Abstract

An early hypothesis for myocardial stunning held that contractile dysfunction was caused by neutrophil-mediated microvascular occlusions which produced focal areas of myocardial ischemia. Although this hypothesis appeared to go against the basic tene that blood flow was normal, or nearly normal in stunned myocardium, an interesting model resembling stunning was described by Hori et al. (1) in which coronary microsphere embolization was used to produce progressive microvascular occlusion and resting contractile dysfunction. Like stunned myocardium, resting flow remained normal and, although resting function was depressed, contractile reserve could be recruited by beta-adrenergic agonists. However, maximal flow reserve progressively declined as the microvasculature became obliterated. Resting flow was maintained at normal levels by local release of adenosine from ischemic areas, resulting in hyperemia of surrounding normal regions.

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