alexa Myocardial ischemia and reperfusion injury
Diabetes & Endocrinology

Diabetes & Endocrinology

Journal of Diabetes & Metabolism

Author(s): Buja LM

Abstract Share this page

Myocardial ischemic injury results from severe impairment of coronary blood supply and produces a spectrum of clinical syndromes. As a result of intensive investigation over decades, a detailed understanding is now available of the complexity of the response of the myocardium to an ischemic insult. Myocardial ischemia results in a characteristic pattern of metabolic and ultrastructural changes that lead to irreversible injury. Recent studies have explored the relationship of myocardial ischemic injury to the major modes of cell death, namely, oncosis and apoptosis. The evidence indicates that apoptotic and oncotic mechanisms can proceed together in ischemic myocytes with oncotic mechanisms and morphology dominating the end stage of irreversible injury. Myocardial infarcts evolve as a wavefront of necrosis, extending from subendocardium to subepicardium over a 3- to 4-hour period. A number of processes can profoundly influence the evolution of myocardial ischemic injury. Timely reperfusion produces major effects on ischemic myocardium, including a component of reperfusion injury and a greater amount of salvage of myocardium. Preconditioning by several short bouts of coronary occlusion and reperfusion can temporarily salvage significant amounts of myocardium and extend the window of myocardial viability. Ongoing research into the mechanisms involved in reperfusion and preconditioning is yielding new insights into basic myocardial pathobiology

This article was published in Cardiovasc Pathol. and referenced in Journal of Diabetes & Metabolism

Relevant Expert PPTs

Relevant Speaker PPTs

Relevant Topics

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

 
© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version
adwords