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

Brain Research

Volumn 912, Issue 2, 2001, Pages 203-205

  Li, Ping An ^a   He, Qing Ping ^a   Csiszar, Katalin ^a   Siesjö, Bo K ^a  

^a UNIVERSITY OF HAWAII   (United States)

Author keywords

Brain damage; Glucose; Histopathology; Hyperglycemia; Ischemia; Seizure

Indexed keywords

GLUCOSE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; BRAIN INJURY; CONTROLLED STUDY; GLUCOSE INFUSION; HYPERGLYCEMIA; LONG TERM CARE; MALE; NONHUMAN; PRIORITY JOURNAL; RAT; TRANSIENT ISCHEMIC ATTACK;

ANIMALS; BRAIN; BRAIN INJURIES; BRAIN ISCHEMIA; CEREBRAL INFARCTION; DRUG ADMINISTRATION SCHEDULE; GLUCOSE; MALE; NERVE DEGENERATION; NEURONS; RATS; RATS, WISTAR; REPERFUSION INJURY; SURVIVAL RATE;

EID: 0035823326     PISSN: 00068993     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0006-8993(01)02724-X     Document Type: Article

References (8)

1. Effects of streptozotocin-induced hyperglycemia on brain damage following transient ischemia
2. Hypothermia ameliorates ischemic brain damage and suppresses the release of extracellular amino acids in both normo- and hyperglycemic subjects
3. Critical values for plasma glucose in aggravating ischemic brain damage: Correlation to extracellular pH
4. Role of hyperglycaemia-related acidosis in ischaemic brain damage
5. Transient focal ischemia in hyperglycemic rats is associated with increased cerebral infarction
6. Corticosterone: A possible candidate for hyperglycemia-enhanced ischemic neuronal damage
7. The glucose paradox in cerebral ischemia. New insights
8. Morphological lesions in the brain preceding the development of postischemic seizures