Detailed analyses of regional myocardial blood flow, function, metabolism and morphology in ischemic and reperfused myocardium have led to the identifi cation of important phenomena, i. e. , myocardial hibernation, myocardial stun ning and ischemic preconditioning. Both the hibernating and the stunned myocardium characterize viable though dysfunctional as distinguished from necrotic tissue. With the advent of reperfusion procedures, the distinction between reversibly injured, hypofunctional myocardium from irreversibly injured, hypofunctional myocardium is of utmost clinical importance. The…mehr
Detailed analyses of regional myocardial blood flow, function, metabolism and morphology in ischemic and reperfused myocardium have led to the identifi cation of important phenomena, i. e. , myocardial hibernation, myocardial stun ning and ischemic preconditioning. Both the hibernating and the stunned myocardium characterize viable though dysfunctional as distinguished from necrotic tissue. With the advent of reperfusion procedures, the distinction between reversibly injured, hypofunctional myocardium from irreversibly injured, hypofunctional myocardium is of utmost clinical importance. The pathophysiological distinction of hibernating and stunned myocardium is con troversial, but reperfusion is mandatory anyway. Ischemic preconditioning is the most powerful maneuver known so far to delay infarct development. Its clinical significance has been suggested from retrospective analyses of data from patients suffering a myocardial infarction as well as from controlled PTCA studies. Whether or not preconditioning can be achieved pharmacologically in the clinical setting remains to be established. The mechanisms and signal cascade underlying myocardial hibernation, myocardial stunning and ischemic preconditioning are not clear in detail. Over the last year, focussed issues on myocardial hibernation, myocardial stunning and ischemic preconditioning were published in Basic Research in Car diology; they have received great interest and a good response. Therefore, these focussed issues are now combined and published as a separate monograph. We express our gratitude once more to all our colleagues who contributed to this monograph, to Ms. Ibkendanz of Steinkopff, and to Ms. Philipp and Mr. Heinrichs from Bayer AG Germany, who supported this additional publication.Hinweis: Dieser Artikel kann nur an eine deutsche Lieferadresse ausgeliefert werden.
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Inhaltsangabe
Myocardial Hibernation.- I. Short-term hibernation: evidence for downregulation of contractile function and metabolic adaptation.- Critical role of energy supply and glycolysis during short-term hibernation.- Hibernating myocardium represents a primary downregulation of regional myocardial oxygen consumption distal to a critical coronary stenosis.- Myocardial hibernation: relationship to a model for segmental dyskinesis.- Myocardial hibernation in terms of the flow- function relationship.- Contractile pattern in acutely hibernating myocardium.- Excitation-contraction coupling in hibernating myocardium.- Hibernating myocardium: a hypometabolic state for energy conservation.- Myocardial hibernation.- Acute adaptation to ischemia: Short-term hibernating myocardium.- II. Long-term hibernation.- Myocardial hibernation: unresolved physiological and clinical issues.- Hibernating myocardium.- Hibernating myocardium: a brief article.- Myocardial hibernation, stunning, or both?.- Structural aspects of the chronic hibernating myocardium in man.- Hibernating myocardium: adaptation or degeneration?.- The hibernating myocardium: identification of viable myocardium in patients with coronary artery disease and chronic left ventricular dysfunction.- Commentary on hibernating myocardium and its clinical relevance.- Hibernating myocardium, a clinical entity.- Identification of "hibernating myocardium" by imaging approaches.- Myocardial Stunning.- I. Definition and occurence.- Ubiquity of myocardial stunning.- II. Methodological and conceptual problems.- Common methodological problems and artifacts associated with studies of myocardial stunning in vivo.- Stunning: Three questions and concerns.- III. Excitation-contraction coupling.- Do ATP-sensitive potassium channels play a role inmyocardial stunning?.- Stunned myocardium: a disease of the myofilaments?.- Stunned myocardium, an opinionated review.- IV. Metabolism.- Myocardial stunning: the role of oxidative substrate metabolism.- Adjustments in competitive substrate utilization in stunned myocardium during early reperfusion.- V. Coronary blood flow alterations.- Is stunned myocardium ischemic on a microvascular level?.- Absolute myocardial blood flow in chronic left ventricular dysfunction.- Coronary vasomotion of the stunned myocardium.- VI. Pharmacotherapy.- Therapy for myocardial stunning.- Stunned myocardium: inotropic reserve and pharmacological attenuation.- VII. Clinical relevance: hibernation vs. stunning.- The elusive difference between hibernation and stunning in patients.- Commentary on myocardial stunning and its clinical relevance.- Chronic stunning: The new switch in thought.- Ischemic Preconditioning.- I. Ischemic preconditioning: the concept.- Ischemic preconditioning: a brief review.- Preconditioning - a reappraisal of protection.- Ischemic preconditioning, remembrances of things past and future.- Three questions about preconditioning.- II. Triggers and mediators of ischemic preconditioning: adenosine, bradykinin, nitric oxide and KATP-channels.- Preconditioning-induced protection against post-ischemic contractile dysfunction: Inhibitory effect of tissue washout.- Adenosine and bradykinin: Are they independent triggers of precondi¬tioning?.- Activation of Ecto-5?-nucleotidase and cardioprotection by ischemic preconditioning.- Endothelial cells, nitric oxide and ischaemic preconditioning.- Criteria for a mediator or effector of myocardial preconditioning: Do KATP channels meet the requirements?.- III. The controversial role of protein kinase C in ischemic preconditioning.-Preconditioning: Markers vs. epiphenomena.- Limitation of infarct size by myocardial ischemic preconditioning.- Role of protein kinase C in ischemic preconditioning: in search of the "pure and simple truth".- IV. Trigger mechanisms other than ischemia: stress and stretch.- Cardioprotection by organs in stress or distress.- An alternative perspective on ischemic preconditioning derived from mathematical modeling.- V. Ischemic preconditioning vs. myocardial hibernation.- Ischemic preconditioning and myocardial hibernation: Is there a common mechanism?.- VI. Second window of protection.- Delayed myocardial protection following ischaemic preconditioning.- The early and late phases of preconditioning against myocardial stunning and the essential role of oxyradicals in the late phase: an overview.
