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Physiological Reviews, Vol. 79, No. 2, April 1999, pp. 609-634
Copyright ©1999 by the American Physiological Society
Experimental Research Laboratory, Division of Cardiology, University of Louisville, Louisville, Kentucky; and Section of Molecular and Cellular Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland
Bolli, Roberto and
Eduardo Marbán.
The past two decades have witnessed an explosive
growth of knowledge regarding postischemic myocardial dysfunction or
myocardial "stunning." The purpose of this review is to summarize
current information regarding the pathophysiology and pathogenesis of this phenomenon. Myocardial stunning should not be regarded as a single
entity but rather as a "syndrome" that has been observed in a wide
variety of experimental settings, which include the following:
1) stunning after a single, completely reversible episode of
regional ischemia in vivo; 2) stunning after multiple,
completely reversible episodes of regional ischemia in vivo;
3) stunning after a partly reversible episode of regional
ischemia in vivo (subendocardial infarction); 4) stunning
after global ischemia in vitro; 5) stunning after global
ischemia in vivo; and 6) stunning after exercise-induced
ischemia (high-flow ischemia). Whether these settings share a common
mechanism is unknown. Although the pathogenesis of myocardial stunning
has not been definitively established, the two major hypotheses are
that it is caused by the generation of oxygen-derived free radicals
(oxyradical hypothesis) and by a transient calcium overload (calcium
hypothesis) on reperfusion. The final lesion responsible for the
contractile depression appears to be a decreased responsiveness of
contractile filaments to calcium. Recent evidence suggests that calcium
overload may activate calpains, resulting in selective proteolysis of
myofibrils; the time required for resynthesis of damaged proteins would
explain in part the delayed recovery of function in stunned myocardium.
The oxyradical and calcium hypotheses are not mutually exclusive and
are likely to represent different facets of the same pathophysiological
cascade. For example, increased free radical formation could cause
cellular calcium overload, which would damage the contractile apparatus of the myocytes. Free radical generation could also directly alter contractile filaments in a manner that renders them less responsive to
calcium (e.g., oxidation of critical thiol groups). However, it remains
unknown whether oxyradicals play a role in all forms of stunning and
whether the calcium hypothesis is applicable to stunning in vivo.
Nevertheless, it is clear that the lesion responsible for myocardial
stunning occurs, at least in part, after reperfusion so that this
contractile dysfunction can be viewed, in part, as a form of
"reperfusion injury." An important implication of the phenomenon of
myocardial stunning is that so-called chronic hibernation may in
fact be the result of repetitive episodes of stunning, which have a
cumulative effect and cause protracted postischemic dysfunction. A
better understanding of myocardial stunning will expand our knowledge
of the pathophysiology of myocardial ischemia and provide a rationale
for developing new therapeutic strategies designed to prevent
postischemic dysfunction in patients.
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