scholarly journals Limb remote ischemia per-conditioning protects the heart against ischemia–reperfusion injury through the opioid system in rats

2018 ◽  
Vol 96 (1) ◽  
pp. 68-75 ◽  
Author(s):  
Li Zhang ◽  
Hui Guo ◽  
Fang Yuan ◽  
Zeng-chao Hong ◽  
Yan-ming Tian ◽  
...  
Keyword(s):  
Protein Expression ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Cardiac Ischemia ◽  
Cardiac Protection ◽  
Expression Levels ◽  
Infarct Area

Remote ischemia per-conditioning (RPerC) has been demonstrated to have cardiac protection, but the underlying mechanism remains unclear. This study aimed to investigate the mechanism underlying cardiac protection of RPerC. Adult male Sprague–Dawley rats were used in this study. Cardiac ischemia/reperfusion (I/R) was induced by 30 min of occlusion and 3 h of reperfusion of the left anterior descending coronary artery. RPerC were performed by 5 min of occlusion of the right femoral artery followed by 5 min of reperfusion for three times during cardiac ischemia. The hemodynamics, left ventricular function, arrhythmia, and infarct area were measured. Protein expression levels of endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), protein kinase C-ε (PKCε), and PKCδ in the myocardium were assayed. During I/R, systolic artery pressure and left ventricular function were decreased, infarct area was increased, and arrhythmia score was increased (P < 0.05). However, changes of the above parameters were significantly attenuated in RPerC-treated rats compared with control rats (P < 0.05). The cardiac protective effects of RPerC were prevented by naloxone or glibenclamide. Also, RPerC increased the protein expression levels of eNOS, iNOS, PKCε, and PKCδ in the myocardium compared with control rats. These effects were blocked by naloxone, an opioid receptor antagonist, and glibenclamide, an ATP-sensitive K+ channel blocker (KATP). In summary, this study suggests that RPerC protects the heart against I/R injury through activation of opioid receptors and the NO–PKC–KATP channel signaling pathways.

scholarly journals Erythropoietin improves left ventricular function and coronary flow in an experimental model of ischemia-reperfusion injury

2004 ◽  
Vol 6 (7) ◽  
pp. 853-859 ◽  
Author(s):  
Peter van der Meer ◽  
Erik Lipsic ◽  
Robert H. Henning ◽  
Rudolf A. de Boer ◽  
Albert J.H. Suurmeijer ◽  
...  
Keyword(s):  
Left Ventricular Function ◽  
Reperfusion Injury ◽  
Ventricular Function ◽  
Experimental Model ◽  
Coronary Flow ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular

scholarly journals Catestatin Improves Post-Ischemic Left Ventricular Function and Decreases Ischemia/Reperfusion Injury in Heart

2010 ◽  
Vol 30 (8) ◽  
pp. 1171-1179 ◽  
Author(s):  
Claudia Penna ◽  
Giuseppe Alloatti ◽  
Maria Pia Gallo ◽  
Maria Carmela Cerra ◽  
Renzo Levi ◽  
...  
Keyword(s):  
Left Ventricular Function ◽  
Reperfusion Injury ◽  
Ventricular Function ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular

Responses of chronically hypoxic rat hearts to ischemia: KATP channel blockade does not abolish increased RV tolerance to ischemia

2004 ◽  
Vol 286 (2) ◽  
pp. H545-H551 ◽  
Author(s):  
Joerg Forkel ◽  
Xiaochao Chen ◽  
Susanne Wandinger ◽  
Florian Keser ◽  
Alexey Duschin ◽  
...  
Keyword(s):  
Protein Expression ◽  
Left Ventricular Function ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Right Ventricular Function ◽  
Chronic Hypoxia ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Rat Hearts ◽  
Left And Right

Chronic hypoxia may precondition the myocardium and protect from ischemia-reperfusion damage. We therefore examined the recovery of left and right ventricular function after ischemia and reperfusion (15 min each) in isolated blood-perfused working hearts from normoxic (Norm) and hypoxic (Hypo; 14 days, 10.5% O2) adult rats. In addition, the mRNA expression of hypoxia-inducible factor (HIF)-1α and the protein expression of endothelial nitric oxide synthase (eNOS) were measured. Postischemic left ventricular function recovered to 66 ± 6% and 67 ± 5% of baseline in Norm and Hypo, respectively. In contrast, postischemic right ventricular function was 93 ± 2% of baseline in Hypo vs. 67 ± 3% in Norm ( P < 0.05). Improved postischemic right ventricular function in Hypo (93 ± 2% and 96 ± 2% of baseline) was observed with 95% O2 or 21% O2 in the perfusate, and it was not attenuated by glibenclamide (5 and 10 μmol/l) (86 ± 4% and 106 ± 6% recovery). HIF-1α mRNA and eNOS protein expression were increased in both left and right hypoxic ventricles. In conclusion, postischemic right, but not left, ventricular function was improved by preceding chronic hypoxia. ATP-sensitive K+ channels are not responsible for the increased right ventricular tolerance to ischemia after chronic hypoxia in adult rat hearts.

A Model of Blood Component–Heart Interaction in Cardiac Ischemia–Reperfusion Injury using a Langendorff-Based Ex Vivo Assay

2019 ◽  
Vol 25 (2) ◽  
pp. 164-173 ◽  
Author(s):  
Johanna M. Muessig ◽  
Sema Kaya ◽  
Luise Moellhoff ◽  
Johanna Noelle ◽  
Leonie Hidalgo Pareja ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular Function ◽  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Cardiac Ischemia ◽  
Transfer Model ◽  
Blood Components ◽  
The Impact ◽  
Human Rbcs

Introduction: Myocardial infarction is one of the leading causes of morbidity and mortality worldwide. Cellular interactions of red blood cells (RBCs) and platelets with endothelial cells and cardiomyocytes play a crucial role in cardiac ischemia/reperfusion (I/R) injury. However, addressing the specific impact of such cell-to-cell interactions in commonly employed in vivo models of cardiac I/R injury is challenging due to overlap of neuronal, hormonal, and immunological pathways. This study aimed to refine a Langendorff-based ex vivo transfer model to evaluate the impact of specific blood components on cardiac I/R injury. Material and methods: Murine whole blood, defined murine blood components (RBCs, platelet-rich plasma [PRP], and platelet-poor plasma [PPP], respectively) as well as human RBCs were loaded to the coronary system of isolated murine hearts in a Langendorff system before initiating global ischemia for 40 minutes. Following 60 minutes of reperfusion with Krebs Henseleit Buffer, left ventricular function and coronary flow were assessed. Infarct size was determined by specific histological staining following 120 minutes of reperfusion. Results: Loading of murine whole blood to the coronary system of isolated murine hearts at the beginning of 40 minutes of global ischemia improved left ventricular function after 60 minutes of reperfusion and reduced the infarct size in comparison to buffer-treated controls. Similarly, isolated murine RBCs, PRP, and PPP mediated a protective effect in the cardiac I/R model. Furthermore, human RBCs showed a comparable protective capacity as murine RBCs. Conclusion: This Langendorff-based transfer model of cardiac I/R injury is a feasible, time-, and cost-effective model to evaluate the impact of blood components on myocardial infarction. The presented method facilitates loading of blood components of genetically modified mice to murine hearts of a different mouse strain, thus complementing time- and cost-intensive chimeric models and contributing to the development of novel targeted therapies.

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