UID:
edoccha_9960073512602883
Format:
1 online resource (1481 p.)
Edition:
Sixth edition.
ISBN:
0-323-29544-4
Content:
Offered in print, online, and downloadable formats, this updated edition of Stroke: Pathophysiology, Diagnosis, and Management delivers convenient access to the latest research findings and management approaches for cerebrovascular disease. Picking up from where J. P. Mohr and colleagues left off, a new team of editors - Drs. Grotta, Albers, Broderick, Kasner, Lo, Mendelow, Sacco, and Wong - head the sixth edition of this classic text, which is authored by the world's foremost stroke experts. Comprehensive, expert clinical guidance enables you to recognize the clinical manifestations of stroke.
Note:
"Get full acces and more at ExpertConsult.com"--Cover.
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Front Cover -- Stroke -- Copyright Page -- Table Of Contents -- Foreword to the Sixth Edition -- Preface -- List of Contributors -- AHA Evidence-based Classifications -- I Pathophysiology -- 1 Vascular Biology and Atherosclerosis of Cerebral Vessels -- Key Points -- Introduction -- Physiological Regulation of Cerebral Vascular Tone -- Cyclic AMP-mediated Mechanisms -- Nitric Oxide (NO) and Cyclic Guanosine Monophosphate -- K+ Channels -- KCa-activated K+ Channels -- KATP Channels -- KV Channels -- KIR Channels -- K2P Channels -- Rho/rho-kinase -- Reactive Oxygen Species (ROS) -- Transient Receptor Potential (TRP) Channels -- Alterations in Cerebral Vascular Function During Hypertension and Atherosclerosis -- Atherosclerosis -- Cerebral Vascular Oxidative Stress in Models of Atherosclerosis -- Cerebral Vascular Endothelial Dysfunction in Models of Atherosclerosis -- Cerebral Vascular Inflammation in Models of Atherosclerosis -- Hypertension -- Oxidative Stress In Hypertension Involving Elevated Ang II -- Endothelial Dysfunction in Hypertension Involving Elevated Ang II -- Cerebrovascular Inflammation in Hypertension Involving Elevated Ang II -- K+ Channel Function in Chronic Hypertension -- BKCa Channels. -- KATP Channels. -- KV Channels. -- KIR Channels. -- Rho-kinase in Hypertension -- Conclusion -- References -- 2 Mechanisms of Thrombosis and Thrombolysis -- Key Points -- Thrombus Formation -- Fibrinolysis -- Plasminogen -- Plasminogen Activation -- Thrombus Dissolution -- Plasminogen Activators -- Endogenous Plasminogen Activators -- Tissue-type Plasminogen Activator -- Urokinase-type Plasminogen Activator (u-PA) -- Exogenous Plasminogen Activators -- Streptokinase -- Staphylokinase -- Plasminogen Activators Derived from Desmodus rotundus -- Novel Plasminogen Activators -- Regulation of Endogenous Fibrinolysis.
