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B Quistorff

Publications and source records attributed to B Quistorff.

At least 91 records · Page 5Linked to original sources
PubMed1986

The deuterium isotope effect on ethanol metabolism in perfused rat liver: effect of reversed perfusion on ethanol and oxygen uptake.

Livers from rats fasted for 24 hr were subjected to nonrecirculating perfusion with Krebs-Ringer bicarbonate solution containing 10 mM ethanol. The deuterium isotope effect was measured using (1-R)-[1-14C,1-2H]ethanol. A value of 2.57 +/- 0.09 (SD) was obtained independent of the direction of perfusion. Oxygen uptake and ethanol metabolism in contrast were significantly increased when reverse perfusion (i.e., from vena cava to vena portae) was used. The magnitude of the isotope effect indicates that contribution from microsomal ethanol-oxidizing system if this is the only supplementary system is 9.8% under the experimental conditions. At high ethanol concentrations, the contribution would approach 18%. Equal activities of microsomal ethanol-oxidizing system and catalase under the experimental conditions would mean that both contribute 7.3% of the total ethanol metabolism. At high ethanol concentrations (80 mM), however, catalase will be 6.8% and microsomal ethanol-oxidizing system is calculated to 13.3%. Preliminary experiments with rats pretreated with phenobarbital showed no change in the isotope effect or in the rate of ethanol metabolism, but a 40-50% increase in oxygen consumption. The acetaldehyde concentration in the effluent medium was below 1 microM.

Alcohol Dehydrogenase↗
PubMed1985

High spatial resolution readout of 3-D metabolic organ structure: an automated, low-temperature redox ratio-scanning instrument.

Intraorgan compartmentation of metabolic processes plays an important role in the understanding of the physiological function of the integrated organ under normal as well as under pathological conditions. We describe here a technique by which 3-D information on tissue redox state may be obtained by means of automated scanning of surface fluorescence. The instrument allows for serial scanning of frozen tissue. A typical scan of a tissue volume of 3 X 3 X 2 mm at a linear resolution of 50 micron and a spatial resolution of ca. 3 X 10(-7) ml includes 144,000 single-point measurements of pyridine nucleotide and flavoprotein fluorescence within the tissue block. The scanning process is fully computerized and programs have been developed which allow 2- or 3-D reconstruction of the data in terms of "redox ratio models," exemplified here by a 3-D model of a spreading depression wave in the cerebral cortex of a gerbil.

Animals↗
PubMed1985

Gluconeogenesis in periportal and perivenous hepatocytes of rat liver, isolated by a new high-yield digitonin/collagenase perfusion technique.

A technique is described which allows preparations of hepatocytes, enriched in either periportal or perivenous hepatocytes ('PP-cells' and 'PV-cells' respectively), in a yield of about 30-50% compared with control cell preparations. The liver is first perfused for 40-60s with digitonin (4 mg/ml) to destroy selectively either the periportal or the perivenous part of the microcirculatory unit, and then the remaining hepatocytes are isolated by the ordinary collagenase perfusion technique. In periportal cells the activities of alanine aminotransferase and pyruvate kinase were 29.4 and 18.7 mumol/min per mg of DNA respectively. The rate of gluconeogenesis was 0.402 mumol/min per mg of DNA. In perivenous cells the corresponding values were 9.55, 22.1 and 0.244 mumol/min per mg of DNA respectively. These data support the concept of a zonation of glucose metabolism within the microcirculatory unit of the liver, with the afferent part (periportal zone) having a 2-fold, more active gluconeogenesis than the efferent part (perivenous zone).

Alanine Transaminase↗
PubMed1985

Digitonin perfusion of rat liver. A new approach in the study of intra-acinar and intracellular compartmentation in the liver.

Perfusing a rat liver with digitonin in the concentration range 2-20 mg/ml results in complete decolorization of the organ within 45-250 s. Decolorization progresses with time in the direction of flow, and it is therefore possible, by collecting the eluate, to obtain material from specific intracellular compartments of hepatocytes in different zones in the microcirculatory unit of the liver. The results demonstrate that cytoplasmic marker enzymes from periportal or perivenous hepatocytes can be collected with as little contamination from the other compartment as is obtained in micro-dissection studies. Furthermore, a fraction enriched in mitochondrial marker enzymes can be achieved with only 10-20% contamination by cytoplasmic material.

Animals↗
PubMed1983

31-P NMR in the study of liver metabolism in vivo.

Continuous noninvasive readout of biochemical events in body tissues is the goal of many techniques and optical and nuclear magnetic resonance (NMR) approaches seem to be at the forefront of these. Here we present a review of NMR methods for studying liver metabolism in vivo with special emphasis on methods of localizing the response appropriate to the liver itself and to the exclusion of surrounding tissues. The simplest and most direct method appears with the use of an implanted coil which enables a variety of NMR magnets to be used in this study.

