: Hua Feng, Ying Mao, John H. Zhang
: Hua Feng, Ying Mao, John H. Zhang
: Early Brain Injury or Cerebral Vasospasm Vol 1: Pathophysiology
: Springer-Verlag
: 9783709103531
: 1
: CHF 189.80
:
: Klinische Fächer
: English
: 256
: Wasserzeichen/DRM
: PC/MAC/eReader/Tablet
: PDF
More than 40 articles provide an extensive coverage of clinical and basic science advances over the last three years of research on subarachnoid hemorrhage-induced brain injuries. Early brain injury, the new frontier of subarachnoid hemorrhage research, which may be a key contributor to the high mortality and morbidity, promotes collaborative efforts from neurosurgery, neurology, neuro-ICU into other interrelated fields and basic neurosciences. For the first time, subarachnoid hemorrhage research is almost equally divided by early brain injury and cerebral vasospasm, mechanistic investigations and therapeutic approaches, demonstrating a translational feature of the future direction.
Preface6
Acknowledgement8
Contents10
Part I: Advances in Subarachnoid Hemorrhage and Cerebral Vasospasm14
Section I: Honored Guest14
1514
A Clinical Review of Cerebral Vasospasm and Delayed Ischaemia Following Aneurysm Rupture16
New Regulatory, Signaling Pathways, and Sources of Nitric Oxide18
Section II: Advances in Subarachnoid Hemorrhage Research24
Advances in Experimental Subarachnoid Hemorrhage25
Advances in Treatment of Cerebral Vasospasm: an Update32
Roles of Signal Transduction Mechanisms in Cerebral Vasospasm Following Subarachnoid Hemorrhage: Overview36
Part II: Mechanistic Studies40
Section III: Early Brain Injury After Subarachnoid Hemorrhage41
Hypoperfusion in the Acute Phase of Subarachnoid Hemorrhage42
Association of APOE Polymorphism with the Change of Brain Function in the Early Stage of Aneurysmal Subarachnoid Hemorrhage46
Apoptotic Mechanisms for Neuronal Cells in Early Brain Injury After Subarachnoid Hemorrhage50
Early Micro Vascular Changes After Subarachnoid Hemorrhage56
Immunological Response in Early Brain Injury After SAH63
Mechanisms of Early Brain Injury After SAH: Matrixmetalloproteinase 968
Tyrosine Phosphatase Inhibition Attenuates Early Brain Injury After Subarachnoid Hemorrhage in Rats71
Protection of Minocycline on Early Brain Injury After Subarachnoid Hemorrhage in Rats75
Role of Osteopontin in Early Brain Injury After Subarachnoid Hemorrhage in Rats79
Matrix Metalloproteinase 9 Inhibition Reduces Early Brain Injury in Cortex After Subarachnoid Hemorrhage84
Section IV: Nitric Oxide84
8884
Nitric Oxide Synthase Inhibitors and Cerebral Vasospasm89
The Role of Nitric Oxide Donors in Treating Cerebral Vasospasm After Subarachnoid Hemorrhage94
Nitric Oxide in Early Brain Injury After Subarachnoid Hemorrhage99
Nitric Oxide Related Pathophysiological Changes Following Subarachnoid Haemorrhage104
Endothelin-1(1–31) Induces Spreading Depolarization in Rats109
The Gamut of Blood Flow Responses Coupled to Spreading Depolarization in Rat and Human Brain: from Hyperemia to Prolonged Ischemia116
Cerebral Microdialysis in Acutely Brain-Injured Patients with Spreading Depolarizations122
Section V: Pathophysiology of Cerebral Vasospasm128
Mitogen-Activated Protein Kinases in Cerebral Vasospasm After Subarachnoid Hemorrhage: A Review129
Association of Apolipoprotein E Polymorphisms with Cerebral Vasospasm After Spontaneous Subarachnoid Hemorrhage136
Impact of Subarachnoid Hemorrhage on Local and Global Calcium Signaling in Cerebral Artery Myocytes140
Enhanced Angiogenesis and Astrocyte Activation by Ecdysterone Treatment in a Focal Cerebral Ischemia Rat Model146
Bilirubin Oxidation Products Seen Post Subarachnoid Hemorrhage Have Greater Effects on Aged Rat Brain Compared to Young151
Preliminary Results of an ICP-Controlled Subarachnoid Hemorrhage Rabbit Model for the Study of Delayed Cerebral Vasospasm157
PKGIa Inhibits the Proliferation of Cerebral Arterial Smooth Muscle Cell Induced by Oxyhemoglobin After Subarachnoid Hemorrhage160
Characteristics of In Vivo Animal Models of Delayed Cerebral Vasospasm165
Endothelin Related Pathophysiology in Cerebral Vasospasm: What Happens to the Cerebral Vessels?168
Expression and Role of COMT in a Rat Subarachnoid Hemorrhage Model172
Section VI: Clinical Manifestations of Subarachnoid Hemorrhage179
Monitoring of the Inflammatory Response After Aneurysmal Subarachnoid Haemorrhage in the Clinical Setting: Review of Literature and Report of Preliminary Clinical Experience180
Perimesencephalic Subarachnoid Hemorrhage: Risk Factors, Clinical Presentations, and Outcome186
The Relationship Between IL-6 in CSF and Occurrence of Vasospasm After Subarachnoid Hemorrhage191
Non-Aneurysm Subarachnoid Hemorrhage in Young Adults197
Cardiac Damage After Subarachnoid Hemorrhage202
Analysis on Death-Associated Factors of Patients with Subarachnoid Hemorrhage During Hospitalization206
Clinical Study of Changes of Cerebral Microcirculation in Cerebral Vasospasm After SAH211
Effect of Weekend Admission on in-Hospital Mortality After Subarachnoid Hemorrhage in Chongqing China215
The Correlation Between COMT Gene Polymorphism and Early Cerebral Vasospasm After Subarachnoid Hemorrhage219
Fever Increased In-Hospital Mortality After Subarachnoid Hemorrhage225
Subarachnoid Hemorrhage in Old Patients in Chongqing China230
Author Index234
Subject Index236
Table of Contents for Vol. 1242
Table of Contents for Vol. 2246