Oxygen supply of the brain cortex (rat) during severe hypoglycemia.
Oxygen supply of the brain cortex together with changes in the electrocorticogram (ECoG) were investigated during and after insulin induced hypoglycemia in 13 anaesthetized rats. Local oxygen partial pressures (pO2) on the parietal cortex were continuously measured with a multiwire surface electrode of the Clark type. During early hypoglycemia with a mean arterial glucose concentration [G]a of 2.81 (SD +/- 0.40) mmol/l, the local tissue pO2 did not change significantly as compared to the pO2 values recorded during the control period with a normal [G]a of 4.51 (SD +/- 0.70) mmol/l. During severe hypoglycemia at a [G]a of 1.39 (SD +/- 0.2) mmol/l, pO2 began to increase continuously on all 104 measuring sites, independently of changes in arterial blood pressure and ECoG. During a period of 7-18 min of isoelectricity, tissue pO2 remained elevated so long as blood pressure did not decrease. After injection of a 25% glucose solution, pO2 gradually decreased to control values within 30-60 min in most experiments. We conclude from these results that oxygen supply is generally improved during severe hypoglycemia. We assume that the increase in tissue pO2 is mainly caused by an increase in microflow. Thus, the neuronal damage occurring after severe hypoglycemia, as reported in literature, cannot primarily be caused by an oxygen deficiency.
D000818:Animals; D001784:Blood Gas Analysis; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D002540:Cerebral Cortex / Q000378:metabolism*; D004569:Electroencephalography; D007003:Hypoglycemia / Q000503:physiopathology*; D007328:Insulin / Q000494:pharmacology; D008297:Male; D010100:Oxygen / Q000502:physiology*; D051381:Rats
D001786:Blood Glucose; D007328:Insulin; D010100:Oxygen