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Development of short-term myocardial hibernation. Its limitation by the severity of ischemia and inotropic stimulation.
Author(s) -
Rainer Schulz,
Johnie Rose,
C Martín,
O.E. Brodde,
Gerd Heusch
Publication year - 1993
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.88.2.684
Subject(s) - dobutamine , medicine , hibernating myocardium , ischemia , inotrope , cardiology , perfusion , creatine , hibernation (computing) , myocardial stunning , anesthesia , hemodynamics , myocardial infarction , revascularization , state (computer science) , algorithm , computer science
Short-term hibernating myocardium is characterized by a decrease in contractile function in proportion to the reduced myocardial blood flow. Myocardial creatine phosphate content, initially decreased during the first minutes of ischemia, returns to near-control values, the ischemia-induced net lactate production is attenuated, and the myocardium remains viable despite ongoing hypoperfusion and contractile dysfunction. Hibernating myocardium after 85 minutes of ischemia maintains an inotropic reserve and responds to short-term intracoronary dobutamine infusion with increased work; however, this inotropic response is at the expense of metabolic recovery. We therefore hypothesized that the development of myocardial hibernation is a delicate process that is easily disturbed by unfavorable alterations in the oxygen-supply demand balance.

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