Cardioprotective effect of the short-acting beta-blocker esmolol in experimental ischemia/reperfusion

Author(s):  
Jorge Nuche ◽  
Sergio Huertas ◽  
Carlos Galán-Arriola ◽  
Pedro López-Ayala ◽  
Manuel Lobo ◽  
...  
2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Ramón Rodrigo ◽  
Matías Libuy ◽  
Felipe Feliú ◽  
Daniel Hasson

Acute myocardial infarction (AMI) is the leading cause of mortality worldwide. Major advances in the treatment of acute coronary syndromes and myocardial infarction, using cardiologic interventions, such as thrombolysis or percutaneous coronary angioplasty (PCA) have improved the clinical outcome of patients. Nevertheless, as a consequence of these procedures, the ischemic zone is reperfused, giving rise to a lethal reperfusion event accompanied by increased production of reactive oxygen species (oxidative stress). These reactive species attack biomolecules such as lipids, DNA, and proteins enhancing the previously established tissue damage, as well as triggering cell death pathways. Studies on animal models of AMI suggest that lethal reperfusion accounts for up to 50% of the final size of a myocardial infarct, a part of the damage likely to be prevented. Although a number of strategies have been aimed at to ameliorate lethal reperfusion injury, up to date the beneficial effects in clinical settings have been disappointing. The use of antioxidant vitamins could be a suitable strategy with this purpose. In this review, we propose a systematic approach to the molecular basis of the cardioprotective effect of antioxidant vitamins in myocardial ischemia-reperfusion injury that could offer a novel therapeutic opportunity against this oxidative tissue damage.


2007 ◽  
Vol 103 (6) ◽  
pp. 2129-2136 ◽  
Author(s):  
David A. Liem ◽  
Henry M. Honda ◽  
Jun Zhang ◽  
David Woo ◽  
Peipei Ping

Despite tremendous advances in cardiovascular research and clinical therapy, ischemic heart disease remains the leading cause of serious morbidity and mortality in western society and is growing in developing countries. For the past 5 decades, many scientists have studied the pathophysiology of myocardial ischemia-reperfusion (I/R) injury leading to infarction. With the exception of reperfusion therapy, attempts to salvage the myocardium during an acute myocardial infarction showed disappointing results in directly decreasing infarct size. Nevertheless, the phenomena of ischemic preconditioning and ischemic postconditioning show a consistent and robust cardioprotective effect in every used experimental animal model. As a result, many studies have focused on the intracellular protective signaling pathways that are involved in preconditioning and postconditioning. More recently, it has been suggested that components of the reperfusion injury salvage kinases pathway, protein kinase B, and the extracellular signal-regulated kinases can induce cardioprotection against I/R injury when they are activated during the postischemic reperfusion period. In addition, inhibition of mitochondrial permeability transition during postischemic reperfusion also shows a strong cardioprotective effect against I/R injury. The present mini-review highlights a short summary of the historical and present course of research into cardioprotection against myocardial I/R injury.


1986 ◽  
Vol 111 (1) ◽  
pp. 42-48 ◽  
Author(s):  
Sheron Anderson ◽  
Lori Blanski ◽  
Randolph C. Byrd ◽  
Gopal Das ◽  
Robert Engler ◽  
...  

2000 ◽  
Vol 51 (1) ◽  
pp. 20-28 ◽  
Author(s):  
Satoshi Takeo ◽  
Hiroshi Kajiwara ◽  
Kouichi Tanonaka ◽  
Yoshihisa Nasa ◽  
Yasuo Nakajima ◽  
...  

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