Brain tissue injury and blood-brain barrier opening induced by injection of LGE2 or PGE2.
The hypothesis that the accumulation of prostaglandin (PG)E2 during reperfusion of severely ischemic tissue contributes to a breakdown in the blood-brain barrier (BBB) was expanded to include a parallel role for levuglandins(LGs), gamma-ketoaldehydes produced by rearrangement of PGH2. LGE2 was shown to be more potent than PGE2 in causing breakdown of the BBB when injected intrahemispherically. Brain tissue necrosis was clearly evident with total doses of levuglandin as low as 100 nmole.
Schmidley
J W
JW
Department of Neurology, Case Western Reserve University, Cleveland, Ohio 44106-2699.
Dadson
J
J
Iyer
R S
RS
Salomon
R G
RG
D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects*; D001834:Body Water; D001921:Brain / Q000187:drug effects* / Q000473:pathology; D001929:Brain Edema / Q000139:chemically induced / Q000473:pathology; D015232:Dinoprostone / Q000633:toxicity*; D005070:Evans Blue; D005260:Female; D008297:Male; D009336:Necrosis; D011458:Prostaglandins E / Q000633:toxicity*; D051381:Rats
D011458:Prostaglandins E; D005070:Evans Blue; C047684:levuglandin E2; D015232:Dinoprostone