AJP - Regulatory, Integrative and Comparative Physiology, Vol 248, Issue 1 72-R77, Copyright © 1985 by American Physiological Society
Insulin hypoglycemia, cerebral metabolism, and neural function in fetal lambs
B. S. Richardson, A. R. Hohimer, J. M. Bissonnette and C. M. Machida
The effect of insulin-induced hypoglycemia on cerebral oxidative metabolism
(CMRO2) was studied in nine late gestational fetal lambs using the
radiolabeled microsphere technique for cerebral blood flow and
brachiocephalic to sagittal sinus blood O2 content differences. After 4 h
insulin infusion to the fetus, arterial glucose fell from control levels of
0.96 +/- 0.11 (SE) to 0.69 +/- 0.09 mmol X l-1. CMRO2 was reduced from 199
+/- 23 to 155 +/- 22 mumol X 100 g-1 X min-1 (P less than 0.05), and
cerebral glucose uptake fell from 31 +/- 4 to 25 +/- 4 mumol X 100 g-1 X
min-1 (P less than 0.02). During both euglycemia and hypoglycemia, 6 mumol
glucose were taken up for each micromole of O2, indicating that glucose was
the sole metabolic substrate for oxidative metabolism. Although there was
no change in fetal electrocortical activity during the hypoglycemia, fetal
breathing movements were present only 19.4 +/- 3.4% of the hypoglycemic
hours compared with 36.8 +/- 2.6% of the control period (P less than or
equal to 0.01). These results suggest that during rapidly induced fetal
hypoglycemia, blood-brain barrier transport of glucose can limit cerebral
glucose and O2 uptake, and this decrease in cerebral metabolism is
associated with a lowered incidence of fetal breathing movements.