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α2-Antiplasmin and α2-Macroglobulin -- Inhibitors of Plasminogen Activators and Fibrinolysis -- Clinical Consequences of Therapeutic Plasminogen Activation -- Limitations to the Clinical Use of Fibrinolytic Agents for Ischemic Stroke -- Plasminogen Activators in Cerebral Tissue -- Plasminogen Activators and Neuronal Functions -- Plasminogen Activators and Cerebral Microvessel Integrity -- Plasminogen Activators in Experimental Cerebral Ischemia -- Plasminogen Activators and Recanalization in Ischemic Stroke -- Plasminogen Activators and Cerebral Hemorrhage in Ischemic Stroke -- Conclusion -- References -- 3 Cerebral Blood Flow and Metabolism: -- Key Points -- Normal Cerebral Energy Metabolism and Hemodynamics -- Introduction -- Cerebral Blood Flow and Other Measurements of Cerebral Perfusion -- Normal Values of Cerebral Blood Flow and Cerebral Metabolism -- Control of Cerebral Blood Flow -- Relationship of Cerebral Blood Flow and Metabolism -- Response of Cerebral Blood Flow to Changes in Arterial Partial Pressure of Oxygen and Oxygen Content -- Response of Cerebral Blood Flow to Changes in Blood Glucose -- Response of Cerebral Blood Flow to Changes in Arterial pCO2 -- Response of Cerebral Blood Flow to Changes in Blood Viscosity -- Autoregulation of Cerebral Blood Flow to Changes in Cerebral Perfusion Pressure -- Compensatory Responses to Reduced Cerebral Blood Flow -- Response of Cerebral Blood Flow to Multiple Simultaneous Stimuli -- Hemodynamic Effects of Arterial Occlusive Disease -- Three-stage Classification System of Cerebral Hemodynamics -- Hemodynamic Effects of Arterial Stenosis -- Correlation of Cerebral Hemodynamics with Stroke Risk -- Ischemic Stroke -- Changes in Cerebral Blood Flow and Metabolism with Acute Ischemic Stroke -- Flow-Metabolism Thresholds of Tissue Function and Viability in Acute Ischemic Stroke.
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Vasoreactivity and Autoregulation in Ischemic Stroke -- Remote Flow and Metabolic Effects of Ischemic Stroke -- Intracerebral Hemorrhage -- Cerebral Blood Flow and Metabolism -- Autoregulation -- Arteriovenous Malformations -- Aneurysmal Subarachnoid Hemorrhage -- Cerebral Blood Flow and Metabolism -- Autoregulation -- Conclusions -- Acknowledgments -- Key References -- References -- 4 Histopathology of Brain Tissue Response to Stroke and Injury -- Key Points -- Four Broad Categories of Cerebral Ischemia -- Large Vessel Strokes -- Heart Disease and Cerebral Emboli -- Carotid Artery Atherosclerosis -- Infarction Versus Selective Neuronal Necrosis -- Small Vessel Strokes -- Hypertensive Arteriolosclerosis -- White Matter Incomplete Infarction -- Amyloid Angiopathy -- CADASIL -- Tissue Response to Therapy of Cerebral Ischemia -- References -- 5 Molecular and Cellular Mechanisms of Ischemia-Induced Neuronal Death -- Key Points -- Global Ischemia -- Focal Ischemia -- Experimental Models of Global and Focal Ischemia -- Models of Global Ischemia -- Models of Focal Ischemia -- Hypoxia/Ischemia -- Modalities of Ischemic Cell Death -- Necrosis -- Apoptosis -- The Caspase Death Cascade -- Alternative Pathways of Caspase Activation -- The Bcl-2 Family of Proteins -- Inhibitors of Apoptosis -- Caspase-Independent Programmed Cell Death -- Autophagy -- Cell Death Pathways -- Triggers of Ischemic Cell Death -- Glutamate Excitotoxicity -- NMDARs -- Ca2+-Permeable AMPARs -- Non-excitotoxic Mechanisms -- TRP Channels -- ASIC Channels -- Calcium -- Zinc -- Mechanisms of Ischemic Cell Death -- Metabolic Stress -- Mitochondrial Permeabilization -- Nitric Oxide -- Free Radicals and Lipid Peroxidation -- Epigenetic Mechanisms and Transcriptional Regulation -- The Transcription Activator CREB -- Nuclear Factor-κB: A Balance between Neuronal Survival and Death.
