The evolving paradigm for blood cell-endothelial cell interactions in the cerebral microcirculation.
Inflammation and microvascular dysfunction have been implicated in a variety of pathologic conditions affecting the brain. Features of the inflammatory response that are common to many of these pathological conditions and that are manifested in the neurovasculature include oxidative stress, diminished endothelial barrier function (increased vascular permeability), increased expression of endothelial cell adhesion molecules, and the recruitment of rolling and adherent leukocytes and platelets. The evidence implicating leukocyte-endothelial cell adhesion in cerebral microvessels as a rate-determining component of the pathophysiology associated with conditions such as ischemia-reperfusion, sickle cell disease, and gamma -irradiation is summarized. Mechanisms that have been proposed to explain the recruitment of adherent leukocytes and platelets in the diseased/injured cerebral microvasculature are also addressed, and a common paradigm for blood cell recruitment induced by seemingly unrelated pathological conditions is outlined. Although there are many structural and functional characteristics of the cerebral microvasculature that distinguish it from other regional vascular beds, the processes that underlie the recruitment of injury-causing inflammatory cells in the brain appear to closely resemble those described for other tissues.
Gavins
Felicity
F
Centre for Biochemical Pharmacology, William Harvey Research Institute, London, UK.
Yilmaz
Gokhan
G
Granger
D Neil
DN
D000818:Animals; D001773:Blood Cells / Q000166:cytology / Q000502:physiology; D002450:Cell Communication / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D002561:Cerebrovascular Disorders / Q000209:etiology* / Q000473:pathology; D004730:Endothelium, Vascular / Q000166:cytology / Q000502:physiology; D006801:Humans; D008833:Microcirculation / Q000166:cytology / Q000502:physiology / Q000503:physiopathology