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Biomedical subjects

A Gjedde

Publications and source records attributed to A Gjedde.

At least 217 records · Page 12Linked to original sources
PubMed1980

Blood-brain glucose transport in the conscious rat: comparison of the intravenous and intracarotid injection methods.

The unidirectioal transfer of D-glucose from blood to parietal cortex tissue of the brain of awake rats was measured by single intravenous injection of tracer glucose, as well as by single intracarotid injection according to the method of Oldendorf. The maximal unidirectional blood-brain glucose transfer rate (Tmax) was 407 mumol (100 g)-1 min-1 when measured by intravenous injection, and 352 mumol (100 g)-1 min-1 when measured by intracarotid injection. The half-saturation constants (Km) were 7.8 mM and 16.8 mM, respectively. The comparison shows that the two methods give similar results when cerebral perfusion is assessed accurately.

Animals↗
PubMed1980

Pentobarbital anesthesia reduces blood-brain glucose transfer in the rat.

Pentobarbital anesthesia (40 mg kg-1) was accompanied by a 50% decrease of blood flow and a 40% decrease of unidirectional blood-brain glucose transfer in the parietal cortex of the rat brain. The correlation was explained by a decrease of the number of perfused capillaries. The maximal transport capacity, Tmax, decreased from 409 to 235 mumol 100 g-1 min-1 and the half-saturation constant, Km, from 8.8 to 4.9 mM. At 8.3-8.7 mM-glucose in arterial plasma, the transfer constant (clearance) for unidirectional blood-brain transfer decreased from 0.195 +/- 0.011 in awake rats to 0.132 +/- 0.005 ml g-1 min-1 in anesthetized rats. Half of the decrease was due to less complete diffusion-limitation of glucose uptake at the low plasma flow rate in brain, the other half to the decreased Tmax.

Animals↗
PubMed1980

Rapid simultaneous determination of regional blood flow and blood-brain glucose transfer in brain of rat.

A new method was developed and used in rat to measure regional and whole-brain blood flow and blood-brain glucose transfer simultaneously and in 20 s. This simple method consisted of i.v. bolus injection of labeled butanol and tracer glucose, determination of the average arterial tracer concentration and subsequent assay of cerebral tissue activity 20 s after bolus injection. The whole-brain blood flow rate averaged 129 ml (100 g)-1 min-1. The unidirectional blood-brain glucose transfer was twice as high as previously estimated in similar studies on rat, or 144 mumol (100 g)-1 min-1 at 10 mM glucose in plasma. The magnitude is sufficient to explain the high cerebral glucose consumption rates recently determined by means of autoradiographic 2-deoxy-D-glucose method of Sokoloff et al. (1977).

Animals↗
PubMed1980

Rapid steady-state analysis of blood-brain glucose transfer in rat.

A new kinetic analysis of blood-brain glucose transport is described, based on a steady-state model that takes account of cerebral blood flow, mean capillary glucose concentration, and cerebral metabolic rate. The maximal rate (Tmax) and half-saturation constant (Km) of glucose transport from blood to brain were determined in rats by measuring the rate of blood-to-brain glucose transfer at different blood glucose concentrations. Each determination lasted 20 seconds. For whole-brain, Tmax and Km averaged 258 +/- 33 (S.E.) mumol L(100 g)-1 min-1 and 5.9 +/- 1.6 (S.E.) mmol 1-1, respectively. The regional variations were insignificant. The new approach permits kinetic parameters to be measured locally in brain in rapidly changing functional states.

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↗
PubMed1980

Post-ischemic coma in rat: effect of different pre-ischemic blood glucose levels on cerebral metabolic recovery after ischemia.

Hyper-, normo-, and hypoglycemic rats were exposed to 10 min of complete cerebral ischemia. Regional cerebral blood flow (CBF), blood-brain glucose transfer, and cerebral consumption of oxygen and glucose were measured before, as well as three and 60 minutes after ischemia. Three min after ischemia, no differences were observed between the 3 groups of rats. One h after ischemia, the hyperglycemic rats in comparison to those of the other groups had similar whole-brain CBF and glucose consumption but appreciately lower oxygen consumption, indicating continued non-oxidative use of glucose in the hyperglycemic group. In general, regional CBF values exceeded the control value by 100-200% 3 min after ischemia and were reduced to 50% of control at 1 h after ischemia, at which time the rats were still comatose. In the brain stem of hyperglycemic rats, blood flow, however, remained elevated after ischemia. Thus, the significantly increased mortality observed in rats hyperglycemic before, during and after ischemia (Siemkowicz & Hansen 1978) was the result, not of impaired postischemic CBF, but of ischemic or postischemic damage to brain cells. We suggest that the damaging factor in the hyperglycemic group is increased lactacidosis associated with prolonged anaerobic glycolysis.

