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Inflammation After Stroke
Is It Harmful?
Gregory J. del Zoppo, MD;
Kyra J. Becker, MD;
John M. Hallenbeck, MD
From the Department of Molecular and Experimental Medicine, The Scripps
Research Institute, and the Division of Hematology/Medical Oncology, Scripps
Clinic, La Jolla, Calif (Dr del Zoppo); the Department of Neurology, University
of Washington, Harborview Medical Center, Seattle (Dr Becker); and the Stroke
Branch, National Institute of Neurological Disorders and Stroke, National
Institutes of Health, Bethesda, Md (Dr Hallenbeck).
Corresponding author and reprints: Gregory J. del Zoppo, MD, Department
of Molecular and Experimental Medicine, Room MEM 132, The Scripps Research
Institute, 10550 N Torrey Pines Rd, La Jolla, CA 92037 (e-mail: grgdlzop@hermes.scripps.edu).
Arch Neurol. 2001;58:669-672.
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TISSUE INJURY stimulates increased local blood flow and an influx of
leukocytes to initiate wound repair. This response involves leukocyte adhesion
receptors, the release of biologically active substances, and microvascular
changes that allow the invasion by leukocytes. Inflammation plays a vital
role in tissue recovery, serving an integral part of the host immune defense
system. In patients with cerebral ischemia, however, the early inflammatory
processes are likely to be deleterious.
INFLAMMATORY RESPONSES TO FOCAL CEREBRAL ISCHEMIA
Cellular and Noncellular Inflammation
Cellular inflammation is initiated by ischemia at the blood–microvascular
endothelial cell interface. Researchers1, 2
have demonstrated that polymorphonuclear leukocytes are early participants
in the cerebral microvascular response to focal ischemia, and rapidly enter
the brain tissue in the ischemic territory, followed by mononuclear cell invasion.
The initial movement of nonresident inflammatory cells into the central nervous
system requires the rapid appearance of the leukocyte adhesion receptors (P
selectin, . . . [Full Text of this Article] Inflammation and Thrombosis Contributions to Secondary Injury
OTHER CONTRIBUTIONS TO INJURY DEVELOPMENT
Ischemic Tolerance
Immune Tolerance
EFFECT OF BLOCKADE
Experimental
Microvascular "No Reflow" Cytokines Cyclooxygenase 2 Inhibitors. Clinical
CONCLUSIONS
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