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The Pro-Death Transcription Activator FOXO -- The Signal Transducer and Activator of Transcription 3 (STAT3) -- The Restrictive Element-1 Silencing Transcription Factor (REST)/Neuron Restrictive Silencing Factor (NRSF) -- Inflammation -- Acknowledgments -- Key References -- References -- 6 Intracellular Signaling: -- Key Points -- Preconditioning -- Windows of Preconditioning -- Induction of Preconditioning -- Cross-Tolerance -- Cellular Defense -- Reactive Oxygen Species -- Mitochondria -- Neurotrophin Support -- Survival Kinases -- Erythropoietin -- Inhibition of Cell Death -- Cellular Maintenance -- Regeneration and Repair -- Clinical Implications -- Acknowledgments -- References -- 7 The Neurovascular Unit and Responses to Ischemia -- Key Points -- Introduction -- Architecture of the CNS and the Neurovascular Unit -- Structural Relationships: Anatomy of the Cerebral Vasculature -- Functional Relationships -- Neuron-Microvessel Communication -- Neuron-Astrocyte Communication. -- Astrocyte-Endothelial Cell (Vascular) Communication. -- Astrocyte-Smooth Muscle Communication. -- Microvessel-Neuron Communication -- Astrocyte-Neuron Communication. -- Endothelial Cell-Astrocyte Communication. -- Evidence for the Neurovascular Unit -- Interactions Suggesting Unit Communication -- Structural Changes During Focal Ischemia. -- Microvessel (Endothelial-Astrocyte) Communication. -- Innate Inflammation. -- Propagating Depolarizations and Neurovascular Unit Dysfunction. -- Summary and Implications -- References -- 8 Mechanisms of Cerebral Hemorrhage -- Key Points -- Experimental Models of Intracerebral Hemorrhage -- Mechanism of Brain Injury after Intracerebral Hemorrhage -- Inflammatory Responses after Intracerebral Hemorrhage -- Oxidative Stress after Intracerebral Hemorrhage -- Blood Components and Intracerebral-Hemorrhage-induced Injury.
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Red Blood Cell Lysis and Hemoglobin Toxicity -- Brain Iron Overload -- Thrombin Formation -- Mechanisms of Cell Death After Intracerebral Hemorrhage -- Apoptosis -- Excitotoxicity and Cell Death after Intracerebral Hemorrhage -- Additional Caveats about the Apoptosis and Other Forms of Death after Intracerebral Hemorrhage -- Blood-Brain Barrier Disruption -- Modifiers of Intracerebral-hemorrhage- induced Injury -- Hypertension -- Gender -- Age -- Therapeutic Approaches Targeting Intracerebral Hemorrhage Pathogenesis in Animal Research -- Surgical Treatment for Intracerebral Hemorrhage -- Pharmacologic and other Experimental Treatment for Intracerebral Hemorrhage -- Conclusion -- Key References -- References -- 9 White Matter Pathophysiology -- Key Points -- White Matter Anatomy and Physiology -- Model Systems for Studying White Matter Ischemia -- Cell Culture -- In vitro Tissue Models -- In vivo Models -- Effects of Ischemia on White Matter -- Derangement of Transmembrane Ion Gradients -- The Ca2+ Hypothesis and Anoxic-Ischemic White Matter Injury -- Mechanisms of White Matter Injury -- Ca2+ Entry and Intracellular Ca2+ Release in Axons during Ischemia -- Reversal of Na+-Ca2+ Exchange -- Activation of Voltage-Gated Ca2+ Channels -- Activation of Intracellular Ca2+ Release -- Excitotoxic Pathways Injure Glia in White Matter -- Autoprotection in White Matter -- Strategies for Protecting White Matter from Anoxic-Ischemic Injury are Diverse -- Acknowledgments -- References -- 10 Inflammation and Immune Response -- Key Points -- Cerebral Ischemia, Cytokines, and Inflammation -- Mechanisms by Which Inflammation Contributes to Ischemic Brain Injury -- Immune Cells Participating in Ischemic Injury and Tissue Repair -- Microglia, Monocytes/Macrophages, and Dendritic Cells -- Neutrophils -- Mast Cells -- Lymphocytes.
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Danger Sensors: Scavenger Receptors and Toll-Like Receptors.
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English
Additional Edition:
ISBN 1-336-23984-0
Additional Edition:
ISBN 0-323-32805-9
Language:
English
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