Evidence that Cardioprotection by Postconditioning Involves Preservation of Myocardial Opioid Content and Selective Opioid Receptor Activation

Zatta, Amanda J.; Kin, Hajime; Yoshishige, Darice; Jiang, Rong; Wang, Ning-Ping; Reeves, James G.; Mykytenko, James; Guyton, Robert A.; Zhao, Zhi‐Qing; Caffrey, James L.; Vinten‐Johansen, Jakob

doi:10.1016/j.hlc.2008.05.567

Cited by 32 publications

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“…Adenosine is increasingly released or focally accumulated upon reperfusion (90), and it is recognized to cause cardioprotection before index ischemia as a trigger of preconditioning, as well as at reperfusion as an effector of both preconditioning (95) and postconditioning (143). In a rodent model, the nonselective opioid receptor antagonist naloxone, as well as the selective antagonists of specific (␦, , or ) opioid receptors, blunted cardioprotective postconditioning; however, the nonselective agonist morphine exerted pharmacological postconditioning (239). There are other possible mediators of postconditioning-induced cardioprotection such as bradykinin or tyrosine kinase receptors (143), but their mechanisms of action are still under discussion.…”

Section: Role Of Transient Reperfusion In the Postconditioning Mechanmentioning

confidence: 99%

Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures

Shoji

Komuro

Kitakaze

2011

American Journal of Physiology-Heart and Circulatory Physiology

328

270

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Sanada S, Komuro I, Kitakaze M. Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures. Am J Physiol Heart Circ Physiol 301: H1723-H1741, 2011. First published August 19, 2011; doi:10.1152/ajpheart.00553.2011.-Heart diseases due to myocardial ischemia, such as myocardial infarction or ischemic heart failure, are major causes of death in developed countries, and their number is unfortunately still growing. Preliminary exploration into the pathophysiology of ischemia-reperfusion injury, together with the accumulation of clinical evidence, led to the discovery of ischemic preconditioning, which has been the main hypothesis for over three decades for how ischemia-reperfusion injury can be attenuated. The subcellular pathophysiological mechanism of ischemia-reperfusion injury and preconditioninginduced cardioprotection is not well understood, but extensive research into components, including autacoids, ion channels, receptors, subcellular signaling cascades, and mitochondrial modulators, as well as strategies for modulating these components, has made evolutional progress. Owing to the accumulation of both basic and clinical evidence, the idea of ischemic postconditioning with a cardioprotective potential has been discovered and established, making it possible to apply this knowledge in the clinical setting after ischemia-reperfusion insult. Another a great outcome has been the launch of translational studies that apply basic findings for manipulating ischemia-reperfusion injury into practical clinical treatments against ischemic heart diseases. In this review, we discuss the current findings regarding the fundamental pathophysiological mechanisms of ischemiareperfusion injury, the associated protective mechanisms of ischemic pre-and postconditioning, and the potential seeds for molecular, pharmacological, or mechanical treatments against ischemia-reperfusion injury, as well as subsequent adverse outcomes by modulation of subcellular signaling mechanisms (especially mitochondrial function). We also review emerging translational clinical trials and the subsistent clinical comorbidities that need to be overcome to make these trials applicable in clinical medicine. calcium overload; reactive oxygen species; mitochondria; transition pore; comorbidities; clinical trials WHAT DO WE KNOW ABOUT ischemia-reperfusion injury? Because the morbidity and mortality due to ischemic heart diseases have come to the fore in developed countries and are still increasing, it is critically important, both scientifically and socially, to know how cardioprotection is achieved in ischemic myocardium. In fact, in the clinical setting, the application of coronary thrombolysis or immediate percutaneous coronary intervention for faster recanalization has been shown to dramatically improve the outcomes of patients with acute or chronic myocardial ischemia due to impaired coronary blood supply. This finding is founded on the premise that a shorter period of index ischemia...

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Section: Role Of Transient Reperfusion In the Postconditioning Mechanmentioning

confidence: 99%

Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures

Shoji

Komuro

Kitakaze

2011

American Journal of Physiology-Heart and Circulatory Physiology

328

270

View full text Add to dashboard Cite

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“…Recently, Zatta and colleagues [208] have linked IPost with the endogenous activation of the opioid GPCR. After demonstrating that the non-specific opioid receptor antagonist, naloxone, was capable of abolishing IPost-protection in the intact rat heart, they investigated the effect of IPost in the presence of pharmacological antagonists of the -, -, and -opioid receptors [208].…”

Section: Cell-surface Receptor Activationmentioning

confidence: 99%

Section: Cell-surface Receptor Activationmentioning

confidence: 99%

“…After demonstrating that the non-specific opioid receptor antagonist, naloxone, was capable of abolishing IPost-protection in the intact rat heart, they investigated the effect of IPost in the presence of pharmacological antagonists of the -, -, and -opioid receptors [208]. The data implicated endogenous stimulation of the -and possibly theopioid receptors in the setting of IPost [208]. In addition, hearts subjected to IPost accumulated higher levels of pro-encephalin, suggesting perhaps that IPost was capable of increasing endogenous opioid content in the reperfused myocardium [208].…”

