TY - JOUR
T1 - CEREBRAL BLOOD FLOW AND CEREBRAL METABOLIC RATES FOR OXYGEN, GLUCOSE, AND KETONE BODIES IN NEWBORN DOGS
AU - Gregoire, N. M.
AU - Gjedde, A.
AU - Plum, F.
AU - Duffy, T. E.
PY - 1978/1
Y1 - 1978/1
N2 - Cerebral blood flow (CBF) and the cerebral metabolic rates for oxygen, glucose, acetoacetate, β‐hydroxybutyrate and lactate were measured in 1‐ to 5‐day old Beagle dogs under nitrous oxide anesthesia. CBF was determined by 133Xe washout with mechanically integrated blood samples withdrawn simultaneously from a femoral artery and from the posterior one‐third of the superior sagittal sinus. CBF and CMRO2 in normocapnia (PaCO2 40 × 1 mm Hg) were 48 × 5 ml/100 g/min and 2.15 ml/100 g/min, respectively. There was a positive, linear relationship between CBF and PaCO2, calculated for PaCO2 values ranging from 26 to 70 mm Hg. Induced hypocapnia (PaCO2 31 × 1 mm Hg) or hypercapnia (PaCO2 58 × 2 mm Hg) did not alter the CMRO2. Glucose and acetoacetate were taken up by the brain at all PaCO2 levels examined; however, the cerebral uptake of glucose always exceeded the combined uptake of ketone bodies by more than a factor of ten. The cerebral metabolic rate for glucose (94.6 × 3.6 μmol/100 g/min) more than accounted for overall cerebral oxygen consumption, and yielded an oxygen:glucose ratio (mol:mol) of 5.1. Thus, as in adult animals, PaCO2 is an important regulator of cerebral blood flow in puppies, and glucose is the major substrate for oxidative energy production in the immature brain. The oxidation of ketone bodies by the newborn dog brain accounts for not more than 6% of the in vivo cerebral oxygen consumption.
AB - Cerebral blood flow (CBF) and the cerebral metabolic rates for oxygen, glucose, acetoacetate, β‐hydroxybutyrate and lactate were measured in 1‐ to 5‐day old Beagle dogs under nitrous oxide anesthesia. CBF was determined by 133Xe washout with mechanically integrated blood samples withdrawn simultaneously from a femoral artery and from the posterior one‐third of the superior sagittal sinus. CBF and CMRO2 in normocapnia (PaCO2 40 × 1 mm Hg) were 48 × 5 ml/100 g/min and 2.15 ml/100 g/min, respectively. There was a positive, linear relationship between CBF and PaCO2, calculated for PaCO2 values ranging from 26 to 70 mm Hg. Induced hypocapnia (PaCO2 31 × 1 mm Hg) or hypercapnia (PaCO2 58 × 2 mm Hg) did not alter the CMRO2. Glucose and acetoacetate were taken up by the brain at all PaCO2 levels examined; however, the cerebral uptake of glucose always exceeded the combined uptake of ketone bodies by more than a factor of ten. The cerebral metabolic rate for glucose (94.6 × 3.6 μmol/100 g/min) more than accounted for overall cerebral oxygen consumption, and yielded an oxygen:glucose ratio (mol:mol) of 5.1. Thus, as in adult animals, PaCO2 is an important regulator of cerebral blood flow in puppies, and glucose is the major substrate for oxidative energy production in the immature brain. The oxidation of ketone bodies by the newborn dog brain accounts for not more than 6% of the in vivo cerebral oxygen consumption.
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U2 - 10.1111/j.1471-4159.1978.tb07035.x
DO - 10.1111/j.1471-4159.1978.tb07035.x
M3 - Article
C2 - 340616
AN - SCOPUS:0017813528
VL - 30
SP - 63
EP - 69
JO - Journal of Neurochemistry
JF - Journal of Neurochemistry
SN - 0022-3042
IS - 1
ER -