Related Experiment Video
Updated: Feb 7, 2026
09:37
Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
Published on: August 1, 2018
15.5K
β-Blockers Improve Presinusoidal Portal Hypertension
Michael Sørensen1, Lars P Larsen2, Gerda E Villadsen3
1Department of Hepatology and Gastroenterology, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99; C116, 8000, Aarhus, Denmark. michsoer@rm.dk.
Digestive Diseases and Sciences
|July 14, 2018
Summary
Beta-blockers significantly reduce portal hypertension in non-cirrhotic patients. This study supports their use to prevent gastric and gastroesophageal varices bleeding in presinusoidal portal hypertension.
Area of Science:
- Hepatology
- Gastroenterology
- Pharmacology
Background:
- Presinusoidal portal hypertension is a key cause of gastric and gastroesophageal varices.
- The efficacy of beta-blockers in presinusoidal portal hypertension remains unestablished, unlike in cirrhotic portal hypertension.
Purpose of the Study:
- To assess the hemodynamic impact of beta-blockers in non-cirrhotic patients experiencing presinusoidal portal hypertension.
Main Methods:
- The study involved 12 patients with presinusoidal portal hypertension.
- Hemodynamic measurements (splenic pulp to hepatic vein pressure gradient) were taken with and without beta-blocker treatment using a randomized sequence.
Main Results:
- Beta-blocker treatment reduced the mean pressure gradient from 32 mm Hg to 26 mm Hg (P < 0.05).
- A clinically significant reduction (≥20%) was observed in 42% of patients.
Conclusions:
- Beta-blocker therapy effectively lowers the pressure gradient in presinusoidal portal hypertension.
- These findings advocate for the prophylactic use of beta-blockers in managing this condition.
Keywords:
Gastroesophageal varicesNon-cirrhotic portal hypertensionPortal vein thrombosisPropranololSplenic vein thrombosisMore Related Videos
Related Concept Videos
01:16Antianginal Drugs: Nitrates and β-Blockers
1.6K
In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
Organic nitrates, such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow....
Organic nitrates, such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow....
1.6K
01:28Antihypertensive Drugs: Types of β-Blockers
1.7K
β receptors are classified into three subclasses: β1, β2, and β3. β1 receptors are primarily located in the heart and kidneys. When they get activated, they increase heart rate, contractility, and renin release. This process enhances blood pressure and aids in stress management. In contrast, β2 receptors are situated mainly in the lungs, blood vessels, and skeletal muscles. Upon activation, they trigger smooth muscle relaxation, causing bronchodilation and...
1.7K
01:22Heart Failure Drugs: β-Blockers
943
β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
943
01:31Adrenergic Antagonists: ɑ and β-Receptor Blockers
1.2K
Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is...
1.2K
01:17Antihypertensive Drugs: Action of β1 Blockers
2.1K
β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this,...
2.1K
01:27Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers
1.8K
β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in...
1.8K