Protective effect of fasting upon cerebral hypoxic-ischemic injury.
This study was designed to determine the effect of fasting upon cerebral hypoxic-ischemic injury. In the first part of the study the effect of fasting was determined for survival, brain tissue water and kation contents, and blood-brain barrier integrity. In the second part of the study the administration of the substrates beta-hydroxybutyrate (BHB) and glucose has been evaluated regarding their influence upon the effect of fasting. The study used the Levine-Klein model of unilateral carotid occlusion and hypoxia because it mimics clinical situations of ischemia with hypoxia. The data show that fasting did protect rats from developing brain infarction following hypoxia-ischemia. Hypoglycemia seems to be involved in the mitigation of ischemic blood-brain barrier disruption. The plasma glucose level seems to be not the only factor involved in the genesis of the tissue kation changes. Starvation-induced ketosis probably does not play a role in the protection mechanism.
Go
K G
KG
Department of Neurosurgery, University of Groningen, The Netherlands.
Prenen
G H
GH
Korf
J
J
D000090:Acetoacetates / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D001812:Blood-Brain Barrier; D002412:Cations / Q000378:metabolism; D002546:Ischemic Attack, Transient / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology*; D051381:Rats; D013217:Starvation / Q000378:metabolism / Q000503:physiopathology*
D000090:Acetoacetates; D001786:Blood Glucose; D002412:Cations; C016635:acetoacetic acid