Section: Cell-surface Receptor Activationmentioning

confidence: 99%

“…The data implicated endogenous stimulation of the -and possibly theopioid receptors in the setting of IPost [208]. In addition, hearts subjected to IPost accumulated higher levels of pro-encephalin, suggesting perhaps that IPost was capable of increasing endogenous opioid content in the reperfused myocardium [208]. Other receptors which have been implicated in IPost include the protease activated receptor 2 (PAR2) [209] and particulate guanylyl cyclase, the natriuretic peptide receptor [210].…”

Section: Cell-surface Receptor Activationmentioning

confidence: 99%

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Cardioprotection Techniques: Preconditioning, Postconditioning and Remote Con-ditioning (Basic Science)

Hausenloy¹

2013

CPD

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Ischemic heart disease (IHD) is the leading cause of death and disability worldwide. The major pathological consequences of IHD arise from the detrimental effects of acute ischemia-reperfusion injury (IRI) on the myocardium. Therefore, in order to improve clinical outcomes in patients with IHD, novel therapeutic strategies are required to protect the myocardium from acute IRI and preserve cardiac function (cardioprotection). In this regard, endogenous cardioprotective strategies such as ischemic preconditioning (IPC), ischemic postconditioning (IPost) and remote ischemic conditioning (RIC) may provide novel approaches for protecting the heart in clinical settings in which the patient experiences acute myocardial IRI. In this review article, we provide an overview of these endogenous cardioprotective strategies with respect to the pre-clinical experimental literature, exploring their major characteristics and underlying signaling mechanisms. The application of these therapeutic strategies in the clinical setting for potential patient benefit is reviewed in another article in this special issue.

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Long‐term outcome following remote ischemic postconditioning during percutaneous coronary interventions—the RIP‐PCI trial long‐term follow‐up

Lavi

Abu-Romeh

Wall

et al. 2017

Clinical Cardiology

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The clinical value of ischemic conditioning during percutaneous coronary intervention (PCI) and mode of administration is controversial. Our aim was to assess the long-term effect of remote ischemic postconditioning among patients undergoing PCI. We randomized 360 patients undergoing PCI who presented with a negative troponin T at baseline into 3 groups: 2 groups received remote ischemic postconditioning (with ischemia applied to the arm in 1 group and to the thigh in the other group), and the third group acted as a control group. Remote ischemic postconditioning was applied during PCI immediately following stent deployment, by 3, 5-minute cycles of blood pressure cuff inflation to >200 mm Hg on the arm or thigh (20 mm Hg to the arm in the control), with 5-minute breaks between each cycle. There were no differences in baseline characteristics among the 3 groups. Periprocedural myocardial injury occurred in 33% (P = 0.64). After 1 year, there was no difference between groups in death (P = 0.91), myocardial infarction (P = 0.78), or repeat revascularization (P = 0.86). During 3 years of follow-up, there was no difference in death, myocardial infarction, and revascularization among the groups there is a debate regarding the prognostic implications of minor periprocedural infarcts, and suggestions for using more restrictive definitions, 4 many reports suggest that even a minor degree of elevation in cardiac markers, either pre-or postprocedure, can have longterm prognostic implications. 5-7 Some investigators consider alleviating periprocedural myocardial injury as a therapeutic target for cardioprotection. 8 One potential method of cardioprotection during PCI is ischemic conditioning. 9,10 The concept of ischemic conditioning for cardioprotection, is that brief, repeated episodes of ischemia and reperfusion, render the heart to be more resistant to subsequent ischemia-reperfusion episodes. 10 The mechanism involves complex neuronal and humoral signal transduction pathways. 11Whereas the effects of ischemic conditioning in animal studies were impressive, even if applied remotely 12 or after the initial ischemic injury (postconditioning), 13 the results from human studies were less consistent. In patients undergoing PCI, remote ischemic preconditioning (RIPre) induced by cyclic prolonged blood pressure cuff inflation on the arm prior to PCI was associated with a decrease in periprocedural myocardial injury, which later translated into a decrease in cardiac events. 14,15 The beneficial effect of RIPre in the setting of PCI was also confirmed in meta-analyses. 16,17 However, in a large meta-analysis that included application of ischemic conditioning in multiple settings, overall ischemic conditioning had no effect on major cardiovascular outcomes, 18 and so far we have not witnessed the translation of ischemic conditioning into clinical practice. 19

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Evidence that Cardioprotection by Postconditioning Involves Preservation of Myocardial Opioid Content and Selective Opioid Receptor Activation

Cited by 32 publications

References 0 publications

Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures

Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures

Cardioprotection Techniques: Preconditioning, Postconditioning and Remote Con-ditioning (Basic Science)

Long‐term outcome following remote ischemic postconditioning during percutaneous coronary interventions—the RIP‐PCI trial long‐term follow‐up

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