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Titolo:
HIBERNATING MYOCARDIUM - A REVIEW
Autore:
HEUSCH G; SCHULZ R;
Indirizzi:
UNIV ESSEN GESAMTHSCH,SCH MED,CTR INTERNAL MED,DEPT PATHOPHYSIOL,HUFELANDSTR 55 D-45122 ESSEN GERMANY
Titolo Testata:
Journal of Molecular and Cellular Cardiology
fascicolo: 12, volume: 28, anno: 1996,
pagine: 2359 - 2372
SICI:
0022-2828(1996)28:12<2359:HM-AR>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
LEFT-VENTRICULAR DYSFUNCTION; CHRONIC CORONARY STENOSIS; SHORT-TERM HIBERNATION; BLOOD-FLOW; INORGANIC-PHOSPHATE; ISCHEMIC-HEART; CONTRACTILE FAILURE; ENERGY-METABOLISM; POSTISCHEMIC DYSFUNCTION; ADENOSINE-TRIPHOSPHATE;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
81
Recensione:
Indirizzi per estratti:
Citazione:
G. Heusch e R. Schulz, "HIBERNATING MYOCARDIUM - A REVIEW", Journal of Molecular and Cellular Cardiology, 28(12), 1996, pp. 2359-2372

Abstract

Within a few seconds after a sudden reduction of coronary blood flow regional contractile dysfunction ensues, The mechanisms responsible for the rapid reduction in contractile function during acute myocardial ischemia remain unclear, but may involve a rise in inorganic phosphate. When severe ischemia, such as resulting from a sudden and complete coronary artery occlusion, is prolonged for more than 20-40 min, myocardial infarction develops, and there is irreversible loss of contractile function. When myocardial ischemia is less severe but nevertheless prolonged, the myocardium is dysfunctional but can remain viable, In such ischemic and dysfunctional myocardium, contractile function is reduced in proportion to the reduction in regional myocardial brood flow; i.e. a state of ''perfusion-contraction matching'' exists. The metabolic status of such myocardium improves over the first few hours, as myocardial lactate production is attenuated and creatine phosphate, afteran initial reduction, returns towards control values. Ischemic myocardium, characterized by perfusion-contraction matching, metabolic recovery and lack of necrosis, has been termed ''short-term hibernating myocardium'', Short-term hibernating myocardium can respond to an inotropic stimulation with increased contractile function, however, at the expense of a renewed worsening of the metabolic status. This situation of an increased regional contractile function at the expense of metabolic recovery during inotropic stimulation can be used to identify short-term hibernating myocardium. When inotropic stimulation is prolonged,the development of short-term hibernation is impaired and myocardial infarction develops. The mechanisms responsible for the development ofshort-term myocardial hibernation remain unclear at present; a significant involvement of adenosine and of activation of ATP-dependent potassium channels has been excluded. Whereas short-term hibernation is well characterized in animal experiments, the existence of hibernation over weeks or months (long-term hibernation) can only be inferred from clinical studies. Hibernation, as defined by Rahimtoola, is a state ofchronic contractile dysfunction which is fully reversible upon reperfusion, Clinical syndromes consistent with the existence of myocardial hibernation include unstable and stable angina, acute myocardial infarction and left ventricular dysfunction and/or congestive heart failure, In long-term hibernating myocardium morphological alterations occur;the myofibrils are reduced in number and disorganized and myocardial glycogen content as well as the extracellular collagen network are increased. Thus, despite the fact that the myocardium remains viable during persistent ischemia and contractile dysfunction is reversible upon reperfusion, there are severe morphological alterations, Understandably, full functional recovery following reperfusion might therefore require weeks or even months. (C) 1996 Academic Press Limited

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 16:31:51