Progressing cerebral infarction in relation to plasma glucose in gerbils.

Abstract

We studied neurologic morbidity and its evolution during hyperglycemia induced immediately after permanent unilateral common carotid artery ligation in Mongolian gerbils. A total of 60 animals were divided into five groups: one experiencing severe hyperglycemia for 1 hour after the onset of ischemia (brief hyperglycemia group, n=13), a normoglycemic control group for the brief hyperglycemia group (n=12), a group with severe hyperglycemia for 4 hours after the onset of ischemia (prolonged hyperglycemia group, n = l l ) , a normoglycemic control group for the prolonged hyperglycemia group (n = 13), and a hyperosmolar normoglycemic control group for the prolonged hyperglycemia group ( n = l l ) . Neurologic morbidity and mortality were higher in the two hyperglycemic groups than in the three normoglycemic control groups. The neurologic deficit progressed according to the duration of severe hyperglycemia. In the three normoglycemic control groups neurologic status stabilized 120 minutes after the onset of ischemia, in the brief hyperglycemia group stabilization occurred at 210 minutes, and in the prolonged hyperglycemia group neurologic deficit progressed for approximately 360 minutes, coinciding with the death of all but one gerbil, in which the neurologic deficit remained stable until death 23 hours after ischemia. We suggest that hyperglycemia is another cause of progressing cerebral infarction. (Stroke 1990;21:1621-1624) P rogressing cerebral infarction refers to that temporal clinical category for which progression or an increase in the severity of the neurologic signs has occurred within recent minutes. Other suggested causes, well-summarized by Price et al, 3 are decreased cardiac output, systemic hypotension/postural hypotension, increased blood viscosity, hypoxia, seizures, and hemorrhage into an infarct.There are no reports on progressing cerebral infarction to date that provide an analysis of plasma glucose level during the acute phase of the illness. Hyperglycemia during either global or regional brain ischemia is widely known to be detrimental.4 -6 High brain glucose Received January 5, 1989; accepted July 25, 1990. levels are thought to mediate their detrimental effect through accentuated tissue lactacidosis during and following ischemia.7 -8 Hence, by controlling hyperglycemia during the acute phase of cerebral ischemia some progressing strokes could be arrested.We examined the influence of hyperglycemia in the setting of progressing cerebral infarction. Specifically, we assessed neurologic morbidity and its temporal profile during hyperglycemia induced immediately after unilateral common carotid artery (CCA) occlusion in Mongolian gerbils. Materials and MethodsWe performed experiments on a total of 60 adult (50-80 g body wt) Mongolian gerbils (Meriones unguiculatus) (Shamrock, Henfield-Sussets, England) of either sex equally distributed among five groups: the brief hyperglycemia group (n = 13), the prolonged hyperglycemia group (« = 11), saline-treated normoglycemic control groups for both the br...

Iron-related damage in acute ischemic stroke.

“…9 Recently attention has been focused on controlling hyperglycemia because it has been related to infarct size 10 and progressing cerebral infarct. 8 - 11 Lactate and unbuffered hydrogen ions produced by anaerobic glycolysis accumulate in tissue in proportion to the carbohydrate stores present at the onset of ischemia. The toxicity of hydrogen ions, especially their ability to facilitate ferrous iron-mediated free-radical injury, may be responsible for the increased tissue damage.…”

Diabetes hyperglycemia and recovery from stroke

“…The ischemic cascade begins within seconds of onset of ischemia and results in cell death when local cerebral blood flow falls below 10-15 mL/100 g per min. 25,[39][40][41] Most of the experimental evidence linking hyperglycemia to enhanced ischemic injury comes from animal models of stroke. 36 The cascade of metabolic events that ensues following focal cerebral ischemia results in a local increase in glycolysis and a rapid decline in tissue glucose levels.…”

“…This raises the potential that glucose treatment thresholds exist in acute stroke above which maximal ischemic damage may occur. 25,[39][40][41] Most of the experimental evidence linking hyperglycemia to enhanced ischemic injury comes from animal models of stroke. Extrapolations to human stroke have been made on the basis of these observations and also on the basis of associations observed in clinical studies.…”