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The Glucose Paradox in Cerebral Ischemia: New Insights
Author(s) -
SCHURR AVITAL,
PAYNE RALPHIEL S.,
TSENG MICHAEL T.,
MILLER JAMES J.,
RIGOR BENJAMIN M.
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb07862.x
Subject(s) - neuroprotection , ischemia , in vivo , medicine , in vitro , brain damage , hormone , ischemic injury , endocrinology , anesthesia , pharmacology , chemistry , biology , biochemistry , microbiology and biotechnology
The present in vivo findings that lactate, accumulated during an ischemic episode, is an essential aerobic energy substrate during the initial postischemic period are in full agreement with out in vitro findings. Moreover, the beneficial effects of hyperglycemia are also in agreement with our and others' in vitro results that have demonstrated a neuroprotective effect of glucose against hypoxic change. The aggravation of ischemic delayed neuronal damage by glucose loading 15 min prior to the ischemic insult is likely the result of glucose induction of a short-acting (30 to 60 min) systemic factor (hormonal?) that, when combined with an ischemic insult, potentiates the ischemic damage.