Post-ischemic coma in rat: effect of different pre-ischemic blood glucose levels on cerebral metabolic recovery after ischemia
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Post-ischemic coma in rat: effect of different pre-ischemic blood glucose levels on cerebral metabolic recovery after ischemia. / Siemkowicz, Eugeniusz; Gjedde, Albert.
In: Acta physiologica Scandinavica, Vol. 110, No. 3, 1980, p. 225-32.Research output: Contribution to journal › Journal article › Research › peer-review
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T1 - Post-ischemic coma in rat: effect of different pre-ischemic blood glucose levels on cerebral metabolic recovery after ischemia
AU - Siemkowicz, Eugeniusz
AU - Gjedde, Albert
PY - 1980
Y1 - 1980
N2 - Hyper-, normo-, and hypoglycemic rats were exposed to 10 min of complete cerebral ischemia. Regional cerebral blood flow (CBF), blood-brain glucose transfer, and cerebral consumption of oxygen and glucose were measured before, as well as three and 60 minutes after ischemia. Three min after ischemia, no differences were observed between the 3 groups of rats. One h after ischemia, the hyperglycemic rats in comparison to those of the other groups had similar whole-brain CBF and glucose consumption but appreciately lower oxygen consumption, indicating continued non-oxidative use of glucose in the hyperglycemic group. In general, regional CBF values exceeded the control value by 100-200% 3 min after ischemia and were reduced to 50% of control at 1 h after ischemia, at which time the rats were still comatose. In the brain stem of hyperglycemic rats, blood flow, however, remained elevated after ischemia. Thus, the significantly increased mortality observed in rats hyperglycemic before, during and after ischemia (Siemkowicz & Hansen 1978) was the result, not of impaired postischemic CBF, but of ischemic or postischemic damage to brain cells. We suggest that the damaging factor in the hyperglycemic group is increased lactacidosis associated with prolonged anaerobic glycolysis.
AB - Hyper-, normo-, and hypoglycemic rats were exposed to 10 min of complete cerebral ischemia. Regional cerebral blood flow (CBF), blood-brain glucose transfer, and cerebral consumption of oxygen and glucose were measured before, as well as three and 60 minutes after ischemia. Three min after ischemia, no differences were observed between the 3 groups of rats. One h after ischemia, the hyperglycemic rats in comparison to those of the other groups had similar whole-brain CBF and glucose consumption but appreciately lower oxygen consumption, indicating continued non-oxidative use of glucose in the hyperglycemic group. In general, regional CBF values exceeded the control value by 100-200% 3 min after ischemia and were reduced to 50% of control at 1 h after ischemia, at which time the rats were still comatose. In the brain stem of hyperglycemic rats, blood flow, however, remained elevated after ischemia. Thus, the significantly increased mortality observed in rats hyperglycemic before, during and after ischemia (Siemkowicz & Hansen 1978) was the result, not of impaired postischemic CBF, but of ischemic or postischemic damage to brain cells. We suggest that the damaging factor in the hyperglycemic group is increased lactacidosis associated with prolonged anaerobic glycolysis.
M3 - Journal article
C2 - 7211409
VL - 110
SP - 225
EP - 232
JO - Acta Physiologica Scandinavica
JF - Acta Physiologica Scandinavica
SN - 0001-6772
IS - 3
ER -
ID: 14944289