Myocardial Hibernation.- I. Short-term hibernation: evidence for downregulation of contractile function and metabolic adaptation.- Critical role of energy supply and glycolysis during short-term hibernation.- Hibernating myocardium represents a primary downregulation of regional myocardial oxygen consumption distal to a critical coronary stenosis.- Myocardial hibernation: relationship to a model for segmental dyskinesis.- Myocardial hibernation in terms of the flow- function relationship.- Contractile pattern in acutely hibernating myocardium.- Excitation-contraction coupling in hibernating myocardium.- Hibernating myocardium: a hypometabolic state for energy conservation.- Myocardial hibernation.- Acute adaptation to ischemia: Short-term hibernating myocardium.- II. Long-term hibernation.- Myocardial hibernation: unresolved physiological and clinical issues.- Hibernating myocardium.- Hibernating myocardium: a brief article.- Myocardial hibernation, stunning, or both?.- Structural aspects of the chronic hibernating myocardium in man.- Hibernating myocardium: adaptation or degeneration?.- The hibernating myocardium: identification of viable myocardium in patients with coronary artery disease and chronic left ventricular dysfunction.- Commentary on hibernating myocardium and its clinical relevance.- Hibernating myocardium, a clinical entity.- Identification of "hibernating myocardium" by imaging approaches.- Myocardial Stunning.- I. Definition and occurence.- Ubiquity of myocardial stunning.- II. Methodological and conceptual problems.- Common methodological problems and artifacts associated with studies of myocardial stunning in vivo.- Stunning: Three questions and concerns.- III. Excitation-contraction coupling.- Do ATP-sensitive potassium channels play a role inmyocardial stunning?.- Stunned myocardium: a disease of the myofilaments?.- Stunned myocardium, an opinionated review.- IV. Metabolism.- Myocardial stunning: the role of oxidative substrate metabolism.- Adjustments in competitive substrate utilization in stunned myocardium during early reperfusion.- V. Coronary blood flow alterations.- Is stunned myocardium ischemic on a microvascular level?.- Absolute myocardial blood flow in chronic left ventricular dysfunction.- Coronary vasomotion of the stunned myocardium.- VI. Pharmacotherapy.- Therapy for myocardial stunning.- Stunned myocardium: inotropic reserve and pharmacological attenuation.- VII. Clinical relevance: hibernation vs. stunning.- The elusive difference between hibernation and stunning in patients.- Commentary on myocardial stunning and its clinical relevance.- Chronic stunning: The new switch in thought.- Ischemic Preconditioning.- I. Ischemic preconditioning: the concept.- Ischemic preconditioning: a brief review.- Preconditioning - a reappraisal of protection.- Ischemic preconditioning, remembrances of things past and future.- Three questions about preconditioning.- II. Triggers and mediators of ischemic preconditioning: adenosine, bradykinin, nitric oxide and KATP-channels.- Preconditioning-induced protection against post-ischemic contractile dysfunction: Inhibitory effect of tissue washout.- Adenosine and bradykinin: Are they independent triggers of precondi¬tioning?.- Activation of Ecto-5?-nucleotidase and cardioprotection by ischemic preconditioning.- Endothelial cells, nitric oxide and ischaemic preconditioning.- Criteria for a mediator or effector of myocardial preconditioning: Do KATP channels meet the requirements?.- III. The controversial role of protein kinase C in ischemic preconditioning.-Preconditioning: Markers vs. epiphenomena.- Limitation of infarct size by myocardial ischemic preconditioning.- Role of protein kinase C in ischemic preconditioning: in search of the "pure and simple truth".- IV. Trigger mechanisms other than ischemia: stress and stretch.- Cardioprotection by organs in stress or distress.- An alternative perspective on ischemic preconditioning derived from mathematical modeling.- V. Ischemic preconditioning vs. myocardial hibernation.- Ischemic preconditioning and myocardial hibernation: Is there a common mechanism?.- VI. Second window of protection.- Delayed myocardial protection following ischaemic preconditioning.- The early and late phases of preconditioning against myocardial stunning and the essential role of oxyradicals in the late phase: an overview.
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