Cardioprotection via adaptation to hypoxia: expanding the timeline and targets?

Przyklenk, Karin; Whittaker, Peter

doi:10.1007/s00395-011-0169-9

Cited by 11 publications

(11 citation statements)

References 31 publications

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“…Although a number of cardioprotective strategies have been discovered, their clinical translation is disappointing, probably because of the inadequacy of animal I/R models to simulate what happens at the bedside (13,34). IHH appears to be a promising therapeutic strategy for coronary heart disease due to its easier manipulation, longer protection duration, and fewer adverse effects (3,37,48). Moreover, we (48) have shown that IHH has a significant therapeutic effect after 1 wk of coronary artery occlusion.…”

Section: Mitochondria As the Main Source Of Ros In Ihh-induced Cardiomentioning

confidence: 77%

“…IHH has also been demonstrated to improve myocardial perfusion in patients with severe coronary heart disease (7). As a relatively simple intervention, IHH may offer profound benefits to patients with acute myocardial infarction upon the elucidation of protective mechanisms (37). Considering the failure of clinical usage of antioxidants (29), understanding the precise regulation of ROS generation and subsequent signaling pathways in IHH is of clinical significance.…”

Section: Mitochondria As the Main Source Of Ros In Ihh-induced Cardiomentioning

confidence: 99%

“…Recently, we (48) revealed a therapeutic effect of IHH on permanent coronary artery ligation-induced myocardial infarction by attenuating infarct size, myocardial fibrosis, and apoptosis and improving cardiac performance. Because IHH is a relatively simple intervention with a longer protection duration and fewer adverse effects and may offer profound benefit to patients with acute myocardial infarction (3,37), elucidating the mechanistic insights underlying the cardioprotective effects of IHH is critical to potential clinic applications.…”

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confidence: 99%

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Intermittent hypobaric hypoxia improves postischemic recovery of myocardial contractile function via redox signaling during early reperfusion

Wang

Chen

Zhang

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Intermittent hypobaric hypoxia improves postischemic recovery of myocardial contractile function via redox signaling during early reperfusion. Am J Physiol Heart Circ Physiol 301: H1695-H1705, 2011. First published August 5, 2011; doi:10.1152/ajpheart.00276.2011.-Intermittent hypobaric hypoxia (IHH) protects hearts against ischemiareperfusion (I/R) injury, but the underlying mechanisms are far from clear. ROS are paradoxically regarded as a major cause of myocardial I/R injury and a trigger of cardioprotection. In the present study, we investigated whether the ROS generated during early reperfusion contribute to IHH-induced cardioprotection. Using isolated perfused rat hearts, we found that IHH significantly improved the postischemic recovery of left ventricular (LV) contractile function with a concurrent reduction of lactate dehydrogenase release and myocardial infarct size (20.5 Ϯ 5.3% in IHH vs. 42.1 Ϯ 3.8% in the normoxic control, P Ͻ 0.01) after I/R. Meanwhile, IHH enhanced the production of protein carbonyls and malondialdehyde, respective products of protein oxidation and lipid peroxidation, in the reperfused myocardium and ROS generation in reperfused cardiomyocytes. Such effects were blocked by the mitochondrial ATP-sensitive K ϩ channel inhibitor 5-hydroxydecanoate. Moreover, the IHH-improved postischemic LV performance, enhanced phosphorylation of PKB (Akt), PKC-ε, and glycogen synthase kinase-3␤, as well as translocation of PKC-ε were not affected by applying H 2O2 (20 mol/l) during early reperfusion but were abolished by the ROS scavengers N-(2-mercaptopropionyl-)glycine (MPG) and manganese (III) tetrakis (1-methyl-4-pyridyl)porphyrin. Furthermore, IHH-reduced lactate dehydrogenase release and infarct size were reversed by MPG. Consistently, inhibition of Akt with wortmannin and PKC-ε with εV1-2 abrogated the IHH-improved postischemic LV performance. These findings suggest that IHHinduced cardioprotection depends on elevated ROS production during early reperfusion.reactive oxygen species; ischemia-reperfusion injury EARLY REPERFUSION during evolving myocardial infarction is essential for saving the myocardium, but lethal reperfusion injury can occur and limit the beneficial effects (49). A number of cardioprotective strategies have been developed to ameliorate or retard the irreversible injury. However, the clinical translation of these strategies has failed to achieve the anticipated results (13, 34). Intermittent hypobaric hypoxia (IHH) has been shown to protect the heart against ischemia-reperfusion (I/R) injury by improving the manifestations including contractile dysfunction (3, 33), arrhythmias (31, 52), and cell death (8,27). Recently, we (48) revealed a therapeutic effect of IHH on permanent coronary artery ligation-induced myocardial infarction by attenuating infarct size, myocardial fibrosis, and apoptosis and improving cardiac performance. Because IHH is a relatively simple intervention with a longer protection duration and fewer adverse effects and may offer profound benefit to patients ...

