Korean J Anesthesiol.  2011 Nov;61(5):358-366. 10.4097/kjae.2011.61.5.358.

Morphine and remifentanil-induced cardioprotection: its experimental and clinical outcomes

Affiliations
  • 1Department of Anesthesiology and Pain Medicine, School of Medicine, Keimyung University, Daegu, Korea. kimjin00@dsmc.or.kr
  • 2Institute of Cardiovascular Research, Pusan National University Yangsan Hospital, Yangsan, Korea.

Abstract

During the past few decades, a large number of animal studies demonstrated that commonly used opioids could provide cardioprotection against ischemia-reperfusion (I/R) injury. Opioid-induced preconditioning or postconditioning mimics ischemic preconditioning (I-Pre) or ischemic postconditioning (I-Post). Both delta- and kappa-opioid receptors (OPRs) play a crucial role in opioid-induced cardioprotection (OIC). Down stream signaling effectors of OIC include ATP-sensitive potassium (KATP) channels, protein kinase C (PKC), tyrosine kinase, phosphatidylinositol-3-kinase (PI3-kinase), extracellular signal regulated kinase1/2 (ERK1/2), glycogen synthase kinase-3beta (GSK-3beta), and mitochondrial permeability transition pore (MPTP), among others. Recently, various reports also suggest that opioids could provide cardioprotection in humans. This review will discuss OIC using mostly morphine and remifentanil which are widely used during cardiac anesthesia in addition to the clinical implications of OIC.

Keyword

Ischemic postconditioning; Ischemic preconditioning; Morphine; Myocardial ischemia; Myocardial reperfusion; Remifentanil

MeSH Terms

Analgesics, Opioid
Anesthesia
Animals
Glycogen Synthase
Humans
Ischemic Postconditioning
Ischemic Preconditioning
Mitochondrial Membrane Transport Proteins
Morphine
Myocardial Ischemia
Myocardial Reperfusion
Permeability
Piperidines
Potassium
Protein Kinase C
Protein-Tyrosine Kinases
Rivers
Analgesics, Opioid
Glycogen Synthase
Mitochondrial Membrane Transport Proteins
Morphine
Piperidines
Potassium
Protein Kinase C
Protein-Tyrosine Kinases
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