Regional cerebral blood flow and glucose utilization during hypoglycemia in newborn dogs

Dennis Mujsce, M. A. Christensen, R. C. Vannucci

Research output: Contribution to journalArticle

42 Citations (Scopus)

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 languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume256
Issue number6
StatePublished - Jan 1 1989

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Cerebrovascular Circulation
Regional Blood Flow
Hypoglycemia
Blood Glucose
Dogs
Glucose
Arterial Pressure
Brain
Radioactive Tracers
Antipyrine
Acid-Base Equilibrium
Pons
Halothane
Thalamus
Intravenous Injections
Homeostasis
Heart Rate
Maintenance
Insulin

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

@article{4a121908b5e74ae7935bb4443c436450,
title = "Regional cerebral blood flow and glucose utilization during hypoglycemia in newborn dogs",
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.",
author = "Dennis Mujsce and Christensen, {M. A.} and Vannucci, {R. C.}",
year = "1989",
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journal = "American Journal of Physiology",
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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 journalArticle

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AU - Christensen, M. A.

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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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