Titlebook: Stunning, Hibernation, and Calcium in Myocardial Ischemia and Reperfusion; Lionel H. Opie (Professor of Medicine, Visiting Pr Book 1992 Kl

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Do Neutrophils Contribute to Myocardial Stunning?cannot be demonstrated in stunned myocardium, and abnormalities of microvascular function can be dissociated from impaired postischemic myocardial function. Based on the weight of accumulated evidence, neutrophils appear to have no important role in the production of stunned myocardium.

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Proclivitiy of Activated Neutrophils to Cause Postischemic Cardiac Dysfunction: Participation in Stuoduction of free radicals and endothelial dysfunction may create conditions propitious for neutrophil recruitment. However, because activated neutrophils synthesize and release various mediators that are potentially toxic to myocardium, once the stage is reached for leukocyte accumulation, it may he

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Stunning: Damaging or Protective to the Myocardium?fter a short period of myocardial ischemia is a transient postischemic ventricular dysfunction, a situation termed .. As in the case of hibernating myocardium, the depressed contractile function occurring during stunning could be a protective mechanism, allowing the reperfused cells to gradually rec

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Hibernation and Myocardial Ischemia: Clinical Detection by Positron Emission Tomographyxyglucose, which measures myocardial glucose utilization, it is possible to identify myocardial tissue that is hypoperfused at rest with preserved or increased glucose uptake. This mismatch of blood flow to metabolism has a high predictive accuracy in the recovery of contractile function. In order t

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Recovery of Myocardial Function in the Hibernating Hearts. A further improvement of systolic function after 15 weeks suggests a biphasic course of recovery. Prospective studies must clarify whether the potential for improvement in function constitutes an indication for revascularization independent of clinical symptoms.

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Recruitment of an Inotropic Reserve in Hibernating and Stunned Myocardiumd and creatine phosphate, after an initial reduction, returns towards control values. Despite the decrease in baseline contractile function, the hypoperfused myocardium can respond to inotropic stimulation by dobutamine. The recruitment of an inotropic reserve implies increased energy utilization. I