Animals↗
PubMed1978

Cerebral blood flow and metabolism in chronically hyperammonemic rats: effect of an acute ammonia challenge.

The effects of chronic hyperammonemia on cerebral metabolism were studied in rats four and eight weeks after the construction of a portacaval shunt. Compared to sham-operated controls, shunted animals had increased arterial concentrations of ammonia and glutamine and decreased glutamate. Cerebral blood flow, measured by xenon 133 washout in animals lightly anesthetized with nitrous oxide, increased from a control of 91 +/- 5 (mean +/- SEM) to 139 +/- 20 ml per 100 gm tissue per minute after shunting for eight weeks; however, the cerebral metabolic rate for oxygen was not different from control four or eight weeks after the shunting procedure. Following intraperitoneal administration of a small ammonium acetate load (2.6 mmol/kg), eight-week portacaval animals consistently underwent a fall in cerebral blood flow and cerebral oxygen consumption and developed high-voltage slow waves in the electroencephalogram. Glutamine was produced by the brains of all groups of animals; the cerebral metabolic rate for glutamine was greater than control in eight-week portacaval rats, the only animals to show a net uptake of ammonia into brain. The findings suggest that increased cerebral sensitivity to ammonia, along with nonspecific effects of chronic portal-systemic shunting, may lead to uncoupling of cerebral blood flow and oxidative metabolism.

Ammonia↗
PubMed1977

Cerebral blood flow and oxygen consumption in rat, measured with microspheres or xenon.

The cerebral blood flow and, in some rats, the cerebral rate of oxygen consumption were measured in three groups of male rats. Fractionation of radioisotope-labeled microspheres was used to measure regional cerebral blood flow in four parts of the rat brain. The arterial and cerebral venous concentrations of radioactive xenon during desaturation were used to measure the blood flow and oxygen consumption of cortex when venous blood was collected from the superior sagittal sinus, or of whole brain when the transverse sinus was sampled. The regional cerebral flow measured with microspheres had a large standard error reflecting the technical difficulty of this method. The cerebral blood flow measured with xenon was higher when venous blood was sampled from the superior sagittal sinus than when sampled from the transverse sinus, but cerebral oxygen consumption rates were similar. The difference reflects the greater trauma involved in the superior sagittal approach and possible extracerebral contamination present in the transverse sinus approach.

Animals↗
PubMed1975

Whole-brain blood flow and oxygen metabolism in the rat after halothane anesthesia.

A recent modification of the Kety-Schmidt wash-out technique for 133xenon was used to measure whole-brain blood flow (CBF) and oxygen consumption (CMRO2) 1 to 4 hours after termination of halothane anesthesia in 15 Wistar rats. In this 3-hour experimental period, mean CBF and CMRO2 were reduced to 29 and 43% of control values, respectively. CBF and CMRO2 determined at the beginning and end of the experimental period were not significantly different from each other. Cerebral venous O2 tension was significantly higher than in the control group, supporting recent suggestions of a primary, intrinsic effect of halothane on the homeostatic control of this variable. It is concluded that halothane is not useful for cerebral metabolic studies in the rat.

Anesthesia, General↗
PubMed1975

Brain uptake of lactate, antipyrine, water and ethanol.

Brain uptake of antipyrine, water and ethanol was studied in rats under normo-, hypo- and hypercapnic conditions. Brain uptake of D- and L-lactate was studied in normal rats. The uptake was determined with the Oldendorf method, using single common carotid arterial injections of a mixture of -14C-labeled test substance and tritiated reference substance. The results demonstrate that L-lactate is taken up by the brain in significant amounts. The results also demonstrate marked differences in the uptakes of antipyrine, water and ethanol. The brain uptake of antipyrine is lower, the brain uptake of ethanol higher, than of water. The brain uptake of all 3 substances was shown not to be affected by changes in cerebral blood flow, although a decrease of brain uptake of antipyrine relative to ethanol was observed during hypo- and hypercapnia.

