Three openings of the blood-brain barrier produced by forebrain ischemia in the rat.
A sensitive radiotracer method was used to explore the time course and regional pattern of blood-brain barrier (BBB) opening that occurs in a rat forebrain ischemia model that mimics temporary cardiac arrest. Immediately following 10 min of ischemia, transfer constants (Ki) for blood to brain permeation of [3H]sucrose were augmented severalfold, indicating widespread BBB opening. After 6 h, a delayed intensification of opening was evident in striatum and hippocampus, regions known to undergo selective, delayed neuronal death. There was generalized BBB recovery by 24 h except in experiments that involved prolonged ischemia (25 min) or concomitant brain hyperthermia (41 degrees C, 10 min). These protocols evoked a third opening; a marked upward increment in Ki and % H2O developed in neocortex between 6 and 24 h post-ischemia. Pharmacological or other manipulations of these temporal and regional patterns of altered transfer constants may aid understanding of the interplay between microvascular damage, edema, and neuronal death following brain ischemia.
Preston
E
E
Biomedical NMR Section, National Research Council, Ottawa, Ont., Canada.
Sutherland
G
G
Finsten
A
A
D000818:Animals; D001812:Blood-Brain Barrier; D001921:Brain / Q000378:metabolism; D002545:Brain Ischemia / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D002199:Capillary Permeability; D008297:Male; D016548:Prosencephalon / Q000098:blood supply*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013395:Sucrose / Q000097:blood / Q000493:pharmacokinetics
D013395:Sucrose