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

Mechanisms of ischemic preconditioning

T Ishida1, K Yarimizu, D C Gute

  • 1Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, School of Medicine, Shreveport 71130, USA.

Shock (Augusta, Ga.)
|August 1, 1997
PubMed
Summary

Ischemic preconditioning (IPC) protects tissues from damage by activating adenosine A1 receptors and protein kinase C. However, the specific protective mechanisms and effectors vary across different organs, influencing outcomes in conditions like ischemia.

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

Experimental models to investigate inflammatory processes in chronic venous insufficiency.

Microcirculation (New York, N.Y. : 1994)·2001
Same author

Postischemic anti-inflammatory effects of bradykinin preconditioning.

American journal of physiology. Heart and circulatory physiology·2000
Same author

Ischemic preconditioning prevents postischemic P-selectin expression in the rat small intestine.

The American journal of physiology·1999
Same author

PR-39, a proline/arginine-rich antimicrobial peptide, prevents postischemic microvascular dysfunction.

The American journal of physiology·1999
Same author

Adhesion molecule expression in postischemic microvascular dysfunction: activity of a micronized purified flavonoid fraction.

Journal of vascular research·1999
Same author

Concentration-dependent effects of bradykinin on leukocyte recruitment and venular hemodynamics in rat mesentery.

The American journal of physiology·1999

Area of Science:

  • Physiology
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Ischemic preconditioning (IPC) is a phenomenon where brief ischemia confers resistance to subsequent prolonged ischemia.
  • Initially observed in the myocardium, IPC's protective effects extend to skeletal muscle, brain, and small intestine, with evidence in humans.
  • The precise molecular mechanisms underlying IPC's protective effects remain incompletely understood.

Purpose of the Study:

  • To review and summarize the current evidence regarding the mechanisms of ischemic preconditioning across different organs.
  • To elucidate the role of adenosine A1 receptors and protein kinase C in initiating IPC's protective effects.
  • To explore the tissue-specific effector pathways involved in the preconditioning phenomenon.

Main Methods:

Related Experiment Videos

  • Review of existing scientific literature on ischemic preconditioning.
  • Analysis of studies investigating the molecular signaling pathways involved in IPC.
  • Comparative examination of IPC mechanisms in various organs, including the heart, skeletal muscle, and small intestine.

Main Results:

  • Adenosine A1 receptor activation during preconditioning ischemia is a common initiating event for IPC in most organs.
  • Protein kinase C activation downstream of adenosine A1 receptors is implicated in mediating IPC's effects.
  • Tissue-specific effectors, such as ATP-sensitive potassium channels in the heart and inhibition of leukocyte adhesion in peripheral tissues, contribute to IPC's protective actions.
  • In the small intestine, IPC preserves nitric oxide bioavailability and reduces P-selectin expression, while in skeletal muscle, it augments adenosine production during reperfusion.

Conclusions:

  • Adenosine-induced protein kinase C activation is a key early step in IPC across multiple tissues.
  • The downstream effector molecules and specific protective mechanisms of IPC differ significantly between organs.
  • Understanding these diverse mechanisms opens avenues for therapeutic preconditioning using agents that target shared signaling cascades.