Heptanol triggers cardioprotection via mitochondrial mechanisms and mitochondrial potassium channel opening in rat hearts

Johansen, David; Sanden, Espen; Hagve, Martin; Chu, Xi; Sundset, Rune; Ytrehus, Kirsti

doi:10.1111/j.1748-1716.2010.02221.x

Cited by 14 publications

(13 citation statements)

References 37 publications

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“…Cx43 is also involved in pathological and physiological processes other than arrhythmias during I/R injury [41, 42], and it may cause uncontrolled opening of hemichannels in the plasma membrane [43] and may be deleterious to the myocardium [44]. Blocking hemichannels may confer cardioprotection by preventing ionic imbalance, excessive entry of Na + and Ca + , ATP leakage, cell swelling, and loss of critical metabolites [40, 45, 46]. Therefore, Cx43-mediated intercellular communication of the injured tissue can be enlarged into other cells, and this may explain that LXA 4 preconditioning induced higher Cx43 expression but caused more serious damage to myocardium.…”

Section: Discussionmentioning

confidence: 99%

Lipoxin A₄Preconditioning and Postconditioning Protect Myocardial Ischemia/Reperfusion Injury in Rats

Zhao

Shao

Xingti

et al. 2013

Mediators of Inflammation

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This study aims to investigate the pre- and postconditioning effects of lipoxin A4 (LXA4) on myocardial damage caused by ischemia/reperfusion (I/R) injury. Seventy-two rats were divided into 6 groups: sham groups (C1 and C2), I/R groups (I/R1 and I/R2), and I/R plus LXA4 preconditioning and postconditioning groups (LX1 and LX2). The serum levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and cardiac troponin I (cTnI) were measured. The content and the activity of Na+-K+-ATPase as well as the superoxide dismutase (SOD), and malondialdehyde (MDA) levels were determined. Along with the examination of myocardium ultrastructure and ventricular arrhythmia scores (VAS), connexin 43 (Cx43) expression were also detected. Lower levels of IL-1β, IL-6, IL-8, TNF-α, cTnI, MDA content, and VAS and higher levels of IL-10, SOD activity, Na+-K+-ATPase content and activity, and Cx43 expression appeared in LX groups than I/R groups. Besides, H&E staining, TEM examination as well as analysis of gene, and protein confirmed that LXA4 preconditioning was more effective than postconditioning in preventing arrhythmogenesis via the upregulation of Cx43. That is, LXA4 postconditioning had better protective effect on Na+-K+-ATPase and myocardial ultrastructure.

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Section: Discussionmentioning

confidence: 99%

Lipoxin A₄Preconditioning and Postconditioning Protect Myocardial Ischemia/Reperfusion Injury in Rats

Zhao

Shao

Xingti

et al. 2013

Mediators of Inflammation

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“…, Johansen et al . ) and include the low mitochondrial Ca 2+ load by reducing the ΔΨm (Murata et al . ) and activation of mitochondrial respiration (Riess et al .…”

Section: Discussionmentioning

confidence: 99%

Energetic study of cardioplegic hearts under ischaemia/reperfusion and [Ca²⁺] changes in cardiomyocytes of guinea‐pig: mitochondrial role

2012

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CPG, diazoxide and clonazepam improve postischaemic recovery, respectively, by increasing the Ca(2+) cycling and by reducing the mitochondrial Ca(2+) uptake either by uniporter or by mNCX. The mitochondria compete with the leaky sarcoplasmic reticulum (SR) as sink of Ca(2+) in guinea-pig hearts, affecting the postischaemic contractility. CPG also prevented the ouabain-induced dysfunction by avoiding the Ca(2+) overload. Ouabain reduced the synergism between CPG and clonazepam suggesting that [Na(+)]i and SR load influence the mNCX role.

