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      Hyperkalemic cardioplegia for adult and pediatric surgery: end of an era?

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          Abstract

          Despite surgical proficiency and innovation driving low mortality rates in cardiac surgery, the disease severity, comorbidity rate, and operative procedural difficulty have increased. Today's cardiac surgery patient is older, has a “sicker” heart and often presents with multiple comorbidities; a scenario that was relatively rare 20 years ago. The global challenge has been to find new ways to make surgery safer for the patient and more predictable for the surgeon. A confounding factor that may influence clinical outcome is high K + cardioplegia. For over 40 years, potassium depolarization has been linked to transmembrane ionic imbalances, arrhythmias and conduction disturbances, vasoconstriction, coronary spasm, contractile stunning, and low output syndrome. Other than inducing rapid electrochemical arrest, high K + cardioplegia offers little or no inherent protection to adult or pediatric patients. This review provides a brief history of high K + cardioplegia, five areas of increasing concern with prolonged membrane K + depolarization, and the basic science and clinical data underpinning a new normokalemic, “polarizing” cardioplegia comprising adenosine and lidocaine (AL) with magnesium (Mg 2+) (ALM™). We argue that improved cardioprotection, better outcomes, faster recoveries and lower healthcare costs are achievable and, despite the early predictions from the stent industry and cardiology, the “cath lab” may not be the place where the new wave of high-risk morbid patients are best served.

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          Most cited references367

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          The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine.

          Despite its very potent vasodilating action in vivo, acetylcholine (ACh) does not always produce relaxation of isolated preparations of blood vessels in vitro. For example, in the helical strip of the rabbit descending thoracic aorta, the only reported response to ACh has been graded contractions, occurring at concentrations above 0.1 muM and mediated by muscarinic receptors. Recently, we observed that in a ring preparation from the rabbit thoracic aorta, ACh produced marked relaxation at concentrations lower than those required to produce contraction (confirming an earlier report by Jelliffe). In investigating this apparent discrepancy, we discovered that the loss of relaxation of ACh in the case of the strip was the result of unintentional rubbing of its intimal surface against foreign surfaces during its preparation. If care was taken to avoid rubbing of the intimal surface during preparation, the tissue, whether ring, transverse strip or helical strip, always exhibited relaxation to ACh, and the possibility was considered that rubbing of the intimal surface had removed endothelial cells. We demonstrate here that relaxation of isolated preparations of rabbit thoracic aorta and other blood vessels by ACh requires the presence of endothelial cells, and that ACh, acting on muscarinic receptors of these cells, stimulates release of a substance(s) that causes relaxation of the vascular smooth muscle. We propose that this may be one of the principal mechanisms for ACh-induced vasodilation in vivo. Preliminary reports on some aspects of the work have been reported elsewhere.
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            Pathophysiology of ischaemia-reperfusion injury.

            Reperfusion of ischaemic tissues is often associated with microvascular dysfunction that is manifested as impaired endothelium-dependent dilation in arterioles, enhanced fluid filtration and leukocyte plugging in capillaries, and the trafficking of leukocytes and plasma protein extravasation in postcapillary venules. Activated endothelial cells in all segments of the microcirculation produce more oxygen radicals, but less nitric oxide, in the initial period following reperfusion. The resulting imbalance between superoxide and nitric oxide in endothelial cells leads to the production and release of inflammatory mediators (e.g. platelet-activating factor, tumour necrosis factor) and enhances the biosynthesis of adhesion molecules that mediate leukocyte-endothelial cell adhesion. Some of the known risk factors for cardiovascular disease (hypercholesterolaemia, hypertension, and diabetes) appear to exaggerate many of the microvascular alterations elicited by ischaemia and reperfusion (I/R). The inflammatory mediators released as a consequence of reperfusion also appear to activate endothelial cells in remote organs that are not exposed to the initial ischaemic insult. This distant response to I/R can result in leukocyte-dependent microvascular injury that is characteristic of the multiple organ dysfunction syndrome. Adaptational responses to I/R injury have been demonstrated that allow for protection of briefly ischaemic tissues against the harmful effects of subsequent, prolonged ischaemia, a phenomenon called ischaemic preconditioning. There are two temporally and mechanistically distinct types of protection afforded by this adaptational response, i.e. acute and delayed preconditioning. The factors (e.g. protein kinase C activation) that initiate the acute and delayed preconditioning responses appear to be similar; however the protective effects of acute preconditioning are protein synthesis-independent, while the effects of delayed preconditioning require protein synthesis. The published literature in this field of investigation suggests that there are several potential targets for therapeutic intervention against I/R-induced microvascular injury. Copyright 2000 John Wiley & Sons, Ltd.
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              Adenosine receptors: therapeutic aspects for inflammatory and immune diseases.

              Adenosine is a key endogenous molecule that regulates tissue function by activating four G-protein-coupled adenosine receptors: A1, A2A, A2B and A3. Cells of the immune system express these receptors and are responsive to the modulatory effects of adenosine in an inflammatory environment. Animal models of asthma, ischaemia, arthritis, sepsis, inflammatory bowel disease and wound healing have helped to elucidate the regulatory roles of the various adenosine receptors in dictating the development and progression of disease. This recent heightened awareness of the role of adenosine in the control of immune and inflammatory systems has generated excitement regarding the potential use of adenosine-receptor-based therapies in the treatment of infection, autoimmunity, ischaemia and degenerative diseases.
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                Author and article information

                Journal
                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                1664-042X
                09 June 2013
                28 August 2013
                2013
                : 4
                : 228
                Affiliations
                [1] 1Department of Physiology and Pharmacology, Heart and Trauma Research Laboratory, James Cook University Townsville, QLD, Australia
                [2] 2Division of Cardiac Surgery, University of Verona Medical School Verona, Italy
                [3] 3Cardiothoracic Research Laboratory of Emory University Hospital Midtown, Carlyle Fraser Heart Center Atlanta, GA, USA
                Author notes

                Edited by: Robert Boushel, University of Copenhagen, Denmark

                Reviewed by: Robert Boushel, University of Copenhagen, Denmark; Andreas Bergdahl, Concordia University, Canada

                *Correspondence: Geoffrey P. Dobson, Department of Physiology and Pharmacology, Heart and Trauma Research Laboratory, James Cook University, Townsville, QLD4811, Australia e-mail: geoffrey.dobson@ 123456jcu.edu.au

                This article was submitted to Clinical and Translational Physiology, a section of the journal Frontiers in Physiology.

                Article
                10.3389/fphys.2013.00228
                3755226
                24009586
                a074a69c-ceb6-4e92-b084-7fd682453138
                Copyright © 2013 Dobson, Faggian, Onorati and Vinten-Johansen.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 15 April 2013
                : 05 August 2013
                Page count
                Figures: 8, Tables: 1, Equations: 0, References: 399, Pages: 28, Words: 25038
                Categories
                Physiology
                Review Article

                Anatomy & Physiology
                cardioplegia,ischemia,cardiac surgery,heart,potassium,hyperkalemia,endothelium,history
                Anatomy & Physiology
                cardioplegia, ischemia, cardiac surgery, heart, potassium, hyperkalemia, endothelium, history

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