-transparent.png){kind=logo}
The influence of hyperglycemic ischemia on tissue damage and cerebral blood flow was studied in rats subjected to short-lasting transient middle cerebral artery (MCA) occlusion. Rats were made hyperglycemic by intravenous infusion of glucose to a blood glucose level of about 20 mmol/L, and MCA occlusion was performed with the intraluminar filament technique for 15, 30, or 60 minutes, followed by 7 days of recovery. Normoglycemic animals received saline infusion. Perfusion-fixed brains were examined microscopically, and the volumes of selective neuronal necrosis and infarctions were calculated. Cerebral blood flow was measured autoradiographically at the end of 30 minutes of MCA occlusion and after 1 hour of recirculation in normoglycemic and hyperglycemic animals. In two additional groups with 30 minutes of MCA occlusion, CO2 was added to the inhaled gases to create a similar tissue acidosis as in hyperglycemic animals. In one group CBF was measured, and the second group was examined for tissue damage after 7 days. Fifteen and 30 minutes of MCA occlusion in combination with hyperglycemia produced larger infarcts and smaller amounts of selective neuronal necrosis than in rats with normal blood glucose levels, a significant difference in the total volume of ischemic damage being found after 30 minutes of MCA occlusion. After 60 minutes of occlusion, when the volume of infarction was larger, only minor differences between normoglycemic and hyperglycemic animals were found. Hypercapnic animals showed volumes of both selective neuronal necrosis and infarction that were almost identical with those observed in normoglycemic, normocapnic animals. When local CBF was measured in the ischemic core after 30 minutes of occlusion, neither the hyperglycemic nor the hypercapnic animals were found to be significantly different from the normoglycemic group. Brief focal cerebral ischemia combined with hyperglycemia leads to larger and more severe tissue damage. Our results do not support the hypothesis that the aggravated injury is caused by any disturbances in CBF.
L Gisselsson, and
M L Smith, and
B K Siesjö
September 2009,
Brain research,
L Gisselsson, and
M L Smith, and
B K Siesjö
January 1996,
Acta neurochirurgica,
L Gisselsson, and
M L Smith, and
B K Siesjö
January 1998,
Acta neurochirurgica. Supplement,
L Gisselsson, and
M L Smith, and
B K Siesjö
July 2003,
Ideggyogyaszati szemle,
L Gisselsson, and
M L Smith, and
B K Siesjö
January 1978,
Critical care medicine,
L Gisselsson, and
M L Smith, and
B K Siesjö
November 1986,
Journal of neurosurgery,
L Gisselsson, and
M L Smith, and
B K Siesjö
March 1998,
Brain research,
L Gisselsson, and
M L Smith, and
B K Siesjö
November 2009,
Experimental & translational stroke medicine,
L Gisselsson, and
M L Smith, and
B K Siesjö
December 2022,
IBRO neuroscience reports,
L Gisselsson, and
M L Smith, and
B K Siesjö
April 1970,
Postgraduate medicine,
