Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure01:16

Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure

691
Oxygen therapy has emerged as a significant tool in enhancing the quality of life for patients suffering from pulmonary arterial hypertension (PAH). While this therapy has principally been studied on patients with significant hypoxemia, this therapeutic approach helps prevent potential organ damage and can be administered in the comfort of one's home.
Oxygen therapy is vital in increasing and maintaining blood oxygen levels in PAH patients. As a result, it aids in reducing fatigue,...
691
Cardiopulmonary Resuscitation IV: Pharmacological Management01:25

Cardiopulmonary Resuscitation IV: Pharmacological Management

1.1K
Pharmacologic intervention is crucial in treating cardiac arrest patients during ACLS or Advanced Cardiovascular Life Support. The ACLS algorithms guide the administration of specific drugs based on the patient's cardiac arrest rhythm, which includes pulseless ventricular tachycardia (VT), ventricular fibrillation (VF), asystole, and pulseless electrical activity (PEA).EpinephrineIndication: Epinephrine is the first-line drug for all cardiac arrest rhythms.Mechanism of Action: Epinephrine...
1.1K

You might also read

Related Articles

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

Sort by
Same author

A Critical Reassessment of Inflammatory and Nutritional Indices (PNI, GNRI, SII, NLR, PLR) for Predicting Arteriovenous Fistula Maturation and Long-Term Patency: A 945-Patient Cohort.

Journal of clinical medicine·2026
Same author

Admission Electrolyte Abnormalities and Clinical Outcomes in Hospitalized COVID-19 Patients.

Medicina (Kaunas, Lithuania)·2026
Same author

Investigation of Sevoflurane-Induced Apoptotic Damage in Human Cardiomyocytes and the Protective Efficacy of Ascorbic Acid.

Medicina (Kaunas, Lithuania)·2026
Same author

Discriminative Ability and Clinical Associations of Serum SIRT1, SIRT3, Apelin, and ELA in Patients with Diabetic Foot Infection.

Life (Basel, Switzerland)·2026
Same author

Emulating a target trial of early compared with late initiation of appropriate antibiotic therapy for hospital-acquired monobacterial Gram-negative bloodstream infections.

The Journal of antimicrobial chemotherapy·2026
Same author

Role of certain adipokines in the pathophysiology of hypertension.

Frontiers in physiology·2026

Related Experiment Video

Updated: Mar 5, 2026

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
08:09

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

10.4K

Hyperbaric Oxygen Preconditioning Provides Preliminary Protection Against Doxorubicin Cardiotoxicity.

Orhan Tezcan1, Oguz Karahan1, Mustafa Alan2

  • 1Department of Cardiovascular Surgery, Medical School of Dicle University.

Acta Cardiologica Sinica
|March 28, 2017
PubMed
Summary

Hyperbaric oxygen therapy (HBOT) may protect against doxorubicin-induced cardiotoxicity. While HBOT increased oxidative stress markers, it preserved cardiac structures in a rat model, suggesting a protective preconditioning effect.

Keywords:
Cardiovascular toxicityDoxorubicinHyperbaric oxygenOxidative stress

More Related Videos

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
05:14

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

5.5K
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
08:22

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model

Published on: October 27, 2020

3.5K

Related Experiment Videos

Last Updated: Mar 5, 2026

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
08:09

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

10.4K
A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
05:14

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

5.5K
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
08:22

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model

Published on: October 27, 2020

3.5K

Area of Science:

  • Cardiology
  • Toxicology
  • Biomedical Engineering

Background:

  • Doxorubicin (DOX) is a widely used chemotherapy agent with known cardiotoxic side effects.
  • The interaction between hyperbaric oxygen (HBO2) therapy and DOX-induced cardiotoxicity is not fully understood, with conflicting study results.
  • HBO2 therapy may induce myocardial preconditioning and generate oxidative stress, necessitating further investigation in the context of DOX treatment.

Purpose of the Study:

  • To investigate the protective effects of HBO2 therapy in a rat model of DOX-induced cardiomyocyte injury.
  • To evaluate the impact of HBO2 on oxidative stress markers and cardiac structure following DOX administration.

Main Methods:

  • Twenty-one rats were divided into three groups: control, DOX-induced cardiotoxicity, and DOX with HBO2 therapy.
  • DOX was administered as a single intraperitoneal dose (20 mg/kg).
  • HBO2 therapy involved exposure to 100% oxygen at 2.5 atmospheres for 90 minutes daily.

Main Results:

  • DOX administration significantly increased cardiac and serum oxidative stress markers and caused severe cardiac injury compared to controls.
  • The highest cardiac oxidative stress index was observed in the group receiving both DOX and HBO2 therapy (p = 0.01 vs. control).
  • Histological examination revealed that cardiac structures were preserved in the DOX + HBO2 group compared to the DOX-only group.

Conclusions:

  • HBO2 preconditioning demonstrates a protective effect against DOX-induced cardiotoxicity in this animal model.
  • Further research is needed to fully elucidate the mechanisms underlying HBO2's preconditioning effect in mitigating DOX cardiotoxicity.