Myocardial ischemia : from mechanisms to therapeutic potentials /

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Bibliographic Details
Imprint:New York : Springer, c2006.
Description:1 online resource (viii, 204 p.) : ill. (some col.)
Language:English
Series:Basic science for the cardiologist ; 21
Basic science for the cardiologist ; 21.
Subject:
Format: E-Resource Book
URL for this record:http://pi.lib.uchicago.edu/1001/cat/bib/8877436
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Other authors / contributors:Cokkinos, Dennis V.
ISBN:0387286578 (alk. paper)
0387286586 (e-book)
9780387286570
9780387286587
661046037X (electronic bk.)
9786610460373 (electronic bk.)
Notes:Includes bibliographical references and index.
Description based on print version record.
Other form:Print version: Myocardial ischemia. New York : Springer, c2006 0387286578
Table of Contents:
  • Preface
  • Introduction: From Fetal to Fatal. Metabolic adaptation of the heart to environmental stress
  • 1. The Logic of Metabolism
  • 2. Substrate Switching and Metabolic Flexibility
  • 3. Pleiotropic Actions of Metabolism
  • Chapter 1. Myocardial Ischemia. Basic concepts
  • 1. The Pathophysiology of Ischemia and Reperfusion Injury
  • 1.1. Cellular injury
  • 1.2. Spread of cell injury
  • 1.2.1. Gap junctions; cell to cell communication
  • 1.2.2. The inflammatory response
  • 1.3. Microvascular injury
  • 1.4. Biochemical aspects of ischemia-reperfusion
  • 1.5. Contractile dysfunction
  • 1.5.1. Ischemic contracture
  • 1.5.2. Hypercontracture
  • 1.5.3. Myocardial Stunning
  • 1.5.4. Myocardial Hibernation
  • 1.6. Ischemia-reperfusion induced arrhythmias
  • 2. Stress Signaling in Myocardial Ischemia
  • 2.1. Membrane bound receptors
  • 2.2. Triggers of cell signaling
  • 2.2.1. Receptor dependent endogenous triggers
  • 2.2.2. Non receptor triggers; reactive oxygen species and nitric oxide
  • 2.3. Intracellular Pathways and End-Effectors
  • 2.3.1. Protein kinase A
  • 2.3.2. Protein kinase C
  • 2.3.3. The Rho signaling
  • 2.3.4. The Ras/Raf signaling
  • 2.3.5. The PI3K signaling
  • 2.3.6. The JAK/STAT signaling
  • 2.3.7. Calcineurin
  • 2.4. Transcription
  • 2.4.1. Hypoxia inducible factor
  • 2.4.2. Heat shock factor- Heat shock proteins
  • 3. The Adapted Heart
  • 3.1. Ischemic preconditioning
  • 3.2. Heat stress induced 'cross tolerance' to myocardial ischemia
  • 3.3. Chronic hypoxia
  • 4. The Diseased and Ageing Heart
  • 4.1. Cardiac hypertrophy
  • 4.2. Heart failure
  • 4.3. Diabetes
  • 4.4. Hypercholesterolemia
  • 4.5. Post-infarcted heart
  • 4.6. Ageing heart
  • 5. Experimental Models
  • 6. Treatment Strategies
  • 6.1. Pharmacological treatments
  • 6.2. Gene and cell based therapies
  • Chapter 2. Hormones Signaling and Myocardial Ischemia
  • 1. Estrogens
  • 2. Androgens
  • 3. Growth Hormone
  • 4. Ghrelin
  • 5. Glucocorticoids
  • 6. Urocortin
  • 7. Melanocortin Peptides
  • 8. Melatonin
  • 9. Erythropoietin
  • 10. Natriuretic Peptides
  • 11. PTH - Parathyroid Hormonerelated Peptide (PTHrP)
  • 12. Aldosterone
  • 13. Leptin
  • 14. Insulin
  • 15. Insulin Like Growth Factor (IGF-1)
  • 16. Peroxisome Proliferated-Activated Receptors (PPARS)
  • 17. Thyroid Hormone
  • 17.1. Thyroid hormone receptors
  • Chapter 3. Ischemic Preconditioning
  • 1. Introduction
  • 2. Ischemic Preconditioning
  • 3. Ischemic Preconditioning is Receptor-Mediated
  • 4. ATP-Sensitive Potassium Channels
  • 5. Mitochondrial K[subscript ATP] Opening Triggers Entrance Into the Preconditioned State
  • 6. The Trigger Pathways are Divergent
  • 7. IPC Appears to Exert Its Protection During Reperfusion by Preventing Mpt Pore Opening
  • 8. Drugs that Protect at Reperfusion Target the Same Pathways as IPC
  • 9. Does Reperfusion Injury Exist?
  • 10. Clinical Implications
  • Chapter 4. Connexin 43 and Ischemic Preconditioning
  • 1. Introduction
  • 2. Regulation of Hemichannels and Gap Junctions
  • 2.1. Protein kinase A (PKA)
  • 2.2. cGMP-dependent protein kinases (PKG)
  • 2.3. Protein kinase C (PKC)
  • 2.4. Protein tyrosine kinase (PTK)
  • 2.5. Mitogen activated protein kinases (MAPKs)
  • 2.6. Casein kinase (CasK)
  • 2.7. Protein phosphatases
  • 2.8. Proton and calcium concentration
  • 3. Myocardial Ischemia/Reperfusion Injury and Its Modification by Ischemic Preconditioning
  • 4. Alterations in CX43 During Ischemia
  • 5. CX43 and Ischemic Preconditioning
  • 6. Clinical Implications
  • Chapter 5. Coronary Microembolization
  • 1. Introduction
  • 2. Coronary Blood Flow Response and Experimental Coronary Microembolization
  • 3. Platelets, Cyclic Coronary Flow Variations and Experimental Coronary Microembolization
  • 4. Coronary Microembolization as an Experimental Model of Unstable Angina: The Role of Inflammatory Cytokines
  • 5. Coronary Microembolization and Ischemic Preconditioning
  • 6. Source and Consequences of Potential Thromboemboli in Patients
  • 7. Protection Devices Against Coronary Microembolization
  • 8. Conclusions and Remaining Questions
  • Chapter 6. Fibroblast Growth Factor-2
  • 1. Introduction
  • 2. FGF-2 in the Heart
  • 3. Preconditioning-Like Cardioprotection by FGF-2
  • 4. Reperfusion (Secondary) Injury Prevention
  • 5. Therapeutic Angiogenesis and FGF-2
  • 6. Repair and Regeneration: Rebuilding, in Addition to Preserving, the Damaged Myocardium
  • 7. Clinical Applications
  • 7.1. Delivery Methods
  • 7.2. Safety considerations
  • 7.3. Clinical Trial Design
  • Chapter 7. Myocardial Protection - From Concepts to Clinical Practice
  • 1. Background
  • 2. Myocardial Protection
  • 2.1. Patient status
  • 2.1.1. Diabetes mellitus
  • 2.1.2. Hypercholesterolemia-atherosclerosis
  • 2.1.3. Hyperthyroidism
  • 2.1.4. Hypothyroidism
  • 2.2. Myocardial status
  • 2.2.1. Myocardial hypertrophy
  • 2.2.2. Myocardial dysfunction
  • 3. The Stage of the Ischemia-Reperfusion Injury Cascade
  • 4. Cardioprotective Agents
  • 5. Synthesis
  • Chapter 8. A Synopsis
  • Index