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Journal of Cardiac Surgery, 1993
The use of animal models is a valuable approach to the elucidation of the pathophysiology of myocardial stunning. Coronary occlusion followed by reperfusion produces stunning experimentally, mimicking a myocardial infarction followed by thrombolysis, angioplasty, or coronary bypass.
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The use of animal models is a valuable approach to the elucidation of the pathophysiology of myocardial stunning. Coronary occlusion followed by reperfusion produces stunning experimentally, mimicking a myocardial infarction followed by thrombolysis, angioplasty, or coronary bypass.
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Mitochondrial function in myocardial stunning
Journal of Molecular and Cellular Cardiology, 1991Mitochondrial respiration parameters were studied in mitochondria isolated from normal, ischemic and post-ischemic rabbit hearts. Mitochondrial function was related to tissue content of high energy phosphates (HEP) and cardiac function in the isolated working rabbit heart preparation.
M. Mattheussen +4 more
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Cellular Mechanisms of Myocardial Stunning
Annual Review of Physiology, 1992Stunning describes the impairment of contraction observed in myocardium that has been reperfused after brief periods of ischemia (12, 31, 90). The critical feature of the definition lies in the premise that no permanent injury has occurred; hence, stunning resolves entirely, albeit slowly (hours to days; 12).
Eduardo Marbán, Hideo Kusuoka
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Myocardial stunning after cerebral infarction
International Journal of Cardiology, 1997Myocardial stunning has not been described in patients with cerebrovascular accidents. We present a patient in whom inferior wall hypokinesis, ST-segment elevations and Q waves developed after acute right hemisphere ischemic stroke. Total recovery ensued within 5 days. Coronary vasospasm induced by stroke-related sympathetic surge might be the cause of
Tzung-Dau Wang +2 more
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Myocardial hibernation, stunning, or both?
Basic Research in Cardiology, 1995Myocardial “hibernation” is a term first used by Rahimtoola (10) for a condition of sustained abnormal contraction presumed due to chronic underperfusion in patients with coronary heart disease, in whom revascularization could lead to recovery of global or regional ventricular function. Braunwald and Rutherford (3) suggested that hibernating myocardium
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Role of Adenosine in the Treatment of Myocardial Stunning
Cardiovascular Drugs and Therapy, 1991Adenosine is an endogenous nucleoside produced from the breakdown of adenosine triphosphate (ATP) that possesses a number of complex cellular and metabolic effects that could ameliorate postischemic contractile dysfunction (myocardial stunning). Potential mechanisms include the repletion of high-energy phosphate stores, reduced myocardial oxygen ...
Mervyn B. Forman, Carlos E. Velasco
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Myocardial “Stunning” and Substrate Metabolism
Journal of Cardiac Surgery, 1994Although many experts have dismissed myocardial substrate metabolism as having a role in the phenomenon known as "myocardial stunning," recent studies using the isolated perfused working rat heart (especially from Lopaschuk's laboratory) have provided evidence that perhaps there is a role for alterations in myocardial substrate metabolism in producing ...
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Myocardial stunning after successful defibrillation
Resuscitation, 2008A 75-year-old man presented to the emergency department with syncope. His ECG rhythm showed a broad complex tachycardia. After synchronized cardioversion with a monophasic 100 J shock he developed coarse ventricular fibrillation. The initial rhythm after the shock was sinus rhythm with no pulse or signs of life.
Sandroni, Claudio +3 more
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Oxygen Radicals and Myocardial Stunning
Journal of Cardiac Surgery, 1994There is compelling, although indirect, evidence that oxygen free radicals, generated during ischemia as well as upon reperfusion and reoxygenation of the ischemic heart, contribute to the reversible ventricular dysfunction characterized as myocardial stunning.
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Clinical and experimental aspects of myocardial stunning
Progress in Cardiovascular Diseases, 1992Although the mechanisms involved in stunning remain incompletely defined, it appears that intracellular calcium overload, sarcoplasmic reticulum dysfunction, and the generation of OFR are important components of post-ischemic myocyte dysfunction. It is likely that a variety of mechanisms, some possibly remaining to be elucidated, are operative in the ...
Richard E. Kerber, Brook D. Scott
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