation avec d’autres facteurs
tels que: la circulation collatérale, la sévérité de l’éventuelle maladie du foie sous-jacente ou l’hypervolémie.
An increased resistance to blood flow in the portal vein causes portal hypertension. This elevated portal pressure is maintained
(and even accentuated) by an increase in portal tributary blood flow (splanchnic hyperdynamic circulation). Splanchnic circulatory
hyperkineticism seems to be partly due to increased levels of certain substances in or near vascular walls. These substances
include nitric oxide, prostacyclin, sympathetic nervous overactivity, β2-adrenergic agonists, neuropeptides (calcitonin gene related-peptide, vasoactive intestinal peptide, substance P), glucagon,
products of tissue hypoxia. In addition, portosystemic shunts, the severity of liver disease and hypervolemia may play a role
in hyperdynamic circulation associated with portal hypertension.
Acta Endoscopica 10/2012; 25(4):307-312. DOI:10.1007/BF02963248 · 0.16 Impact Factor
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