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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1989-6-13
pubmed:abstractText
Two post-ischemic circulatory disturbances that play a significant role in pathophysiology of an ischemic lesion are: (1) reactive hyperemia or hyperperfusion and (2) hypoperfusion. The reactive hyperemia promptly follows release of major cerebral artery occlusion, and it is associated with the opening of the blood-brain barrier to serum proteins and ensuing edema. Prevention or reduction of reactive hyperemia results in significant amelioration of edema and the resulting ischemic brain tissue injury. The post-ischemic hypoperfusion, studied in gerbils, develops soon after recirculation and usually lasts up to 6 h. Its relationship to post-ischemic edema is evident in repeated ischemic insults. In these studies, three ischemic insults of 5 min duration when applied at 1 h intervals, i.e., during the period of hypoperfusion, resulted in a cumulative effect, post-ischemic edema and tissue injury becoming considerably more pronounced that those following a single 15 min ischemia. There was no cumulative effect when the ischemic insults were spaced 3 min or longer than 6 h apart. These observations indicate that repeated ischemic insults taking place during the phase of post-ischemic hypoperfusion may significantly increase the development of edema and brain tissue injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
0734-600X
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
21-9
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:articleTitle
Role of circulatory disturbances in the development of post-ischemic brain edema.
pubmed:affiliation
Laboratory of Neuropathology and Neuroanatomical Sciences, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, MD 20892.
pubmed:publicationType
Journal Article