A myocardialis ischaemia es reperfuzio patofiziologiaja

Translated title of the contribution: Pathophysiology of myocardial ischemia and reperfusion

Research output: Contribution to journalArticle

Abstract

Complete and long lasting loss of coronary circulation results in myocardial cell death (ischemic necrosis). Short lasting ischemia (few minutes) is well tolerated and it may bring certain protection against recurrent ischemia (ischemic preconditioning). Contractile force promptly diminishes following the onset of ischemia and the changes in the intracellular ATP or Ca2+ concentration do not explain this phenomenon. With the progression of ischemia, myocardial relaxation ceases and hypertonic muscle activation appears (ischemic contracture). During myocardial reperfusion following short-term ischemia, arrhythmias often develop and pump function is regularly depressed transiently (myocardial stunning). Permanent reduction in coronary blood supply results in sustained ventricular dysfunction (hibernation). It has been established, that pathologic processes leading to ischemic injury are distinct from those of reperfusion injury. Cellular events are complicated (Ca2+-overload, free radical injuries, activation of proteolytic processes, energy loss, membrane damage, hypercontracture, etc.), and complete understanding of the background of ischemic/reperfusion disorders is still awaited.

Original languageHungarian
Pages (from-to)501-511
Number of pages11
JournalLege Artis Medicinae
Volume10
Issue number6
Publication statusPublished - 2000

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Myocardial Reperfusion
Myocardial Ischemia
Ischemia
Ischemic Contracture
Myocardial Stunning
Ventricular Dysfunction
Hibernation
Ischemic Preconditioning
Coronary Circulation
Wounds and Injuries
Pathologic Processes
Reperfusion Injury
Reperfusion
Free Radicals
Cardiac Arrhythmias
Cell Death
Necrosis
Adenosine Triphosphate
Muscles
Membranes

ASJC Scopus subject areas

  • Medicine(all)

Cite this

A myocardialis ischaemia es reperfuzio patofiziologiaja. / Papp, Z.; Édes, I.

In: Lege Artis Medicinae, Vol. 10, No. 6, 2000, p. 501-511.

Research output: Contribution to journalArticle

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