| Organ arrest, protection and preservation: natural hibernation to cardiac surgery. | |
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MedLine Citation:
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PMID: 15544969 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cardiac surgery continues to be limited by an inability to achieve complete myocardial protection from ischemia-reperfusion injury. This paper considers the following questions: (1) what lessons can be learned from mammalian hibernators to improve current methods of human myocardial arrest, protection and preservation? and (2) can the human heart be pharmacologically manipulated during acute global ischemia to act more like the heart of a hibernating mammal? After reviewing the major entropy-slowing strategies of hibernation, a major player identified in the armortarium is maintenance of the membrane potential. The resting membrane potential of the hibernator's heart appears to be maintained close to its pre-torpid state of around -85 mV. In open-heart surgery, 99% of all surgical heart arrest solutions (cardioplegia) employ high potassium (>16 mM) which depolarises the membrane voltage from -85 to around -50 mV. However, depolarising potassium cardioplegia has been increasingly linked to myocyte and microvascular damage leading to functional loss during reperfusion. Our recent work has been borrowed from hibernation biology and is focused on a very different arrest strategy which 'clamps' the membrane near its resting potential and depresses O2 consumption from baseline by about 90%. The new 'polarising' cardioplegia incorporates adenosine and lidocaine (AL) as the arresting combination, not high potassium. Studies in the isolated rat heart show that AL cardioplegia delivered at 37 degrees C can arrest the heart for up to 4 h with 70-80% recovery of the cardiac output, 85-100% recovery of heart rate, systolic pressure and rate-pressure product and 70-80% of baseline coronary flows. Only 14% of hearts arrested with crystalloid St. Thomas' solution No. 2 cardioplegia survived after 4 h. In conclusion, maintenance of the myocardial membrane potential near or close to its resting state appears to be an important feature of the hibernator's heart that may find great utility in surgical arrest and cellular preservation strategies. Identifying and safely turning 'off' and 'on' the entropy-slowing genes to down-regulate the hibernator's heart and applying this to human organs and tissues remains a major challenge for future genomics and proteomics. |
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Authors:
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Geoffrey P Dobson |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology Volume: 139 ISSN: 1096-4959 ISO Abbreviation: Comp. Biochem. Physiol. B, Biochem. Mol. Biol. Publication Date: 2004 Nov |
Date Detail:
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Created Date: 2004-11-16 Completed Date: 2005-04-14 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9516061 Medline TA: Comp Biochem Physiol B Biochem Mol Biol Country: England |
Other Details:
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Languages: eng Pagination: 469-85 Citation Subset: IM |
Affiliation:
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Department of Physiology and Pharmacology, School of Biomedical Sciences, James Cook University, Molecular Science Building, Townsville, Qld 4811, Australia. geoffrey.dobson@jcu.edu.au |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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metabolism Animals Calcium / metabolism Cell Membrane Heart Arrest* / prevention & control, surgery Hibernation* Humans Myocardial Reperfusion Injury / prevention & control* Myocardium / cytology, metabolism Oxygen Consumption |
| Chemical | |
Reg. No./Substance:
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56-65-5/Adenosine Triphosphate; 7440-70-2/Calcium |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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