Abstract

The aim of pharmacological conditioning is to protect the heart against myocardial ischemia-reperfusion (I/R) injury and its consequences. There is extensive literature that reports a multitude of different cardioprotective signaling molecules and mechanisms in diverse experimental protocols. Several pharmacological agents have been evaluated in terms of myocardial I/R injury. While results from experimental studies are immensely encouraging, translation into the clinical setting remains unsatisfactory. This narrative review wants to focus on two aspects: (1) give a comprehensive update on new developments of pharmacological conditioning in the experimental setting concentrating on recent literature of the last two years and (2) briefly summarize clinical evidence of these cardioprotective substances in the perioperative setting highlighting their clinical implications. By directly opposing each pharmacological agent regarding its recent experimental knowledge and most important available clinical data, a clear overview is given demonstrating the remaining gap between basic research and clinical practice. Finally, future perspectives are given on how we might overcome the limited translatability in the field of pharmacological conditioning.

Highlights

  • Conditioning is still the strongest cardioprotective mechanism to reduce ischemiareperfusion (I/R) injury and cell death after myocardial infarction (MI)

  • Another way to protect the heart against the consequences of I/R injury is pharmacological conditioning, a concept that is based on the administration of specific drugs mimicking the effect of ischemic preconditioning (IPC)

  • Volatile compared with total intravenous anaesthesia in patients undergoing high-risk cardiac surgery: a randomized multicentre study [33]

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Summary

Introduction

Conditioning is still the strongest cardioprotective mechanism to reduce ischemiareperfusion (I/R) injury and cell death after myocardial infarction (MI). Preconditioning with sevoflurane is not negatively affected by diabetic conditions, which is a promising approach regarding successful translation into the clinical setting In this context, Xie et al showed that treatment with sevoflurane protects the heart via AMP-activated protein kinase (AMPK)-dependent inhibition of pro-death mitogen-activated protein kinase p38 (p38 MAPK) in non-diabetic mice [14]. A variety of previous studies have demonstrated cardioprotective effects against I/R injury by increased autophagy; excessive autophagy plays a pivotal role in the reperfusion-induced damage on cardiac function (as reviewed in [21]). These controversial findings are just examples emphasizing the importance of further unravelling the basic mechanisms of cardioprotection. Further studies are needed regarding desflurane and its effectiveness in pharmacological cardiac conditioning

Clinical Implications
Results
Experimental Developments
Future Perspectives
10. Conclusions
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