Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...

Peptic Ulcer Disease IV: Management

Peptic Ulcer Disease IV: Management

Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current medication...

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Access toward Fluorenone Derivatives through Solvent-Free Ruthenium Trichloride Mediated [2 + 2 + 2] Cycloadditions.

Organic letters·2016

Same author

Identification of SNPs in a nonmodel macrofungus (<i>Lepista nuda</i>, Basidiomycota) through RAD sequencing.

SpringerPlus·2016

Same author

The role of HYAL2 in LSS-induced glycocalyx impairment and the PKA-mediated decrease in eNOS-Ser-633 phosphorylation and nitric oxide production.

Molecular biology of the cell·2016

Same author

Mesenchymal stem cells with Sirt1 overexpression suppress breast tumor growth via chemokine-dependent natural killer cells recruitment.

Scientific reports·2016

Same author

RNA Sequencing of Formalin-Fixed, Paraffin-Embedded Specimens for Gene Expression Quantification and Data Mining.

International journal of genomics·2016

Same author

Babao Dan attenuates hepatic fibrosis by inhibiting hepatic stellate cells activation and proliferation via TLR4 signaling pathway.

Oncotarget·2016

Search research articles

Related Experiment Video

Updated: May 11, 2026

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function

Published on: March 15, 2022

Proton-pump inhibitors can decrease gastrointestinal bleeding after percutaneous coronary intervention.

Zongdan Jiang¹, Hailu Wu, Zhaotao Duan

¹Department of Gastroenterology, Nanjing First Hospital Affiliated to Nanjing Medical University, 68, Changle Road, Nanjing 210006, China.

Clinics and Research in Hepatology and Gastroenterology

|May 21, 2013

Summary

Gastrointestinal bleeding occurred in 1.3% of patients after percutaneous coronary intervention (PCI). Proton-pump inhibitor (PPI) use was found to be safe and effective in preventing bleeding events in patients receiving aspirin and clopidogrel.

More Related Videos

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction

Published on: May 28, 2019

Related Experiment Videos

Last Updated: May 11, 2026

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function

Published on: March 15, 2022

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction

Published on: May 28, 2019

Area of Science:

Cardiology
Gastroenterology
Clinical Research

Background:

Current acute coronary syndrome (ACS) therapies target coagulation and platelet inhibition, reducing morbidity and mortality.
However, these treatments increase the risk of bleeding, necessitating further investigation into associated complications.

Purpose of the Study:

To determine the incidence of gastrointestinal bleeding (GIB) following percutaneous coronary intervention (PCI).
To evaluate the efficacy of proton-pump inhibitor (PPI) treatment in mitigating GIB risk in patients undergoing PCI.

Main Methods:

A case-control study was conducted at Nanjing First Hospital from 2008-2011.
Gastrointestinal bleeding events within one year post-PCI were identified and analyzed using linked departmental databases.
Statistical analyses included independent two-sample Student's t-test, Fisher's exact P value, and logistic regression to identify risk and protective factors.

Main Results:

The incidence of GIB after PCI was 1.3% (35/2680 patients).
Identified risk factors for GIB included advanced age, female gender, smoking, alcohol consumption, history of peptic ulcer, and prior GIB.
Proton-pump inhibitor (PPI) use post-PCI was significantly associated with a reduced risk of GIB (P=0.000).

Conclusions:

The incidence of GIB with dual antiplatelet therapy (aspirin and clopidogrel) post-PCI is 1.3%.
Advanced age, female sex, smoking, drinking, and a history of peptic ulcer or GIB are significant risk factors.
PPIs are safe and effective for preventing and treating GIB in patients on dual antiplatelet therapy after PCI.