Adenosine Monophosphate↗
PubMed1981

Blood-brain glucose transfer in spreading depression.

Spreading depression in rat brain cortex is associated with a twofold increase of cerebral blood flow. It is not known whether this increase is coupled to increases of cerebral metabolic rate and glucose transport from blood to brain. During the passage of a single spreading depression, we measured blood-brain glucose transport and glucose metabolism in rat cerebral cortex by single intravenous injection of tracer glucose. Blood flow and tissue content of glucose were measure as well. Reduction of tissue glucose and the consequent increase of net transfer of glucose from blood to brain were consistent with a threefold increase of the consumption of glucose before the increase of blood flow. There was no increase of unidirectional blood-brain transfer.

Animals↗
PubMed1980

Relationship between local changes in cortical blood flow and extracellular K+ during spreading depression.

Change of local cerebral blood flow in response to a single cortical spreading depression of Leão was studied in the brain. During a spreading depression, potassium briefly accumulates in the brain extracellular space. The cortical blood flow was normal during the maximal rate of increase of the extracellular potassium concentration. The blood flow doubled during the subsequent period of normalization of potassium and remained high for one minute thereafter. Thus, potassium cannot be the immediate mediator of the blood flow increase.

Animals↗
PubMed1977

Alcohol metabolism at high alcohol concentrations.

The incorporation rate of tritium from (R,S)ethanol-1-3H, (R)ethanol-1-3H and (S)ethanol-1-3H in lactate and beta-hydroxybutyrate is investigated by means of a GLC method. Preliminary results show no decrease in incorporation of 3H from (R)ethanol during the period of labelling (15 min). These results indicate that either a shift in the isotope effect occurs at high concentrations of ethanol, or the results may indicate that ethanol does not exhibit a substrate inhibitory effect on alcohol dehydrogenase in the liver cells. Furthermore, the fraction of acetaldehyde metabolized in the cytosol is determined.

Acetaldehyde↗
PubMed1976

Metabolism of 1-3H-ethanol by isolated liver cells. Time-course of the transfer of tritium from R,S-1-3H-ethanol to lactate and beta-hydroxybutyrate.

Parenchymal cells isolated from the liver of 24 h fasted rats were incubated with 65 mM R,S-1-3H -ethanol plus 3 mM pyruvate as substrates in the absence and presence of 1.7 mM 4-methylpyrazole. Metabolite levels and the time-course of the transfer of tritum from ethanol to lactate and beta-hydroxybutyrate was measured during the first 15 min of ethanol metabolism. The time-course of the loss of tritium from 2-3H-L-lactate and 3-3H-beta-D-hydroxybutyrate in experiments identical to the above-mentioned was estimated. A GLC method for the isolation of lactate and beta-hydroxybutyrate and the preparation of 2-3H-L-lactate and O-3H-beta-D-hydroxybutyrate is described. The incorporation rate of tritium from ethanol into lactate and beta-hydroxybutyrate decreased with time. Addition of 4-methyl-pyrazole decreased the incorporation rate roughly proportional to the decrease in ethanol and acetaldehyde metabolism. The observed incorporation rates of tritium to lactate were corrected for the detritiation rates measured in experiments with I-3H-L-lactate and 3-3H-beta-D-hydroxybutyrate as substrates. The rate of extramitochondrial acetaldehyde oxidation was calculated from the corrected initial rates of incorporation of tritium into lactate to 0-0.4 mumol min-1 (ml of cells)-1.

Acetaldehyde↗
PubMed1975

Effects of hypoxia of 10-45 seconds duration on energy metabolism in the cerebral cortex of unanesthetized and anesthetized rats.

Glycolytic and citric acid cycle intermediates, as well as organic phosphates, were measured in the cerebral cortex of unanesthetized rats following arterial hypoxia (administration of 6-8% O2) of 10 and 20 s duration. There were decreases in glucose-6-phosphate and fructose-6-phosphate, and increases in fructose-1,6-diphosphate, dihydroxyacetone phosphate and 3-phosphoglycerate, even before pyruvate accumulated. Since measurements of the lactate concentration showed that there was an increased glycolytic rate, the results demonstrate that phosphofructokinase was activated. The glycolytic changes were accompanied by, and probably due to, minor changes in phosphocreatine, ATP, ADP and AMP. Experiments of anesthetized animals showed that hypoxia for 45 s was accompanied by signs of phosphofructokinase activation, even if tissue PCO2 was kept constant. It is concluded that, irrespective of the tissue CO2 tension, hypoxia is accompanied by activation of phosphofructokinase which, at least initially, is responsible for the increased glycolytic rate.

Adenosine Diphosphate↗