Abstract
To assess alterations in regional cerebral blood flow and glucose utilization during perinatal hypoglycemia, newborn dogs (2-7 days postnatal age) were anesthetized with halothane, tracheostomized, paralyzed, and artificially ventilated with 70% N2O-30% O2 to maintain arterial normoxia and normocapnia (arterial PO2>60 mmHg; arterial PCO2: 35-42 mmHg; arterial pH: 7.35-7.45). Regional cerebral blood flow (rCBF) and glucose utilization (rCGU) were determined with iodo-[14C]antipyrine and 2-deoxy-[14C]glucose as the radioactive tracers, respectively. Hypoglycemia with blood glucose concentrations averaging 0.9 mmol/l was achieved within 90-120 min in 10 animals using intermittent intravenous injections of regular insulin; 10 control animals received 0.9% saline (blood glucose = 9 mmol/l). During hypoglycemia, mean arterial blood pressure was 81% of control, whereas heart rate was unchanged. Arterial O2 and acid-base balance were well maintained (arterial PO2 = 68 mmHg; PCO2 = 37 mmHg; pH = 7.35). Hypoglycemia was associated with significant increases in rCBF in all of 16 analyzed structures, ranging from 172% (parietal white matter) to 249% (thalamus) of control values (17-65 ml·100 g-1·min-1). During hypoglycemia, rCGU was relatively unchanged from normoglycemic values in 11 of 16 brain structures. Significant reductions in rCGU were seen only in occipital white matter -31%) and in the cerebellar vermis and hemisphere (-31 and -43%, respectively). CGU actually increased slightly in the pons and medulla (+12 and +19%, respectively). Calculation of the extent to which glucose transport into brain during hypoglycemia was enhanced by the increase in CBF suggested that glucose delivery (CBF x blood glucose concentration) contributed little (<10%) to the maintenance of CGU. Presumably, other factors, notably low cerebral energy demands, serve to maintain cerebral glucose homeostasis of the immature brain during hypoglycemia.
| Original language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 256 |
| Issue number | 6 |
| State | Published - Jan 1 1989 |
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All Science Journal Classification (ASJC) codes
- Physiology
- Cardiology and Cardiovascular Medicine
- Physiology (medical)
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Regional cerebral blood flow and glucose utilization during hypoglycemia in newborn dogs. / Mujsce, Dennis; Christensen, M. A.; Vannucci, R. C.
In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 256, No. 6, 01.01.1989.Research output: Contribution to journal › Article
TY - JOUR
T1 - Regional cerebral blood flow and glucose utilization during hypoglycemia in newborn dogs
AU - Mujsce, Dennis
AU - Christensen, M. A.
AU - Vannucci, R. C.
PY - 1989/1/1
Y1 - 1989/1/1
N2 - To assess alterations in regional cerebral blood flow and glucose utilization during perinatal hypoglycemia, newborn dogs (2-7 days postnatal age) were anesthetized with halothane, tracheostomized, paralyzed, and artificially ventilated with 70% N2O-30% O2 to maintain arterial normoxia and normocapnia (arterial PO2>60 mmHg; arterial PCO2: 35-42 mmHg; arterial pH: 7.35-7.45). Regional cerebral blood flow (rCBF) and glucose utilization (rCGU) were determined with iodo-[14C]antipyrine and 2-deoxy-[14C]glucose as the radioactive tracers, respectively. Hypoglycemia with blood glucose concentrations averaging 0.9 mmol/l was achieved within 90-120 min in 10 animals using intermittent intravenous injections of regular insulin; 10 control animals received 0.9% saline (blood glucose = 9 mmol/l). During hypoglycemia, mean arterial blood pressure was 81% of control, whereas heart rate was unchanged. Arterial O2 and acid-base balance were well maintained (arterial PO2 = 68 mmHg; PCO2 = 37 mmHg; pH = 7.35). Hypoglycemia was associated with significant increases in rCBF in all of 16 analyzed structures, ranging from 172% (parietal white matter) to 249% (thalamus) of control values (17-65 ml·100 g-1·min-1). During hypoglycemia, rCGU was relatively unchanged from normoglycemic values in 11 of 16 brain structures. Significant reductions in rCGU were seen only in occipital white matter -31%) and in the cerebellar vermis and hemisphere (-31 and -43%, respectively). CGU actually increased slightly in the pons and medulla (+12 and +19%, respectively). Calculation of the extent to which glucose transport into brain during hypoglycemia was enhanced by the increase in CBF suggested that glucose delivery (CBF x blood glucose concentration) contributed little (<10%) to the maintenance of CGU. Presumably, other factors, notably low cerebral energy demands, serve to maintain cerebral glucose homeostasis of the immature brain during hypoglycemia.
AB - To assess alterations in regional cerebral blood flow and glucose utilization during perinatal hypoglycemia, newborn dogs (2-7 days postnatal age) were anesthetized with halothane, tracheostomized, paralyzed, and artificially ventilated with 70% N2O-30% O2 to maintain arterial normoxia and normocapnia (arterial PO2>60 mmHg; arterial PCO2: 35-42 mmHg; arterial pH: 7.35-7.45). Regional cerebral blood flow (rCBF) and glucose utilization (rCGU) were determined with iodo-[14C]antipyrine and 2-deoxy-[14C]glucose as the radioactive tracers, respectively. Hypoglycemia with blood glucose concentrations averaging 0.9 mmol/l was achieved within 90-120 min in 10 animals using intermittent intravenous injections of regular insulin; 10 control animals received 0.9% saline (blood glucose = 9 mmol/l). During hypoglycemia, mean arterial blood pressure was 81% of control, whereas heart rate was unchanged. Arterial O2 and acid-base balance were well maintained (arterial PO2 = 68 mmHg; PCO2 = 37 mmHg; pH = 7.35). Hypoglycemia was associated with significant increases in rCBF in all of 16 analyzed structures, ranging from 172% (parietal white matter) to 249% (thalamus) of control values (17-65 ml·100 g-1·min-1). During hypoglycemia, rCGU was relatively unchanged from normoglycemic values in 11 of 16 brain structures. Significant reductions in rCGU were seen only in occipital white matter -31%) and in the cerebellar vermis and hemisphere (-31 and -43%, respectively). CGU actually increased slightly in the pons and medulla (+12 and +19%, respectively). Calculation of the extent to which glucose transport into brain during hypoglycemia was enhanced by the increase in CBF suggested that glucose delivery (CBF x blood glucose concentration) contributed little (<10%) to the maintenance of CGU. Presumably, other factors, notably low cerebral energy demands, serve to maintain cerebral glucose homeostasis of the immature brain during hypoglycemia.
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M3 - Article
C2 - 2500033
AN - SCOPUS:0024379490
VL - 256
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6135
IS - 6
ER -