Daily reoxygenation decreases myocardial injury and improves post-ischaemic recovery after chronic hypoxia☆

Milano, Giuseppina; Corno, Antonio F.; Samaja, Michele; Morel, Sandrine; Vassalli, Giuseppe; Segesser, Ludwig K. von

doi:10.1016/j.ejcts.2009.10.030

Cited by 21 publications

(22 citation statements)

References 24 publications

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“…The measurement of the infarct area following LAD occlusion/reperfusion is related to the functional recovery of Langendorff-perfused hearts after I/R [10]. The LAD occlusion challenged ≈ 40% of the left ventricle in all groups, yet the infarct area at the end of the reperfusion was 50% of the risk area in control hearts, which reduced by half in IH hearts, as a result of effective cardioprotection.…”

Section: Discussionmentioning

confidence: 99%

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Impact of the Phosphatidylinositide 3-Kinase Signaling Pathway on the Cardioprotection Induced by Intermittent Hypoxia

et al. 2013

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BackgroundExposure to intermittent hypoxia (IH) may enhance cardiac function and protects heart against ischemia-reperfusion (I/R) injury. To elucidate the underlying mechanisms, we developed a cardioprotective IH model that was characterized at hemodynamic, biochemical and molecular levels.MethodsMice were exposed to 4 daily IH cycles (each composed of 2-min at 6-8% O2 followed by 3-min reoxygenation for 5 times) for 14 days, with normoxic mice as controls. Mice were then anesthetized and subdivided in various subgroups for analysis of contractility (pressure-volume loop), morphology, biochemistry or resistance to I/R (30-min occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion and measurement of the area at risk and infarct size). In some mice, the phosphatidylinositide 3-kinase (PI3K) inhibitor wortmannin was administered (24 µg/kg ip) 15 min before LAD.ResultsWe found that IH did not induce myocardial hypertrophy; rather both contractility and cardiac function improved with greater number of capillaries per unit volume and greater expression of VEGF-R2, but not of VEGF. Besides increasing the phosphorylation of protein kinase B (Akt) and the endothelial isoform of NO synthase with respect to control, IH reduced the infarct size and post-LAD proteins carbonylation, index of oxidative damage. Administration of wortmannin reduced the level of Akt phosphorylation and worsened the infarct size.ConclusionWe conclude that the PI3K/Akt pathway is crucial for IH-induced cardioprotection and may represent a viable target to reduce myocardial I/R injury.

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Section: Discussionmentioning

confidence: 99%

“…To address cardioprotection, we adopted a validated method [10]. Angiogenesis was addressed by measuring the vascular endothelial growth factors (VEGFs), a family of glycoproteins involved in the regulation of vasculogenesis.…”

Section: Introductionmentioning

confidence: 99%

Impact of the Phosphatidylinositide 3-Kinase Signaling Pathway on the Cardioprotection Induced by Intermittent Hypoxia

et al. 2013

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“…T8877) in PBS for 20 min at 37°C. Sections were fixed in 10% buffered formalin overnight at 4°C and then weighed and photographed for infarct size calculations (3,36,47,51). TTC stains the viable tissue red due to dehydrogenases, and nonviable while infarcted tissue remains a pale white.…”

Section: Generation Of Transgene Construct and Transgenic Micementioning

confidence: 99%

Cardiomyocyte sulfonylurea receptor 2-K_ATPchannel mediates cardioprotection and ST segment elevation

Stoller

Fahrenbach

Chalupský

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Sulfonylurea receptor-containing ATP-sensitive potassium (K(ATP)) channels have been implicated in cardioprotection, but the cell type and constitution of channels responsible for this protection have not been clear. Mice deleted for the first nucleotide binding region of sulfonylurea receptor 2 (SUR2) are referred to as SUR2 null since they lack full-length SUR2 and glibenclamide-responsive K(ATP) channels in cardiac, skeletal, and smooth muscle. As previously reported, SUR2 null mice develop electrocardiographic changes of ST segment elevation that were shown to correlate with coronary artery vasospasm. Here we restored expression of the cardiomyocyte SUR2-K(ATP) channel in SUR2 null mice by generating transgenic mice with ventricular cardiomyocyte-restricted expression of SUR2A. Introduction of the cardiomyocyte SUR2A transgene into the SUR2 null background restored functional cardiac K(ATP) channels. Hearts isolated from rescued mice, referred to as MLC2A, had significantly reduced infarct size (27 ± 3% of area at risk) compared with SUR2 null mice (36 ± 3% of area at risk). Compared with SUR2 null hearts, MLC2A hearts exhibited significantly improved cardiac function during the postischemia reperfusion period primarily because of preservation of low diastolic pressures. Additionally, restoration of cardiac SUR2-K(ATP) channels significantly reduced the degree and frequency of ST segment elevation episodes in MLC2A mice. Therefore, cardioprotective mechanisms both dependent and independent of SUR2-K(ATP) channels contribute to cardiac function.

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“…These findings could help in the design of www.intechopen.com Cardiac Arrhythmias -New Considerations 202 new treatments based on NO pharmacology against hypoxia/reoxygenation dysfunctions (Rus et al, 2011). In contrast to previous evidence about the harmful effect of reoxygenation on myocardium, Milano et al (2010) refer to the protective effect of chronic hypoxia against ischemia/reperfusion damage. In rat experiments, exposure to chronic hypoxia results in impairment of myocardial tolerance to ischemia/reperfusion, greater injury and reduced recovery of performance.…”

Section: Wwwintechopencom Chronobiological Aspects Of the Heart Rhymentioning

confidence: 60%

Chronobiological Aspects of the Heart Rhythm Disorders at the Change of Pulmonary Ventilation in Rat Model

Švorc¹,

Marossy²,

Grešová³

et al. 2012

Cardiac Arrhythmias - New Considerations

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Daily reoxygenation decreases myocardial injury and improves post-ischaemic recovery after chronic hypoxia☆

Cited by 21 publications

References 24 publications

Impact of the Phosphatidylinositide 3-Kinase Signaling Pathway on the Cardioprotection Induced by Intermittent Hypoxia

Impact of the Phosphatidylinositide 3-Kinase Signaling Pathway on the Cardioprotection Induced by Intermittent Hypoxia

Cardiomyocyte sulfonylurea receptor 2-K_ATPchannel mediates cardioprotection and ST segment elevation

Chronobiological Aspects of the Heart Rhythm Disorders at the Change of Pulmonary Ventilation in Rat Model

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Daily reoxygenation decreases myocardial injury and improves post-ischaemic recovery after chronic hypoxia☆

Cited by 21 publications

References 24 publications

Impact of the Phosphatidylinositide 3-Kinase Signaling Pathway on the Cardioprotection Induced by Intermittent Hypoxia

Impact of the Phosphatidylinositide 3-Kinase Signaling Pathway on the Cardioprotection Induced by Intermittent Hypoxia

Cardiomyocyte sulfonylurea receptor 2-KATPchannel mediates cardioprotection and ST segment elevation

Chronobiological Aspects of the Heart Rhythm Disorders at the Change of Pulmonary Ventilation in Rat Model

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Cardiomyocyte sulfonylurea receptor 2-K_ATPchannel mediates cardioprotection and ST segment elevation