Blood to brain transport after newborn cerebral ischemia/reperfusion injury.
These experiments examine the transfer of urea, sodium, and sucrose from blood to brain in an animal model of newborn cerebral ischemia-reperfusion injury. Cerebral ischemia (20 min) was produced in anesthetized, ventilated piglets by increasing intracranial pressure above mean arterial blood pressure, thereby reducing cerebral perfusion pressure to zero. The blood to brain transfer of urea, sodium, and sucrose was then measured in sham control piglets and at 30 min and 2 hr of reperfusion following ischemia. At 30 min of reperfusion, urea and sodium transfer were increased while sucrose transfer was unchanged. However, at 2 hr of reperfusion, transfer of all three tracers was elevated. The difference in the time course of increased transport of these substances into the brain following ischemia cannot be explained by size differences, indicating that changes in the blood-brain barrier following ischemia are more complex than merely opening junctions between cells and creating leaky sites. Alterations in blood-brain barrier transport could participate in altered neuronal function after ischemia-reperfusion injury.
Mirro
R
R
Department of Physiology and Biophysics, Laboratory for Research in Neonatal Physiology, University of Tennessee, Memphis 38163.
Armstead
W M
WM
Busija
D W
DW
Leffler
C W
CW
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D001692:Biological Transport; D001812:Blood-Brain Barrier; D002545:Brain Ischemia / Q000378:metabolism* / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D015427:Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology; D012995:Solubility; D013552:Swine