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 Experiment Videos

Nitric oxide signaling in ischemic heart

N Maulik1, D T Engelman, M Watanabe

  • 1Department of Surgery, University of Connecticut School of Medicine, Farmington 06030-1110, USA.

Cardiovascular Research
|October 1, 1995
PubMed
Summary

Nitric oxide (NO) signaling via cGMP protects ischemic hearts by inhibiting phosphodiesterases, but this effect diminishes with reperfusion duration. This NO signaling may be modulated by superoxide radicals during reperfusion.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Magnetic nanoparticle-catalysed synthesis of quinoline derivatives: A green and sustainable method.

Heliyon·2024
Same author

Isoniazid preventive therapy among child contacts of TB patients, India.

The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease·2022
Same author

Postoperative care: who should look after patients following surgery?

Anaesthesia·2020
Same author

Chest wall lymphomas: Fine needle aspiration cytodiagnosis and review of the literature.

Cytopathology : official journal of the British Society for Clinical Cytology·2017
Same author

MRF-ANN: a machine learning approach for automated ER scoring of breast cancer immunohistochemical images.

Journal of microscopy·2017
Same author

RETRACTED ARTICLE: Expression of a bacterial chitinase (<i>ChiB</i>) gene enhances resistance against E. polygoni induced powdery mildew disease in the transgenic Black gram (<i>Vigna mungo</i> L.) (cv. T9).

Physiology and molecular biology of plants : an international journal of functional plant biology·2016

Area of Science:

  • Cardiovascular Physiology
  • Biochemistry
  • Cell Signaling

Background:

  • Endogenous nitric oxide (NO) is implicated in myocardial ischemic/reperfusion (I/R) injury.
  • The precise intracellular signaling mechanisms of NO in I/R injury remain unclear.
  • This study investigates the role of the NO-cGMP pathway in phosphoinositide metabolism during I/R.

Purpose of the Study:

  • To elucidate the role of the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) signaling pathway.
  • To examine the impact of NO on phosphodiesterase activity and phosphoinositide turnover during myocardial ischemia and reperfusion.
  • To investigate the potential protective effects of L-arginine on I/R injury via NO modulation.

Main Methods:

  • Isolated working rat hearts subjected to 30 min ischemia and 30 min reperfusion.

Related Experiment Videos

  • Monitoring NO release using amperometric sensors and assessing myocardial function (aortic flow, developed pressure).
  • Radiolabeling of sarcolemmal membranes with [3H]myoinositol and [14C]arachidonic acid to analyze phosphoinositide breakdown and diacylglycerol/phosphatidic acid formation. cGMP and SOD levels were also measured.

    • Main Results:

    • L-arginine administration augmented NO release and significantly reduced I/R injury, improving myocardial functional recovery.
    • Ischemia/reperfusion induced significant phosphodiesteratic breakdown of phosphoinositides, which was reversed by L-arginine.
    • cGMP levels increased with L-arginine treatment, suggesting NO-cGMP pathway activation, while SOD activity decreased during reperfusion.

    Conclusions:

    • Nitric oxide plays a significant role in transmembrane signaling within the ischemic myocardium.
    • The NO-cGMP pathway opposes ischemia/reperfusion-induced phosphodiesteratic breakdown, indicating a protective mechanism.
    • The modulation of NO signaling by superoxide radicals during reperfusion may explain its dynamic effects.