Cerebral metabolism in sheep: a comparative study of the adult, the lamb, and the fetus

1975 ◽  
Vol 229 (1) ◽  
pp. 235-239 ◽  
Author(s):  
Jones MD ◽  
LI Burd ◽  
EL Makowski ◽  
G Meschia ◽  
FC Battaglia
Keyword(s):  
Steady State ◽  
Comparative Study ◽  
Cerebral Metabolism ◽  
Lactate Production ◽  
Fetal Sheep ◽  
Sagittal Sinus ◽  
Sheep Brain ◽  
Beta Hydroxybutyrate ◽  
Arteriovenous Difference

The cerebral uptakes of glucose, oxygen, lactate, pyruvate, acetoacetate and beta-hydroxybutyrate were compared in the adult, the fetal, and the newborn sheep. Beginning 1-2 days after surgery, we withdrew samples simultaneously from an artery and from the sagittal sinus for up to 2 wk. At all ages glucose was the only substrate taken up in significant quantity relative to oxygen. The glucose-oxygen quotients were 0.98 less than 1.03 less than 1.08 in adults; 0.92 less than 0.99 less than 1.06 in lambs; 0.92 less than 0.98 less than 1.03 in fetuses. These quotients were not significantly different. There was a significant (P less than .05) arteriovenous difference for lactate in the adult (-0.031 mM), but not in the lamb or fetus. A significant (P less than .05) arteriovenous difference pyruvate was found in the adult (-0.013 mM) and in the fetus (-0.020 mM). The findings of a glucose-oxygen quotient of approximately 1 and the lack of significant lactate production in fetal sheep brain are consistent with the hypothesis that anerobic glycolysis is unimportant to the steady-state cerebral metabolism of the fetal sheep.

Effect of hypoglycemia on cerebral metabolism and carbon dioxide responsivity

1989 ◽  
Vol 256 (3) ◽  
pp. H697-H706 ◽  
Author(s):  
F. E. Sieber ◽  
S. A. Derrer ◽  
C. D. Saudek ◽  
R. J. Traystman
Keyword(s):  
Carbon Dioxide ◽  
Cerebral Metabolism ◽  
Carbon Dioxide Tension ◽  
Cerebrovascular Reactivity ◽  
Cerebral Oxygen ◽  
Cerebral Vasoconstriction ◽  
Sagittal Sinus ◽  
Cerebral Metabolites ◽  
Anesthetized Dogs ◽  
Beta Hydroxybutyrate

This study examined the effects of hypoglycemia (HG) on cerebral metabolism and cerebrovascular reactivity to carbon dioxide. Cerebral blood flow (CBF) was determined using radiolabeled microspheres in pentobarbital-anesthetized dogs. Cerebral oxygen, glucose, lactate, pyruvate, acetoacetate, and beta-hydroxybutyrate uptakes were calculated using the respective concentrations measured in arterial and sagittal sinus blood samples. EEG was recorded throughout each experiment. HG was induced with insulin to obtain a blood glucose less than 30 mg/100 ml. Hypercapnia was studied in 10 animals (3 control, 7 HG) by increasing arterial carbon dioxide tension (PaCO2) from control (35 +/- 4; mean +/- SE) to 54 +/- 2 Torr during normoglycemia (NG) and HG. Hypocapnia was studied in 11 animals (3 control, 8 HG) by decreasing PaCO2 from control (39 +/- 1) to 14 +/- 1 Torr in NG and HG. Measurements were taken after reaching steady-state PaCO2 in both groups at each control and altered PaCO2 state. In the hypercapnic group, glucose decreased from 71 +/- 3 to 28 +/- 3 mg/100 ml. CBF increased with hypercapnia to 175% of control in both NG and HG. Cerebral metabolic rate of oxygen and electroencephalogram (EEG) did not change in the hypercapnic group. In the hypocapnic group glucose decreased from 71 +/- 3 to 19 +/- 2 mg/100 ml. CBF decreased with hypocapnia to 62 +/- 5% of control in NG but remained at control in HG. This was not accompanied by changes in cerebral oxygen consumption; however, a flat EEG occurred in all HG hypocapnic animals. No change occurred in uptake of the other cerebral metabolites measured in any group. This study shows that the CBF hypercapnic response remains intact during HG; however, hypocapnia causes severe EEG disturbances and impairs the cerebral vasoconstriction response.