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“…Cardiac subsarcolemmal (SSM) and interfibrillar mitochondria (IFM) were isolated from the left ventricle as previously described [22], [23]. Renal and hepatic mitochondria were also isolated by the procedure used to isolate SSM mitochondria.…”

Section: Methodsmentioning

confidence: 99%

The Acute Phase of Experimental Cardiogenic Shock Is Counteracted by Microcirculatory and Mitochondrial Adaptations

et al. 2014

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The mechanisms contributing to multiorgan dysfunction during cardiogenic shock are poorly understood. Our goal was to characterize the microcirculatory and mitochondrial responses following ≥10 hours of severe left ventricular failure and cardiogenic shock. We employed a closed-chest porcine model of cardiogenic shock induced by left coronary microembolization (n = 12) and a time-matched control group (n = 6). Hemodynamics and metabolism were measured hourly by intravascular pressure catheters, thermodilution, arterial and organ specific blood gases. Echocardiography and assessment of the sublingual microcirculation by sidestream darkfield imaging were performed at baseline, 2±1 and 13±3 (mean±SD) hours after coronary microembolization. Upon hemodynamic decompensation, cardiac, renal and hepatic mitochondria were isolated and evaluated by high-resolution respirometry. Low cardiac output, hypotension, oliguria and severe reductions in mixed-venous and hepatic O2 saturations were evident in cardiogenic shock. The sublingual total and perfused vessel densities were fully preserved throughout the experiments. Cardiac mitochondrial respiration was unaltered, whereas state 2, 3 and 4 respiration of renal and hepatic mitochondria were increased in cardiogenic shock. Mitochondrial viability (RCR; state 3/state 4) and efficiency (ADP/O ratio) were unaffected. Our study demonstrates that the microcirculation is preserved in a porcine model of untreated cardiogenic shock despite vital organ hypoperfusion. Renal and hepatic mitochondrial respiration is upregulated, possibly through demand-related adaptations, and the endogenous shock response is thus compensatory and protective, even after several hours of global hypoperfusion.

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Heptanol triggers cardioprotection via mitochondrial mechanisms and mitochondrial potassium channel opening in rat hearts

Abstract: Pre-treatment with Hp protects the heart against ischaemia-reperfusion injury. This protection is most likely mediated via mitochondrial mechanisms which initiate a signalling cascade that converges on inhibition of opening of MPTP.

Cited by 14 publications

References 37 publications

Lipoxin A₄Preconditioning and Postconditioning Protect Myocardial Ischemia/Reperfusion Injury in Rats

Lipoxin A₄Preconditioning and Postconditioning Protect Myocardial Ischemia/Reperfusion Injury in Rats

Energetic study of cardioplegic hearts under ischaemia/reperfusion and [Ca²⁺] changes in cardiomyocytes of guinea‐pig: mitochondrial role

The Acute Phase of Experimental Cardiogenic Shock Is Counteracted by Microcirculatory and Mitochondrial Adaptations

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Heptanol triggers cardioprotection via mitochondrial mechanisms and mitochondrial potassium channel opening in rat hearts

Abstract: Pre-treatment with Hp protects the heart against ischaemia-reperfusion injury. This protection is most likely mediated via mitochondrial mechanisms which initiate a signalling cascade that converges on inhibition of opening of MPTP.

Cited by 14 publications

References 37 publications

Lipoxin A4Preconditioning and Postconditioning Protect Myocardial Ischemia/Reperfusion Injury in Rats

Lipoxin A4Preconditioning and Postconditioning Protect Myocardial Ischemia/Reperfusion Injury in Rats

Energetic study of cardioplegic hearts under ischaemia/reperfusion and [Ca2+] changes in cardiomyocytes of guinea‐pig: mitochondrial role

The Acute Phase of Experimental Cardiogenic Shock Is Counteracted by Microcirculatory and Mitochondrial Adaptations

Contact Info

Product

Resources

About

Lipoxin A₄Preconditioning and Postconditioning Protect Myocardial Ischemia/Reperfusion Injury in Rats

Lipoxin A₄Preconditioning and Postconditioning Protect Myocardial Ischemia/Reperfusion Injury in Rats

Energetic study of cardioplegic hearts under ischaemia/reperfusion and [Ca²⁺] changes in cardiomyocytes of guinea‐pig: mitochondrial role