Injection of Sca-1+/CD45+/CD31+ mouse bone mesenchymal stromal-like cells improves cardiac function in a mouse myocardial infarct model

2013 ◽  
Vol 86 (1-2) ◽  
pp. 57-64 ◽  
Author(s):  
Jigang He ◽  
Xiaomei Teng ◽  
Yunsheng Yu ◽  
Haoyue Huang ◽  
Wenxue Ye ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Myocardial Infarct ◽  
Myocardial Infarct Model

scholarly journals Utility of Glycosylated TIMP3 molecules: Inhibition of MMPs and TACE to improve cardiac function in rat myocardial infarct model

2018 ◽  
Vol 6 (6) ◽  
pp. e00442 ◽  
Author(s):  
Vishnu Chintalgattu ◽  
Joanne Greenberg ◽  
Shivani Singh ◽  
Venice Chiueh ◽  
Amy Gilbert ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Myocardial Infarct ◽  
Myocardial Infarct Model

Cardioprotection with esmolol-based cardioplegia for non-infarcted and infarcted rat hearts

2021 ◽  
Author(s):  
Alexander B Veitinger ◽  
Audrey Komguem ◽  
Lena Assling-Simon ◽  
Martina Heep ◽  
Julia Schipke ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Lactate Production ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Cardioplegic Arrest ◽  
Blood Cardioplegia ◽  
Rat Hearts

Abstract OBJECTIVES Esmolol-based cardioplegic arrest offers better cardioprotection than crystalloid cardioplegia but has been compared experimentally with blood cardioplegia only once. We investigated the influence of esmolol crystalloid cardioplegia (ECCP), esmolol blood cardioplegia (EBCP) and Calafiore blood cardioplegia (Cala) on cardiac function, metabolism and infarct size in non-infarcted and infarcted isolated rat hearts. METHODS Two studies were performed: (i) the hearts were subjected to a 90-min cardioplegic arrest with ECCP, EBCP or Cala and (ii) a regional myocardial infarction was created 30 min before a 90-min cardioplegic arrest. Left ventricular peak developed pressure (LVpdP), velocity of contractility (dLVP/dtmax), velocity of relaxation over time (dLVP/dtmin), heart rate and coronary flow were recorded. In addition, the metabolic parameters were analysed. The infarct size was determined by planimetry, and the myocardial damage was determined by electron microscopy. RESULTS In non-infarcted hearts, cardiac function was better preserved with ECCP than with EBCP or Cala relative to baseline values (LVpdP: 100 ± 28% vs 86 ± 11% vs 57 ± 7%; P = 0.002). Infarcted hearts showed similar haemodynamic recovery for ECCP, EBCP and Cala (LVpdP: 85 ± 46% vs 89 ± 55% vs 56 ± 26%; P = 0.30). The lactate production with EBCP was lower than with ECCP (0.6 ± 0.7 vs 1.4 ± 0.5 μmol/min; P = 0.017). The myocardial infarct size and (ECCP vs EBCP vs Cala: 16 ± 7% vs 15 ± 9% vs 24 ± 13%; P = 0.21) the ultrastructural preservation was similar in all groups. CONCLUSIONS In non-infarcted rat hearts, esmolol-based cardioplegia, particularly ECCP, offers better myocardial protection than Calafiore. After an acute myocardial infarction, cardioprotection with esmolol-based cardioplegia is similar to that with Calafiore.

Mesenchymal stem cell implantation in a swine myocardial infarct model: engraftment and functional effects

2002 ◽  
Vol 73 (6) ◽  
pp. 1919-1926 ◽  
Author(s):  
Jay G. Shake ◽  
Peter J. Gruber ◽  
William A. Baumgartner ◽  
Guylaine Senechal ◽  
Jennifer Meyers ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Myocardial Infarct ◽  
Myocardial Infarct Model ◽  
Cell Implantation

scholarly journals Long-term effects of hepatocyte growth factor gene therapy in rat myocardial infarct model

Gene Therapy ◽  
2011 ◽  
Vol 19 (8) ◽  
pp. 836-843 ◽  
Author(s):  
Y-N Jin ◽  
M Inubushi ◽  
K Masamoto ◽  
K Odaka ◽  
I Aoki ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Myocardial Infarct ◽  
Long Term Effects ◽  
Factor Gene ◽  
Growth Factor Gene ◽  
Myocardial Infarct Model ◽  
Hepatocyte Growth

Postconditioning attenuates myocardial injury by reducing nitro-oxidative stress in vivo in rats and in humans

2010 ◽  
Vol 120 (6) ◽  
pp. 251-261 ◽  
Author(s):  
Qian Fan ◽  
Xin-Chun Yang ◽  
Yu Liu ◽  
Le-Feng Wang ◽  
Sheng-Hui Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Function ◽  
Myocardial Infarct ◽  
White Blood Cells ◽  
Coronary Intervention ◽  
Myocardial Infarct Size ◽  
Ischaemia Reperfusion Injury ◽  
Acute Myocardial Infarct ◽  
Inos Activity

In the present study, we hypothesized that postcon (postconditioning) confers cardioprotection in vivo by reducing the production of ONOO− (peroxynitrite) and nitro-oxidative stress subsequent to the inhibition of the iNOS (inducible NO synthase). Patients with AMI (acute myocardial infarct) were randomly assigned to undergo percutaneous coronary intervention without (control) or with ischaemic postcon by three episodes of 30-s inflation and 30-s deflation of the angioplasty balloon. Animal models of MI/R (myocardial ischaemia/reperfusion) injury were induced in rats by occluding the left coronary artery for 40 min followed by 4-h reperfusion. Rats were randomized to receive vehicle, postcon (three cycles of 10-s reperfusion and 10-s coronary re-occlusion preceding full reperfusion), the selective iNOS inhibitor 1400W or postcon plus 3-morpholinosydnonimine (an ONOO− donor). Postcon in patients reduced iNOS activity in white blood cells, decreased plasma nitrotyrosine, a fingerprint of ONOO− and an index of nitro-oxidative stress, and improved cardiac function (P<0.01 compared with control). In rats, postcon reduced post-ischaemic myocardial iNOS activity and nitrotyrosine formation, reduced myocardial infarct size (all P<0.05 compared with control) and improved cardiac function. Administration of 1400W resembled, whereas 3-morpholinosydnonimine abolished, the effects of postcon. In conclusion, reduction in ONOO−-induced nitro-oxidative stress subsequent to the inhibition of iNOS represents a major mechanism whereby postcon confers cardioprotection in vivo.

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