An attempt to demonstrate cerebral anoxia during hyperventilation of anesthetized dogs

1963 ◽  
Vol 204 (2) ◽  
pp. 323-326 ◽  
Author(s):  
Stephen M. Cain
Keyword(s):  
Lactic Acid ◽  
Cerebral Oxygenation ◽  
Lactate Production ◽  
Blood Samples ◽  
Cerebral Anoxia ◽  
Sagittal Sinus ◽  
Hemoglobin Saturation ◽  
Anesthetized Dogs ◽  
Arteriovenous Difference ◽  
Pyruvic Acids

Eight anesthetized, curarized dogs were ventilated to alveolar Pco2 of 40, 20, and 10 mm Hg. Blood samples were drawn from an artery and sagittal sinus and analyzed for Pco2, Po2, pH, hemoglobin saturation, lactic acid, and pyruvic acid. The vasoconstriction of the cerebral vessels was clearly demonstrated by the increased arteriovenous difference in hemoglobin saturation which increased on the average from 26% to 45% and to 48% during the two periods of hyperventilation. Sagittal sinus Po2 declined from 41 mm Hg during the control to 29 and to 25 mm Hg with hyperventilation. Calculation of the cerebral "excess lactate" production from the measurements of lactic and pyruvic acids showed no significant increase with hyperventilation. The conclusion was made, with reservation, that cerebral oxygenation during even severe hyperventilation was sufficient to maintain normal oxidative metabolism.

Changes in cerebral blood flow, cerebral metabolites, and breathing movements in the sheep fetus following asphyxia produced by occlusion of the umbilical cord

2009 ◽  
Vol 297 (1) ◽  
pp. R60-R69 ◽  
Author(s):  
Edwin B. Yan ◽  
Ana A. Baburamani ◽  
Adrian M. Walker ◽  
David W. Walker
Keyword(s):  
Blood Flow ◽  
Cerebral Cortex ◽  
Umbilical Cord ◽  
Cerebral Metabolism ◽  
Membrane Integrity ◽  
Brain Regions ◽  
Distinct Pattern ◽  
Cerebral Hypoperfusion ◽  
Fetal Sheep ◽  
Sagittal Sinus

Severe global fetal asphyxia, if caused by a brief occlusion of the umbilical cord, results in prolonged cerebral hypoperfusion in fetal sheep. In this study, we sought evidence to support the hypothesis that cerebral hypoperfusion is a consequence of suppressed cerebral metabolism. In the 24 h following complete occlusion of the umbilical cord for 10 min, sagittal sinus blood flow velocity was significantly decreased for up to 12 h. Capillary blood flow, measured using microspheres, decreased at 1 and 5 h after cord occlusion in many brain regions, including cortical gray and white matter. Microdialysis probes implanted in the cerebral cortex revealed an increase in extracellular glucose concentrations in gray matter for 7–8 h postasphyxia, while lactate increased only briefly, suggesting decreased cerebral glucose utilization over this time. Although these data, as well as the concurrent suppression of breathing movements and electrocortical activity, support the concept of hypometabolic hypoperfusion, the significant increase of pyruvate and glycerol concentrations in dialysate fluid obtained from the cerebral cortex at 3–8 h after cord occlusion suggests an eventual loss of membrane integrity. The prolonged increase of breathing movements for many hours suggests loss of the pontine/thalamic control that produces the distinct pattern of fetal breathing movements.

Regulation of cytochrome oxidase redox state during umbilical cord occlusion in preterm fetal sheep

2007 ◽  
Vol 292 (4) ◽  
pp. R1569-R1576 ◽  
Author(s):  
Laura Bennet ◽  
Vincent Roelfsema ◽  
Justin M. Dean ◽  
Guido Wassink ◽  
Gordon G. Power ◽  
...  
Keyword(s):  
Cytochrome Oxidase ◽  
Umbilical Cord ◽  
Redox State ◽  
Cerebral Oxygenation ◽  
Cerebral Metabolism ◽  
Electron Flow ◽  
Initial Response ◽  
Severe Hypoxia ◽  
Fetal Sheep ◽  
Severe Hypotension

The preterm fetus is capable of surviving prolonged periods of severe hypoxia without neural injury for much longer than at term. To evaluate the hypothesis that regulated suppression of brain metabolism contributes to this remarkable tolerance, we assessed changes in the redox state of cytochrome oxidase (CytOx) relative to cerebral heat production, and cytotoxic edema measured using cerebral impedance, during 25 min of complete umbilical cord occlusion or sham occlusion in fetal sheep at 0.7 gestation. Occlusion was followed by rapid, profound reduction in relative cerebral oxygenation and EEG intensity and an immediate increase in oxidized CytOx, indicating a reduction in electron flow down the mitochondrial electron transfer chain. Confirming rapid suppression of cerebral metabolism there was a loss of the temperature difference between parietal cortex and body at a time when carotid blood flow was maintained at control values. As occlusion continued, severe hypotension/hypoperfusion developed, with a further increase in CytOx levels to a plateau between 8 and 13 min and a progressive rise in cerebral impedance. In conclusion, these data strongly suggest active regulation of cerebral metabolism during the initial response to severe hypoxia, which may help to protect the immature brain from injury.

