Ischemic preconditioning prevents reperfusion heart injury in cardiac hypertrophy by activation of mitochondrial KATP channels

Katare, Rajesh; Sasaguri, Shiro; Suzuki, Ryoko; Xing, Yanfeng; Maeda, Hironori

doi:10.1016/j.ijcard.2003.06.010

Cited by 42 publications

(25 citation statements)

References 32 publications

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“…The role of mitochondrial K þ -ATP channels as one the end effectors of hyperoxic preconditioning has been also established [22]. Thus according to these results, and evidence for the proved antiarrhythmic role of mitochondrial K þ -ATP channels in IPC [30], it can be suggested that the antiarrhythmia effect of hyperoxia mediates through the pathway of nitric oxide-cGMP-PKG-mitochondrial K þ -ATP channels.…”

Section: Discussionmentioning

confidence: 90%

Ischemia and reperfusion-induced arrhythmias: role of hyperoxic preconditioning

Pourkhalili

Hajizadeh

Tiraihi

et al. 2009

Journal of Cardiovascular Medicine

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f Background Hyperoxic preconditioning is known to protect the heart against necrosis and contractile dysfunction, but protection against arrhythmias has not been well characterized.Objective The authors hypothesized that pre-exposure to normobaric hyperoxia (H) reduces ischemia and reperfusion-induced arrhythmias in isolated rat hearts.Methods Following 60 and 180 min of hyperoxia treatment, rat hearts were isolated immediately (H60 and H180) or 24 h afterward (H60/24 and H180/24), and subjected to 30 min of regional ischemia followed by 120 min of reperfusion. Occurrence, number, and duration of arrhythmias were analyzed during ischemia and reperfusion. In addition, cardiac infarct size was also assessed.Results Sixty and 180 min of breathing hyperoxic gas induced significant protection against severe ischemia and reperfusion-induced arrhythmias. Total number of premature ventricular beats was markedly attenuated by hyperoxia pre-exposure, especially in H60 and H180 groups. Duration of ventricular tachycardia and ventricular fibrillation was also affected by hyperoxia. Hyperoxia reduced the number of ventricular tachycardia episodes in ischemia and reperfusion phase. Accordingly, severity of arrhythmias (arrhythmia score) and infarct size were lower in hyperoxia-treated groups. The effects were more pronounced using hyperoxia immediately before harvesting the heart.Conclusion These results indicate that hyperoxic preconditioning attenuates ventricular ischemia and reperfusion-induced arrhythmias in isolated rat hearts, decreases cardiac infarct size, and improves postischemic heart function. The effects seem to depend on the time course after hyperoxia treatment.

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Section: Discussionmentioning

confidence: 90%

Ischemia and reperfusion-induced arrhythmias: role of hyperoxic preconditioning

Pourkhalili

Hajizadeh

Tiraihi

et al. 2009

Journal of Cardiovascular Medicine

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“…After the initial study of Speechly-Dick et al (1994), subsequent studies in isolated heart preparations have confirmed the ability of classic ischemic preconditioning protocols to elicit a cardioprotective response, with postischemic recovery of contractile function as the principal endpoint, using other rodent models of hypertension including the SHR strain (Boutros and Wang, 1995), abdominal aortic banding (Pantos et al, 1996), the (mREN-2)27 transgenic rat (Randall et al, 1997), and the Dahl salt-sensitive rat strain (Butler et al, 1999). Rajesh et al (2004) have reported that in pressure overload due to abdominal aortic banding, preconditioning with four 3-min coronary artery occlusion-reperfusion cycles before a 30-min coronary occlusion limited infarct size as effectively as it did in normotensive hearts in vivo and that the protection afforded by preconditioning in LVH was abolished by glibenclamide or 5-HD, implying that the involvement of K ATP channels in the protection afforded by preconditioning extends to hypertrophied hearts. Considered together, the above studies suggest that in moderate pressure-overload LVH, before the onset of decompensation, the ischemic preconditioning mechanism remains intact.…”

Section: B Experimental Ischemia/reperfusion Injury In Left Ventricumentioning

confidence: 97%

Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning

Ferdinándy¹,

Schulz²,

Baxter³

2007

Pharmacol Rev

652

615

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“…Delayed acquisition of tolerance to ischemia (late-phase preconditioning) arises 12-24 h after the initial preconditioning stimulus is applied, is longer lived (24 h or longer), and requires the expression of new gene products to mediate cardioprotection. Many of these preconditioning stimuli appear to promote the production of the gaseous monoxide nitric oxide (NO), phosphorylation and activation of p38 MAPK, and activation of plasmalemmal ATP-sensitive potassium (K ATP ) channels as initial triggering events in the acquisition of tolerance to I/R (10,46), whereas formation of the diatomic gas carbon monoxide (CO) and activation of mitochondrial K ATP channels appear to serve as important effectors of protection during I/R (5,34,40,51). In addition, preconditioning with NO donors, p38 MAPK activators, and K ATP channel agonists prevents postischemic leukocyte infiltration and exerts infarct-sparing effects in postischemic tissues (53).…”

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confidence: 99%