scholarly journals Influence of Intrinsic Aerobic Exercise Capacity and Sex on Cardiac Injury Following Acute Myocardial Ischemia and Reperfusion

2021 ◽  
Vol 8 ◽  
Author(s):  
Musaad B. Alsahly ◽  
Madaniah O. Zakari ◽  
Lauren G. Koch ◽  
Steven Britton ◽  
Laxmansa C. Katwa ◽  
...  
Keyword(s):  
Sex Differences ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
Phenotypic Selection ◽  
Acute Myocardial Ischemia ◽  
Myocardial Ischemia And Reperfusion ◽  
Phenotypic Differences

Purpose: Previous reports have suggested that active exercise aside, intrinsic aerobic running capacity (Low = LCR, high = HCR) in otherwise sedentary animals may influence several cardiovascular health-related indicators. Relative to the HCR phenotype, the LCR phenotype is characterized by decreased endothelial reactivity, increased susceptibility to reperfusion-induced arrhythmias following short, non-infarction ischemia, and increased diet-induced insulin resistance. More broadly, the LCR phenotype has come to be characterized as a “disease prone” model, with the HCRs as “disease resistant.” Whether these effects extend to injury outcomes in an overt infarction or whether the effects are gender specific is not known. This study was designed to determine whether HCR/LCR phenotypic differences would be evident in injury responses to acute myocardial ischemia-reperfusion injury (AIR), measured as infarct size and to determine whether sex differences in infarction size were preserved with phenotypic selection.Methods: Regional myocardial AIR was induced in vivo by either 15 or 30 min ligation of the left anterior descending coronary artery, followed by 2 h of reperfusion. Global ischemia was induced in isolated hearts ex vivo using a Langendorff perfusion system and cessation of perfusion for either 15 or 30 min followed by 2 h of reperfusion. Infarct size was determined using 2, 3, 5–triphenyltetrazolium chloride (TTC) staining, and normalized to area at risk in the regional model, or whole heart in the global model. Portions of the tissue were paraffin embedded for H&E staining and histology analysis.Results: Phenotype dependent differences in infarct size were seen with 15 min occlusion/2 h reperfusion (LCR > HCR, p < 0.05) in both regional and global models. In both models, longer occlusion times (30 min/2 h) produced significantly larger infarctions in both phenotypes, but phenotypic differences were no longer present (LCR vs. HCR, p = n.s.). Sex differences in infarct size were present in each phenotype (LCR male > LCR female, p < 0.05; HCR male > HCR female, p < 0.05 regardless of length of occlusion, or ischemia model.Conclusions: There is cardioprotection afforded by high intrinsic aerobic capacity, but it is not infinite/continuous, and may be overcome with sufficient injury burden. Phenotypic selection based on endurance running capacity preserved sex differences in response to both short and longer term coronary occlusive challenges. Outcomes could not be associated with differences in system characteristics such as circulating inflammatory mediators or autonomic nervous system influences, as similar phenotypic injury patterns were seen in vivo, and in isolated crystalloid perfused heart ex vivo.

scholarly journals A Meta-Analysis of Resveratrol Protects against Myocardial Ischemia/Reperfusion Injury: Evidence from Small Animal Studies and Insight into Molecular Mechanisms

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Zhi-Jie Mao ◽  
Hui Lin ◽  
Jian-Wen Hou ◽  
Qian Zhou ◽  
Qian Wang ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Infarct Size ◽  
Animal Studies ◽  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
Meta Analysis ◽  
Small Animal ◽  
Route Of Administration ◽  
Myocardial Ischemia Reperfusion

