High magnesium dialysate does not improve intradialytic hemodynamics or abrogate myocardial stunning

2020 ◽  
Vol 24 (4) ◽  
pp. 506-515 ◽  
Author(s):  
Helen J. Jefferies ◽  
Sandrine Lemoine ◽  
Christopher W. McIntyre
Keyword(s):  
Myocardial Stunning

Myocardial stunning after extracorporal circulation: myth or fact? An experimental analysis in piglets

2012 ◽  
Vol 60 (S 01) ◽  
Author(s):  
P Kiefer ◽  
A Salameh ◽  
M Krausch ◽  
K Oelmann ◽  
F Emrich ◽  
...  
Keyword(s):  
Experimental Analysis ◽  
Myocardial Stunning ◽  
Extracorporal Circulation

Mechanical Unloading Properties of Axial Flow Pumps and their Effect on Myocardial Stunning

1995 ◽  
Vol 18 (12) ◽  
pp. 766-771 ◽  
Author(s):  
F. R. Waldenberger ◽  
B. Meyns ◽  
P. Wouters ◽  
E. De Ruyter ◽  
E. Pongo ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Myocardial Stunning ◽  
Myocardial Dysfunction ◽  
Axial Flow ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Wall Thickening ◽  
Myocardial Wall Motion ◽  
Mechanical Unloading ◽  
Artery Disease

Postischemic myocardial dysfunction affects morbidity and mortality in patients with coronary artery disease. It is known that mechanical unloading of the left heart ventricle can positively influence postischemic myocardial dysfunction. In this respect we tested two miniaturised axial flow pumps, i.e. the 14-F and the 21-F Hemopump®. An experimental study was carried out on 30 open chest sheep where regional myocardial wall motion was followed using sonomicrometry in a preparation of transient coronary artery occlusion. Only the larger 21-F Hemopump® showed hemodynamically significant unloading of the left ventricle. Furthermore, as far as stunning is concerned, systolic wall thickening recovered better when this type of pump was used during reperfusion. Also postejection thickening, which is an indication of diastolic postischemic dysfunction, is reduced significantly in the postischemic area (ANOVA, p<0.05). Thus, the 21F Hemopump®, but not the 14F Hemopump®, provides adequate mechanical unloading in order to beneficially influence myocardial stunning.

Volatile Anesthetics and Myocardial Stunning

1993 ◽  
Vol 77 (4) ◽  
pp. 866
Author(s):  
Jure Marijic ◽  
Nediljka Buljubasic
Keyword(s):  
Myocardial Stunning ◽  
Volatile Anesthetics

Preconditioning prevents myocardial stunning after cardiac transplantation

1998 ◽  
Vol 66 (6) ◽  
pp. 1953-1957 ◽  
Author(s):  
Roderick W Landymore ◽  
Alexander J Bayes ◽  
J.Thomas Murphy ◽  
John H Fris
Keyword(s):  
Myocardial Stunning ◽  
Cardiac Transplantation

scholarly journals 811-2 Evidence that Myocardial Stunning Occurs in Humans Following Unstable Angina

1995 ◽  
Vol 25 (2) ◽  
pp. 427A
Author(s):  
William Wijns ◽  
Jean L. Vanoverschelde ◽  
Bernhard Gerber ◽  
Joszef Bartunek ◽  
Bernard De Bruyne ◽  
...  
Keyword(s):  
Unstable Angina ◽  
Myocardial Stunning

Molecular and Cellular Mechanisms of Myocardial Stunning

1999 ◽  
Vol 79 (2) ◽  
pp. 609-634 ◽  
Author(s):  
Roberto Bolli ◽  
Eduardo Marbán
Keyword(s):  
Free Radical ◽  
Myocardial Stunning ◽  
Recovery Of Function ◽  
Myocardial Dysfunction ◽  
Calcium Overload ◽  
Global Ischemia ◽  
Stunned Myocardium ◽  
Common Mechanism ◽  
Regional Ischemia

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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