scholarly journals Intracoronary Infusion of Allogeneic Mesenchymal Precursor Cells Directly After Experimental Acute Myocardial Infarction Reduces Infarct Size, Abrogates Adverse Remodeling, and Improves Cardiac Function

2013 ◽  
Vol 113 (2) ◽  
pp. 153-166 ◽  
Author(s):  
Jaco H. Houtgraaf ◽  
Renate de Jong ◽  
Kushan Kazemi ◽  
Daphne de Groot ◽  
Tycho I.G. van der Spoel ◽  
...  
2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Andreas Boening ◽  
Maximilian Hinke ◽  
Martina Heep ◽  
Kerstin Boengler ◽  
Bernd Niemann ◽  
...  

Abstract Background Because hearts in acute myocardial infarction are often prone to ischemia-reperfusion damage during cardiac surgery, we investigated the influence of intracellular crystalloid cardioplegia solution (CCP) and extracellular blood cardioplegia solution (BCP) on cardiac function, metabolism, and infarct size in a rat heart model of myocardial infarction. Methods Following euthanasia, the hearts of 50 rats were quickly excised, cannulated, and inserted into a blood-perfused isolated heart apparatus. A regional myocardial infarction was created in the infarction group (18 hearts) for 120 min; the control group (32 hearts) was not subjected to infarction. In each group, either Buckberg BCP or Bretschneider CCP was administered for an aortic clamping time of 90 min. Functional parameters were recorded during reperfusion: coronary blood flow, left ventricular developed pressure (LVDP) and contractility (dp/dt max). Infarct size was determined by planimetry. The results were compared between the groups using analysis of variance or parametric tests, as appropriate. Results Cardiac function after acute myocardial infarction, 90 min of cardioplegic arrest, and 90 min of reperfusion was better preserved with Buckberg BCP than with Bretschneider CCP relative to baseline (BL) values (LVDP 54 ± 11% vs. 9 ± 2.9% [p = 0.0062]; dp/dt max. 73 ± 11% vs. 23 ± 2.7% [p = 0.0001]), whereas coronary flow was similarly impaired (BCP 55 ± 15%, CCP 63 ± 17% [p = 0.99]). The infarct in BCP-treated hearts was smaller (25% of myocardium) and limited to the area of coronary artery ligation, whereas in CCP hearts the infarct was larger (48% of myocardium; p = 0.029) and myocardial necrosis was distributed unevenly to the left ventricular wall. Conclusions In a rat model of acute myocardial infarction followed by cardioplegic arrest, application of BCP leads to better myocardial recovery than CCP.


2018 ◽  
Vol 82 (5) ◽  
pp. 1379-1386 ◽  
Author(s):  
Léo Cuenin ◽  
Sophie Lamoureux ◽  
Mathieu Schaaf ◽  
Thomas Bochaton ◽  
Jean-Pierre Monassier ◽  
...  

2012 ◽  
Vol 40 (3) ◽  
pp. 740-746 ◽  
Author(s):  
Houxiang Hu ◽  
Anargyros Xenocostas ◽  
Nicolas Chin-Yee ◽  
Xiangru Lu ◽  
Ian Chin-Yee ◽  
...  

2013 ◽  
Vol 22 (12) ◽  
pp. 2299-2309 ◽  
Author(s):  
Yanping Cheng ◽  
Genghua Yi ◽  
Gerard B. Conditt ◽  
Alexander Sheehy ◽  
Frank D. Kolodgie ◽  
...  

Author(s):  
Timur Yagudin ◽  
Yue Zhao ◽  
Haiyu Gao ◽  
Yang Zhang ◽  
Ying Yang ◽  
...  

Abstract Currently, there remains a great need to elucidate the molecular mechanism of acute myocardial infarction in order to facilitate the development of novel therapy. Inhibitor of apoptosis-stimulating protein of p53 (iASPP) is a member of the ASPP family proteins and an evolutionarily preserved inhibitor of p53 that is involved in many cellular processes, including apoptosis of cancer cells. The purpose of this study was to investigate the possible role of iASPP in acute myocardial infarction. The protein level of iASPP was markedly reduced in the ischemic hearts in vivo and hydrogen peroxide-exposed cardiomyocytes in vitro. Overexpression of iASPP reduced the infarct size and cardiomyocyte apoptosis of mice subjected to 24 h of coronary artery ligation. Echocardiography showed that cardiac function was improved as indicated by the increase in ejection fraction and fractional shortening. In contrast, knockdown of iASPP exacerbated cardiac injury as manifested by impaired cardiac function, increased infarct size, and apoptosis rate. Mechanistically, overexpression of iASPP inhibited, while knockdown of iASPP increased the expressions of p53 and Bax, the key regulators of apoptosis. Taken together, our results suggested that iASPP is an important regulator of cardiomyocyte apoptosis, which represents a potential target in the therapy of myocardial infarction.


2006 ◽  
Vol 48 (11) ◽  
pp. 2192-2194 ◽  
Author(s):  
Henning Steen ◽  
Evangelos Giannitsis ◽  
Simon Futterer ◽  
Constanze Merten ◽  
Claus Juenger ◽  
...  

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