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[Nitric oxide and myocardial ischemic preconditioning].

B Ghaleh¹, R Tissier, A Berdeaux

¹Département de Pharmacologie, INSERM E 00.01, Faculté de Médecine Paris-Sud, 63, rue Gabriel Péri, 94270 Le Kremlin-Bicêtre.

Journal De La Societe De Biologie

|April 28, 2001

Summary

Preconditioning protects the heart from damage by brief ischemia. Late preconditioning involves nitric oxide, which triggers delayed cardioprotection and mimics effects of nitric oxide donors.

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Area of Science:

Cardiovascular Physiology
Molecular Cardiology
Ischemic Heart Disease Research

Context:

Preconditioning is an endogenous cardioprotective mechanism triggered by brief ischemia.
It significantly reduces myocardial infarct size during subsequent prolonged ischemia.
The phenomenon exhibits a biphasic kinetic: early (1-3 hours) and late (24-48 hours) windows.

Purpose:

To elucidate the mechanisms underlying the late phase of preconditioning.
To investigate the role of nitric oxide in delayed cardioprotection.
To explore the potential of mimicking late preconditioning pharmacologically.

Summary:

Late preconditioning's protective effects against infarction are debated, but its mechanism involves nitric oxide.
Nitric oxide initiates delayed cardioprotection via oxiradical formation, leading to protein kinase C translocation.

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This activates tyrosine kinases and NF-kappa B, inducing iNOS, with nitric oxide acting as a key mediator.

Impact:

Understanding preconditioning mechanisms is crucial for developing novel cardioprotective therapies.
Nitric oxide donors show potential in mimicking late preconditioning effects.
Further research is needed to identify the final effector of nitric oxide-mediated late preconditioning.