Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Cerebral circulation and metabolism.

B K Siesjö

    Journal of Neurosurgery
    |May 1, 1984
    PubMed
    Summary

    This review covers cerebral circulation and metabolism, highlighting how disruptions in energy state, ion balance, and phospholipid metabolism contribute to brain damage during ischemia. Acidosis and calcium disturbances worsen brain injury, leading to edema, infarction, and selective neuronal damage.

    Related Concept Videos

    You might also read

    Related Articles

    Articles linked to this work by shared authors, journal, and citation graph.

    Sort by
    Same author

    Acidosis promotes the permeability transition in energized mitochondria: implications for reperfusion injury.

    Journal of neurotrauma·2001
    Same author

    Does long-term glucose infusion reduce brain damage after transient cerebral ischemia?

    Brain research·2001
    Same author

    Protein aggregation after focal brain ischemia and reperfusion.

    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·2001
    Same author

    Hyperglycemia enhances DNA fragmentation after transient cerebral ischemia.

    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·2001
    Same author

    Cyclosporin A, but not FK506, prevents the downregulation of phosphorylated Akt after transient focal ischemia in the rat.

    Brain research·2001
    Same author

    Early release of cytochrome C and activation of caspase-3 in hyperglycemic rats subjected to transient forebrain ischemia.

    Brain research·2001

    Area of Science:

    • Neuroscience
    • Cerebrovascular Research
    • Metabolic Medicine

    Background:

    • Cerebral circulation and metabolism are critical for brain function.
    • Ischemic events can lead to significant brain damage.
    • Understanding these processes is key to developing therapeutic strategies.

    Purpose of the Study:

    • To review recent developments in cerebral circulation and metabolism.
    • To emphasize the link between metabolic events and brain damage in ischemia.
    • To elucidate the mechanisms underlying neuronal and gross brain injury.

    Main Methods:

    • Review of current literature on cerebral metabolism and blood flow.
    • Analysis of metabolic pathways affecting cellular energy state and homeostasis.
    • Examination of the role of ion fluxes, acid-base balance, and lipid metabolism in ischemic brain injury.

    Main Results:

    • Perturbations in cellular energy state, ionic homeostasis, and phospholipid metabolism are linked to blood flow-metabolism coupling.
    • Derangements in energy metabolism affect ion fluxes, acid-base homeostasis, and lipid metabolism.
    • Tissue acidosis exacerbates brain damage (edema, infarction).
    • Disturbed calcium (Ca2+) homeostasis and Ca2+-triggered events (lipolysis, proteolysis) contribute to selective neuronal damage.

    Conclusions:

    • Metabolic and circulatory factors significantly influence ischemic brain damage.
    • Tissue acidosis and calcium dysregulation are key mediators of brain injury.
    • Further research into these mechanisms can inform treatments for stroke and other ischemic conditions.

    Related Experiment Videos