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Section: Mitochondria As the Main Source Of Ros In Ihh-induced Cardiomentioning

confidence: 77%

Section: Mitochondria As the Main Source Of Ros In Ihh-induced Cardiomentioning

confidence: 99%

mentioning

confidence: 99%

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Intermittent hypobaric hypoxia improves postischemic recovery of myocardial contractile function via redox signaling during early reperfusion

Wang

Chen

Zhang

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…It has the advantages of noninvasive, easier manipulation, and long-lasting protection (up to 5 weeks even stopped the exposure to hypoxia) compared with IPC or IPoC [20,[32][33][34][35]. However, the cardioprotective mechanisms of IHH have not yet been fully understood.…”

Section: Discussionmentioning

confidence: 99%

ROS generated during early reperfusion contribute to intermittent hypobaric hypoxia-afforded cardioprotection against postischemia-induced Ca2+ overload and contractile dysfunction via the JAK2/STAT3 pathway

Tan

Wang

et al. 2015

Journal of Molecular and Cellular Cardiology

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“…This phenomenon was named remote IPC (RIPC). [14151617181920212223242526272829] The remote ischemic conditioning (RIC) stimulus could be noninvasively induced using a standard blood pressure cuff placed on the upper arm or leg. [30]…”

Section: Introductionmentioning

confidence: 99%

Repeated Remote Ischemic Conditioning Effect on Ankle-brachial Index in Diabetic Patients - A Randomized Control Trial

et al. 2017

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Background:Remote ischemic preconditioning (RIPC) is a phenomenon where a short period of ischemia in one organ protects against further ischemia in the other organs. We hypothesized that RIPC occurring in diabetic patients with ankle brachial index (ABI) between 0.70 and 0.90 were included with peripheral arterial disease, would make the better coronary flow resulted in the increasing ABI.Materials and Methods:This randomized clinical trial study was done in the Afshar Cardiovascular Hospital in Yazd between 2013 and 2014. Sixty participants were randomly divided into two groups (intervention and control groups). The intervention group was undergoing RIPC, and the control group was tested without RIPC. RIPC was stimulated by giving three cycles of 5 min of ischemia followed by 5 min of reperfusion of both upper arms using a blood pressure cuff inflated to 200 mm Hg (n = 30). This was compared with no RIPC group which consisted of placing a deflated blood pressure cuff on the upper limbs (n = 30).Results:The mean of ABI level before intervention in the RIPC and control group group was 0.82 ± 0.055 and 0.83 ± 0.0603 (P = 0.347) respectively, with no significant difference. It was 0.86 ± 0.066 in the RIPC group compared the control 0.83 ± 0.0603 (P = 0.046). So levels of ABI were greater after intervention in the RIPC group. The mean of ABI level increase from 0.82 ± 0.05 to 0.86 ± 0.06 in RIPC group (P = 0.008). So the intervention group showed a significant increase in ABI.Conclusions:RIPC through using a simple, noninvasive technique, composing three cycles of 5 min-ischemia of both upper arms, showing a significant increase in ABI level in diabetic patients.

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Cardioprotection via adaptation to hypoxia: expanding the timeline and targets?

Cited by 11 publications

References 31 publications

Intermittent hypobaric hypoxia improves postischemic recovery of myocardial contractile function via redox signaling during early reperfusion

Intermittent hypobaric hypoxia improves postischemic recovery of myocardial contractile function via redox signaling during early reperfusion

ROS generated during early reperfusion contribute to intermittent hypobaric hypoxia-afforded cardioprotection against postischemia-induced Ca2+ overload and contractile dysfunction via the JAK2/STAT3 pathway

Repeated Remote Ischemic Conditioning Effect on Ankle-brachial Index in Diabetic Patients - A Randomized Control Trial

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