Experimental Models of Myocardial Ischemia, Reperfusion, and Coronary Steal: Scientific Foundations and Clinical Significance

1988 ◽  
Vol 6 (3) ◽  
pp. 485-503
Author(s):  
John H. Tinker
2018 ◽  
Vol 314 (4) ◽  
pp. H812-H838 ◽  
Author(s):  
Merry L. Lindsey ◽  
Roberto Bolli ◽  
John M. Canty ◽  
Xiao-Jun Du ◽  
Nikolaos G. Frangogiannis ◽  
...  

Myocardial infarction is a prevalent major cardiovascular event that arises from myocardial ischemia with or without reperfusion, and basic and translational research is needed to better understand its underlying mechanisms and consequences for cardiac structure and function. Ischemia underlies a broad range of clinical scenarios ranging from angina to hibernation to permanent occlusion, and while reperfusion is mandatory for salvage from ischemic injury, reperfusion also inflicts injury on its own. In this consensus statement, we present recommendations for animal models of myocardial ischemia and infarction. With increasing awareness of the need for rigor and reproducibility in designing and performing scientific research to ensure validation of results, the goal of this review is to provide best practice information regarding myocardial ischemia-reperfusion and infarction models. Listen to this article’s corresponding podcast at ajpheart.podbean.com/e/guidelines-for-experimental-models-of-myocardial-ischemia-and-infarction/.


2011 ◽  
Vol 127 (2) ◽  
pp. 111-118 ◽  
Author(s):  
Prem Prakash ◽  
Ankita Misra ◽  
William R. Surin ◽  
Manish Jain ◽  
Rabi S. Bhatta ◽  
...  

2018 ◽  
Vol 315 (6) ◽  
pp. H1553-H1568 ◽  
Author(s):  
Stefano Toldo ◽  
Adolfo G. Mauro ◽  
Zachary Cutter ◽  
Antonio Abbate

Myocardial ischemia-reperfusion injury induces a sterile inflammatory response, leading to further injury that contributes to the final infarct size. Locally released danger-associated molecular patterns lead to priming and triggering of the NOD-like receptor protein 3 inflammasome and amplification of the inflammatory response and cell death by activation of caspase-1. We review strategies inhibiting priming, triggering, or caspase-1 activity or blockade of the inflammasome-related cytokines interleukin-1β and interleukin-18, focusing on the beneficial effects in experimental models of acute myocardial infarction in animals and the initial results of clinical translational research trials.


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