Aims. Myocardial ischemia/reperfusion (I/R) injury is a leading cause of cardiomyocyte loss and subsequent ventricular dysfunction after restoring the coronary blood flow and contributes to considerable increase in morbidity and mortality. Resveratrol has been declared to confer cardioprotection against in vivo and ex vivo myocardial I/R injury. Here, we have sought to investigate the effects of preconditioning with resveratrol on myocardial I/R damage across the small animal studies. Methods and Results. The MEDLINE, Google Scholar, PubMed, and Cochrane databases were searched for preclinical studies investigating resveratrol vs. vehicle published from the inception to July 2018. Eventually, 10 in vivo and 7 ex vivo studies with 261 animals (130 for resveratrol; 131 for vehicle) were included for meta-analysis. Pooled estimates for primary outcomes demonstrated that pretreatment with resveratrol significantly reduced the infarct size after myocardial I/R injury irrespective of in vivo (weighted mean difference (WMD): -13.42, 95% CI: -16.63 to -10.21, P≤0.001) or ex vivo (WMD: -15.05, 95% CI: -18.23 to -11.86, P≤0.001) studies. Consistently, stratified analysis according to the reperfusion duration, route of administration, or timing regimen of pretreatment all showed the infarct-sparing benefit of resveratrol. Metaregression did not indicate any difference in infarct size based on species, sample size, state, route of administration, reperfusion duration, and timing regimen of pretreatment. Meanwhile, sensitivity analysis also identified the cardioprotection of resveratrol with robust results in spite of significant heterogeneity. Conclusions. Preconditioning with resveratrol appears to prevent the heart from I/R injury in comparison with vehicle, as evidenced by limited infarct size in a preclinical setting. Studies with large animals or randomized controlled trials will add more evidence and provide the rationale for clinical use.

In Vivo MRI Visualization of Acute Myocardial Ischemia and Reperfusion in Ferrets by the Persistent Action of the Contrast Agent Gd(BME-DTTA)

Circulation ◽  
1995 ◽  
Vol 92 (12) ◽  
pp. 3549-3559 ◽  
Author(s):  
Tamás Simor ◽  
Wen-Jang Chu ◽  
Lynne Johnson ◽  
Andras Safranko ◽  
Mark Doyle ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Contrast Agent ◽  
Acute Myocardial Ischemia ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

scholarly journals Metabolic alterations in acute myocardial ischemia-reperfusion injury and necrosis using in vivo hyperpolarized [1-13C] pyruvate MR spectroscopy

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Chung-Man Moon ◽  
Yun-Hyeon Kim ◽  
Young-Keun Ahn ◽  
Myung-Ho Jeong ◽  
Gwang-Woo Jeong
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Real Time ◽  
Intracellular Ph ◽  
Ischemia Reperfusion ◽  
Acute Myocardial Ischemia ◽  
Total Carbon ◽  
Myocardial Ischemia Reperfusion ◽  
Ph Level

AbstractThis study aimed to investigate real-time early detection of metabolic alteration in a rat model with acute myocardial ischemia-reperfusion (AMI/R) injury and myocardial necrosis, as well as its correlation with intracellular pH level using in vivo hyperpolarized [1-13C] pyruvate magnetic resonance spectroscopy (MRS). Hyperpolarized 13C MRS was performed on the myocardium of 8 sham-operated control rats and 8 rats with AMI/R injury, and 8 sham-operated control rats and 8 rats with AMI-induced necrosis. Also, the correlations of levels of [1-13C] metabolites with pH were analyzed by Spearman’s correlation test. The AMI/R and necrosis groups showed significantly higher ratios of [1-13C] lactate (Lac)/bicarbonate (Bicar) and [1-13C] Lac/total carbon (tC), and lower ratios of 13C Bicar/Lac + alanine (Ala), and 13C Bicar/tC than those of the sham-operated control group. Moreover, the necrosis group showed significantly higher ratios of [1-13C] Lac/Bicar and [1-13C] Lac/tC, and lower ratios of 13C Bicar/Lac + Ala and 13C Bicar/tC than those of the AMI/R group. These results were consistent with the pattern for in vivo the area under the curve (AUC) ratios. In addition, levels of [1-13C] Lac/Bicar and [1-13C] Lac/tC were negatively correlated with pH levels, whereas 13C Bicar/Lac + Ala and 13C Bicar/tC levels were positively correlated with pH levels. The levels of [1-13C] Lac and 13C Bicar will be helpful for non-invasively evaluating the early stage of AMI/R and necrosis in conjunction with reperfusion injury of the heart. These findings have potential application to real-time evaluation of cardiac malfunction accompanied by changes in intracellular pH level and enzymatic activity.

scholarly journals Protective effect and mechanistic evaluation of linalool against acute myocardial ischemia and reperfusion injury in rats

RSC Advances ◽  
2017 ◽  
Vol 7 (55) ◽  
pp. 34473-34481 ◽  
Author(s):  
Xiao-Hui Zheng ◽  
Chun-Ping Liu ◽  
Zeng-Guang Hao ◽  
Yan-Fang Wang ◽  
Xian-Li Li
Keyword(s):  
Cell Death ◽  
Myocardial Ischemia ◽  
Protective Effect ◽  
Reperfusion Injury ◽  
Acute Myocardial Ischemia ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Myocardial Ischemia And Reperfusion

Linalool causes attenuation of IR induced cell death and apoptosis eitherin vitroorin vivo.

