Beta-adrenergic blockade in cirrhosis – harmful or helpful?
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Introduction Portal hypertension exacerbates the disease course of cirrhosis and is responsible for major complications, including bleeding from esophageal varices, ascites, and encephalopathy. More than 40 years ago, Lebrec and colleagues introduced beta-blockers to prevent esophageal bleeding. However, evidence now suggests that beta-blockers may cause adverse reactions in patients with advanced cirrhosis.Keywords:
BETA (programming language)
Adrenergic beta-Antagonists
In this paper we described the participation of beta-adrenoceptors in the regulation of the cardiovascular system. We characterized mainly the low-affinty state of beta1-adrenoceptors and beta3-adrenoceptors, which are insensitive to propranolol (the antagonist of beta1-/beta2-adrenoceptors). We also illustrated their function in the healthy and failing heart. In addition the vasodilatory effects of these receptors ligands were described.
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Phenylephrine
Adrenergic antagonist
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Blocking (statistics)
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In two consecutive series of hypertensive patients the hypotensive effect, the hyporeninaemic effect and the blockade of cardiac beta-receptors was studied using weekly increasing doses of propranolol or atenolol. With both beta-blockers, cardiac blockade and hypotensive effect increased in a parallel fashion when the dosage was increased suggesting that the hypotensive effect is related to cardiac beta-blockade. On the other hand lack of parallelism between the hypotensive effect and the hyporeninaemic effect suggests that the hypotensive effect was not related to a major extent to the hyporeninaemic effect of the drugs in the dosage range studied here.
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Propranolol is a widely used beta blocker that consists of a racemic mixture of R and S stereoisomers. Only the S stereoisomer has significant activity against the beta-adrenergic receptor. A fortuitous clinical observation was made in an infant who received propranolol for cardiac disease, and regression of a hemangioma of infancy was noted. This has led to the widespread use of propranolol for the treatment of large and life-threatening hemangiomas of infancy. Infants receiving propranolol require monitoring to ensure that they do not suffer from side effects related to beta blockade. The exact mechanism of activity of propranolol in hemangioma of infancy is unknown. In this study, we treated hemangioma stem cells with both beta blockade active S- and inactive R-propranolol and looked for genes that were coordinately regulated by this treatment. Among the genes commonly downregulated, Angiopoietin-like 4 (ANGPTL4) was among the most regulated. We confirmed that propranolol isomers downregulated ANGPTL4 in endothelial cells, with greater downregulation of ANGPTL4 using the beta blockade inactive R-propranolol. ANGPTL4 is present in human hemangiomas of infancy. Finally, R-propranolol inhibited the growth of bEnd.3 hemangioma cells in vivo. The implication of this is that hemangioma growth can be blocked without the side effects of beta blockade. Given that humans have been exposed to racemic propranolol for decades and thus to R-propranolol, clinical development of R-propranolol for hemangiomas of infancy and other angiogenic diseases is warranted.
Infantile hemangioma
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Beta blocker
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Quinidine
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Beta adrenoceptor
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Propranolol is a beta-adrenergic blocking drug with a wide spectrum of use and many diverse pharmacologic effects. This case report is an example of a parturient who was on a large dose of propranolol for idiopathic hypertrophic subaortic stenosis. The effects of this drug on pregnancy, labor, and above all, the fetus are discussed.
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Phenylephrine
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Adrenergic beta-Antagonists
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Adrenergic antagonist
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Adrenergic beta-Antagonists
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