Myocardial Preservation and Cellular Adaptation ( Volume 6 )

Publication series :Volume 6

Author: Das   D. K.  

Publisher: Elsevier Science‎

Publication year: 1998

E-ISBN: 9780080877235

P-ISBN(Paperback): 9780762303915

P-ISBN(Hardback):  9780762303915

Subject: Q2 Cytobiology;Q7 Molecular Biology

Language: ENG

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Description

Living organisms exhibit specific responses when confronted with sudden changes in their environmental conditions. The ability of the cells to acclimate to their new environment is the integral driving force for adaptive modification of the cells. Such adaptation involves a number of cellular and biochemical alteration including metabolic homeostasis and reprogramming of gene expression. Changes in metabolic pathways are generally short-lived and reversible, while the consequences of gene expression are a long-term process and may lead to permanent alternation in the pattern of adaptive responses.

The heart possesses remarkable ability to adapt itself against any stressful situation by increasing resistance to the adverse consequences. Stress composes the foundation of many degenerative heart diseases including atherosclerosis, spasm, thrombosis, cardiomyopathy, and congestive heart failure. Based on the concept that excessive stress may play a crucial role in the pathogenesis of ischemic heart disease, attempts were made to design methods for preventing of myocardial injury. Creation of stress reactions by repeated ischemia and reperfusion or subjecting the hearts to heat or oxidative stress enables them to meet the future stress challenge. Repeated stress exposures adapt the heart to withstand more severe stress reactions probably by upregulating the cellular defense and direct accumulation of intracellular mediators, which presumably constitute the material basis

Chapter

Front Cover

pp.:  1 – 4

Copyright Page

pp.:  5 – 6

CONTENTS

pp.:  6 – 8

LIST OF CONTRIBUTORS

pp.:  8 – 14

PREFACE

pp.:  14 – 16

CHAPTER 1. PRECONDITIONING INDUCES BOTH IMMEDIATE AND DELAYED PROTECTION AGAINST ARRHYTHMIAS RESULTING FROM ISCHEMIA AND REPERFUSION

pp.:  16 – 36

CHAPTER 2. MYOCARDIAL PROTECTION BY BRIEF ISCHEMIC AND NONISCHEMIC STRESS

pp.:  36 – 58

CHAPTER 3. CARDIAC ADAPTATION TO CHRONIC HYPOXIA

pp.:  58 – 76

CHAPTER 4. ANALYSIS OF ALTERED GENE EXPRESSION DURING ISCHEMlC PRECONDITIONING

pp.:  76 – 96

CHAPTER 5. MYOCARDIAL PRECONDITIONING VIA ATP-SENSITIVE POTASSIUM CHANNELS: INTERACTIONS WITH ADENOSINE

pp.:  96 – 116

CHAPTER 6. ISCHEMIC PRECONDITIONING: ROLE OF MULTIPLE KINASES IN SIGNAL AMPLIFICATION AND MODULATION

pp.:  116 – 140

CHAPTER 7. EARLY AND LATE PRECONDITIONING AGAINST MYOCARDIAL STUNNING: PATHOGENESIS AND PATHOPHYSIOLOGY

pp.:  140 – 154

CHAPTER 8. CHANGES IN CARDIAC ENERGETICS DURING PRECONDITIONING AND ADAPTATION

pp.:  154 – 160

CHAPTER 9. MOLECULAR ADAPTATION OF TRANSCRIPTIONAL APPARATUS IN CARDIAC HYPERTROPHY AND EMBRYONIC DEVELOPMENT

pp.:  160 – 170

CHAPTER 10. SIGNAL DIVERGENCE AND CONVERGENCE IN CARDIAC ADAPTATION

pp.:  170 – 196

CHAPTER 11. THE ROLE OF ATP-SENSITIVE POTASSIUM CHANNELS IN MYOCARDIAL ISCHEMIC STRESS

pp.:  196 – 212

CHAPTER 12. DELAYED PRECONDlTlONING: MECHANISMS OF ENDOGENOUS AND PHARMACOLOGIC INDUCTION OF THIS ADAPTIVE RESPONSE TO ISCHEMIA

pp.:  212 – 234

CHAPTER 13. ADAPTATION OF CELLULAR THERMOGENIC REACTIONS

pp.:  234 – 256

CHAPTER 14. FROM RAYNAUD’S PHENOMENON TO SYSTEMIC SCLEROSIS (SCLERODERMA): LACK OR EXHAUSTION OF ADAPTATION?

pp.:  256 – 270

CHAPTER 15. MOLECULAR ADAPTATION TO TOXIC CHEMICALS AND DRUGS

pp.:  270 – 286

INDEX

pp.:  286 – 298

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