Intercellular barriers to and transcellular transfer of albumin in the fetal sheep brain

1997 ◽  
Vol 195 (3) ◽  
pp. 229-236 ◽  
Author(s):  
Y. Balslev ◽  
K. M. Dziegielewska ◽  
K. Møllgård ◽  
N. R. Saunders
Keyword(s):  
Fetal Sheep ◽  
Sheep Brain

Endurance training enhances lactate clearance during hyperlactatemia

1989 ◽  
Vol 257 (5) ◽  
pp. E782-E789 ◽  
Author(s):  
C. M. Donovan ◽  
M. J. Pagliassotti
Keyword(s):  
Steady State ◽  
Endurance Training ◽  
Specific Activity ◽  
Lactate Production ◽  
Lactate Clearance ◽  
Lactate Removal ◽  
Lactate Levels ◽  
Infusion Period ◽  
Mixed Venous ◽  
Blood Lactate Levels

Constant infusions of cold molar lactate (178.0 +/- 1.6 mumol.kg-1.min-1), [U-14C]lactate (0.50 muCi/min), and [6-3H]glucose (0.5 muCi/min) were employed to study the effects of endurance training (running 1 h/day, at 38 m/min, 10% grade) on lactate clearance in resting, hyperlactatemic rats. Before infusion, resting blood lactate levels were not significantly different between controls, 1.10 +/- 0.04 mM, and trained animals, 1.16 +/- 0.04 mM. Lactate levels increased significantly during the infusion period, attaining steady-state mixed venous concentrations of 11.32 +/- 0.24 mM and 5.44 +/- 0.09 mM, respectively, for controls and trained animals. Lactate clearance rates, based on net lactate removal (i.e., not tracer-estimated lactate removal), were twofold greater in trained animals vs. controls, 33.0 +/- 0.7 and 15.4 +/- 0.4 ml.kg-1. min-1, respectively. Lactate specific activity values during the infusion period were not significantly different between controls, 22,243 +/- 236 dpm/mumol, and trained animals, 21,270 +/- 374 dpm/mumol, indicating similar endogenous dilution of the pyruvate-lactate pool. For both control and trained animals, essentially 100% of the 14C infused as lactate was recovered as either glucose or CO2; however, trained animals demonstrated a 25% greater rate of gluconeogenesis. At a given lactate production rate, trained animals maintain lower lactate levels through enhanced clearance via gluconeogenesis and oxidation.

Repeated isoflurane exposure and neuroapoptosis in the midgestation fetal sheep brain

2016 ◽  
Vol 214 (4) ◽  
pp. 542.e1-542.e8 ◽  
Author(s):  
Olutoyin A. Olutoye ◽  
Fariha Sheikh ◽  
Irving J. Zamora ◽  
Ling Yu ◽  
Adesola C. Akinkuotu ◽  
...  
Keyword(s):  
Fetal Sheep ◽  
Sheep Brain

Role of glucose in corneal metabolism

1985 ◽  
Vol 249 (5) ◽  
pp. C409-C416 ◽  
Author(s):  
R. S. Thies ◽  
L. J. Mandel
Keyword(s):  
Oxygen Consumption ◽  
Steady State ◽  
Specific Activity ◽  
Krebs Cycle ◽  
Lactate Production ◽  
Minor Component ◽  
Acid Oxidation ◽  
Endogenous Fatty Acid ◽  
Nonsteady State ◽  
A Minor

Glucose catabolism by glycolysis and the Krebs cycle was examined in the isolated rabbit cornea incubated with [6-14C]glucose. The production of [14C]lactate and 14CO2 from this substrate provided minimal values for the fluxes through these pathways since the tissue was in metabolic steady state but not isotopic steady state during the 40-min incubation. The specific activity of lactate under these conditions was one-third of that for [6-14C]glucose, and label dilution by exchange with unlabeled alanine was minimal, suggesting that glycogen degradation was primarily responsible for this dilution of label in the Embden-Meyerhof pathway. In addition, considerable label accumulation was found in glutamate and aspartate. Calculations revealed that these endogenous amino acid pools were not isotopically equilibrated after the incubation period, suggesting that they were responsible for the isotopic nonsteady state by exchange dilution through transaminase reactions with labeled intermediates. An estimate of glucose oxidation by the Krebs cycle, which was corrected for label dilution by exchange, indicated that glucose could account for most of the measured corneal oxygen consumption that was coupled to oxidative phosphorylation. A minor component of this respiration could not be accounted for by glucose or glycogen oxidation. Additional experiments suggested that endogenous fatty acid oxidation was probably also active under these conditions. Finally, reciprocal changes in plasma membrane Na+-K+-ATPase activity induced by ouabain and nystatin were found to concomitantly alter oxygen consumption rates and [14C]lactate production from [6-14C]glucose. These results demonstrated the capacity for regulating glycolysis and the Krebs cycle in response to changing energy demands in the cornea.

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