Role of heme oxygenase-1 in the cardioprotective effects of erythropoietin during myocardial ischemia and reperfusion

2009 ◽  
Vol 296 (1) ◽  
pp. H84-H93 ◽  
Author(s):  
Dylan Burger ◽  
Fuli Xiang ◽  
Lamis Hammoud ◽  
Xiangru Lu ◽  
Qingping Feng
Keyword(s):  
Myocardial Ischemia ◽  
Infarct Size ◽  
Heme Oxygenase ◽  
Ischemia Reperfusion ◽  
Primary Cultures ◽  
Heme Oxygenase 1 ◽  
Wild Type ◽  
Myocardial Ischemia And Reperfusion ◽  
Cardioprotective Effects

We have recently demonstrated that erythropoietin (EPO) protects cardiomyocytes from apoptosis during myocardial ischemia-reperfusion (I/R). The objective of the present study was to investigate the role of heme oxygenase (HO)-1 in the antiapoptotic effects of EPO. Primary cultures of neonatal mouse cardiomyocytes were subjected to anoxia-reoxygenation (A/R). Pretreatment with EPO significantly reduced apoptosis in A/R-treated cells. This reduction in apoptosis was preceded by an increase in the mRNA and protein expression of HO-1. Selective inhibition of HO-1 using chromium mesoporphyrin (CrMP) significantly diminished the ability of EPO to inhibit apoptosis. Cotreatment of EPO with SB-202190, an inhibitor of p38 activation, blocked the EPO-mediated HO-1 expression and antiapoptotic effects, suggesting a p38-dependent mechanism. The in vivo significance of p38 and HO-1 as mediators of EPO's cardioprotection was investigated in mice subjected to myocardial I/R. Pretreatment with EPO decreased infarct size as well as I/R-induced apoptosis in wild-type mice. However, these effects were significantly diminished in HO-1−/−mice. Furthermore, EPO given during ischemia reduced infarct size in mice subjected to I/R, and this effect was blocked by CrMP treatment in wild-type mice. Moreover, inhibition of p38 diminished the cardioprotective effects of EPO. We conclude that upregulation of HO-1 expression via p38 signaling contributes to EPO-mediated cardioprotection during myocardial I/R.

Long-term infusion of Met5-enkephalin fails to protect murine hearts against ischemia-reperfusion injury

2005 ◽  
Vol 288 (4) ◽  
pp. H1717-H1723 ◽  
Author(s):  
Koh Kuzume ◽  
Kazuyo Kuzume ◽  
Zhiping Cao ◽  
Lijuan Liu ◽  
Donna M. Van Winkle
Keyword(s):  
Myocardial Ischemia ◽  
Infarct Size ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Opioid Peptide ◽  
Area At Risk ◽  
Regional Myocardial Ischemia ◽  
Chronic Infusion ◽  
Myocardial Ischemia Reperfusion

Recently, we reported that exogenous administration of Met5-enkephalin (ME) for 24 h reduces infarct size after ischemia-reperfusion in rabbits. In the present study, we tested whether ME-induced cardioprotection is exhibited in murine hearts and whether chronic infusion of this peptide can render hearts tolerant to ischemia. Barbiturate-anesthetized open-chest mice (C57BL/6J) were subjected to regional myocardial ischemia-reperfusion (45 min of occlusion and 20 min of reperfusion). Mice received saline vehicle or ME for 24 h or 2 wk before undergoing regional myocardial ischemia-reperfusion or for 24 h followed by a 24-h delay before regional myocardial ischemia-reperfusion. Infarct size was measured with propidium iodide and is expressed as a percentage of the area at risk. Infarcts were smaller after infusion of ME for 24 h than with vehicle control: 49.2 ± 9.0% vs. 22.2 ± 3.2% ( P < 0.01). In contrast, administration of ME for 2 wk failed to elicit cardioprotection: 36.5 ± 9.1% and 41.4 ± 8.2% for control and ME, respectively ( P = not significant). When a 24-h delay was imposed between the end of drug treatment and the onset of the ischemic insult, cardioprotection was lost: 38.5 ± 6.1% and 42.8 ± 6.6% for control and ME, respectively ( P = not significant). Chronic sustained exogenous infusion of the endogenously produced opioid peptide ME is associated with loss of the cardioprotection that is observed with 24 h of infusion. Furthermore, in this in vivo murine model, ME failed to induce delayed tolerance to myocardial ischemia-reperfusion.

Coronary endothelial P-selectin in pathogenesis of myocardial ischemia-reperfusion injury

1998 ◽  
Vol 275 (5) ◽  
pp. H1865-H1872 ◽  
Author(s):  
Anthony J. Palazzo ◽  
Steven P. Jones ◽  
Donald C. Anderson ◽  
D. Neil Granger ◽  
David J. Lefer
Keyword(s):  
Myocardial Ischemia ◽  
Infarct Size ◽  
Ischemia Reperfusion Injury ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Myocardial Infarct Size ◽  
Wild Type ◽  
Area At Risk ◽  
Myocardial Ischemia Reperfusion

We investigated in vivo coronary P-selectin expression and its pathophysiological consequences in a murine model of myocardial ischemia-reperfusion (MI/R) using wild-type and P-selectin deficient (−/−) mice. Coronary P-selectin expression [μg monoclonal antibody (MAb)/g tissue] was measured using a radiolabeled MAb method after 30 min of myocardial ischemia and 20 min of reperfusion. P-selectin expression in wild-type mice was significantly ( P< 0.01) elevated in the ischemic zone (0.070 ± 0.010) compared with the nonischemic zone (0.037 ± 0.008). Myocardial P-selectin expression was nearly undetectable in P-selectin −/− mice after MI/R. Furthermore, myocardial infarct size (% of area at risk) after 30 min of myocardial ischemia and 120 min of reperfusion was 42.5 ± 4.4 in wild-type mice and 24.4 ± 4.0 in P-selectin −/− mice ( P < 0.05). In additional experiments of prolonged myocardial ischemia (60 min) and reperfusion (120 min), myocardial infarct size was similar in P-selectin −/− mice and wild-type mice. Our results clearly demonstrate the involvement of coronary P-selectin in the development of myocardial infarction after MI/R.

scholarly journals Leukocyte trafficking and myocardial reperfusion injury in ICAM-1/P-selectin-knockout mice

2001 ◽  
Vol 280 (1) ◽  
pp. H60-H67 ◽  
Author(s):  
Stephanie A. Briaud ◽  
Zhi-Ming Ding ◽  
Lloyd H. Michael ◽  
Mark L. Entman ◽  
Sherita Daniel ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Infarct Size ◽  
Ischemia Reperfusion ◽  
Intercellular Adhesion Molecule ◽  
Myeloperoxidase Activity ◽  
Wild Type ◽  
Area At Risk ◽  
Myocardial Ischemia And Reperfusion ◽  
Significant Difference ◽  
Deficient Mice

P-selectin and intercellular adhesion molecule-1 (ICAM-1) mediate early interaction and adhesion of neutrophils to coronary endothelial cells and myocytes after myocardial ischemia and reperfusion. In the present study, we examined the physiological consequences of genetic deletions of ICAM-1 and P-selectin in mice. In wild-type mice, after 1 h of ischemia followed by reperfusion, neutrophil influx into the area of ischemia was increased by 3 h with a peak at 24 h and a decline by 72 h. ICAM-1/P-selectin-deficient mice showed a significant reduction in neutrophils by immunohistochemistry or by myeloperoxidase activity at 24 h but no significant difference at 3 h. Infarct size (area of necrosis/area at risk) assessed 24 h after reperfusion was not different between wild-type and deficient mice after 30 min and 1 h of occlusion. Mice with a deficiency in both ICAM-1 and P-selectin have impaired neutrophil trafficking without a difference in infarct size due to myocardial ischemia-reperfusion.

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