Animals↗
PubMed1975

Whole-brain blood flow and oxygen metabolism in the rat during nitrous oxide anesthesia.

The Kety-Schmidt washout technique has been modified to measure whole-brain blood flow and metabolism in the rat. During nitrous oxide anesthesia, 14 rats exhaled (133)Xe, and continuous and simultaneous arterial and cerebral venous samples were drawn from a femoral artery and the transverse sinus of the brain. Extracerebral contamination of the venous sample was minimal, and equilibration of (133)Xe in brain tissue and blood was obtained after 10-24 min of inhalation. Cerebral blood flow was calculated from the total activity of the mechanically integrated arterial and venous samples according to the principle of Scheinberg and Stead. At a mean Paco2 of 40 mmHg, CBF averaged 98 +/- 6 (SEM) ml/100 g-min and CMRO2 averaged 5.4 +/- 0.7 (SEM) ml/100 g-min. CBF changed 2.4% with each millimeter Hg change of Paco2 while CMRO2 changed only insignificantly. The values obtained for CBF are higher than reported for man and large laboratory animals bur reflect the proportionately greater amount of gray matter in the rat brain.

Anesthesia, Inhalation↗
PubMed1975

Induction processes in blood-brain transfer of ketone bodies during starvation.

Fed and starved rats were studied on successive days during a 5-day starvation period. The ability of ketone bodies to pass the blood-brain barrier was estimated by single common carotid injections of labeled ketone bodies and water, and results were expressed as the ratio between the normalized activities of tracers in tissue and blood, the brain uptake index (BUI). BUI of D-3-hydroxybutyrate and acetoacetate decreased as their total concentrations increased in the injectate bolus: BUI of D-3-hydroxybutyrate decreased significantly from 8% at 0.2 mM to 3--4% at 20.2 mM in fed rats and from 11.5% at 0.2 mM to 6% at 20.2 mM in starved rats, indicating saturation of the uptake mechanism. The BUI of both ketone bodies increased significantly with increasing duration of starvation, indicating adaptation to ketonemia. Enzymatic kinetics explained the uptake behavior of D-3-hydroxybutyrate in both fed and starved rats and involved a rise of Km and Vmax during starvation consistent with a doubling of the transport rate at the degree of ketonemia found in starved rats. The uptake of glucose was not influenced by starvation or ketonemia.

Acetoacetates↗
PubMedDate not supplied

Glucose uptake and lumped constant variability in normal human hearts determined with [18F]fluorodeoxyglucose.

BACKGROUND: Myocardial glucose uptake can be measured with [18F]fluoro-2-deoxyglucose (FDG) and positron emission tomography (PET). However, changes of myocardial metabolism may alter the ratio between the net rates of FDG and glucose uptake, known as the lumped constant. We tested the hypothesis that the variability of the lumped constant determined in animals explains the disagreement between human net myocardial glucose uptake calculated from aortocoronary sinus deficits and measured with PET. METHODS AND RESULTS: In the three-compartment model of glucose transfer into cells, the lumped constant is a function of the relationship between the net and the unidirectional rates of uptake of glucose and glucose tracers such as FDG. Using this principle, validated in the human brain and the animal heart under experimental conditions, we estimated the lumped constant of the human heart by PET in 10 healthy men under several metabolic conditions established by altering the circulating insulin level during a euglycemic clamp and with somatostatin and heparin infusions. The lumped constant varied systematically between 0.44 and 1.35. At insulin levels below 100 pmol/L, free fatty acids were inversely related to serum insulin levels and the lumped constant increased linearly with serum insulin concentration. At insulin levels above 100 pmol/L, free fatty acids were suppressed and the lumped constant varied in inverse proportion to the insulin level. When the lumped constant was estimated in this manner, net myocardial glucose uptake agreed with that determined in previous measurements of blood flow and aortocoronary sinus deficit. CONCLUSION: In the intact human organism, the cardiac lumped constant varies with the metabolic condition, as predicted from studies of the brain and animal heart under experimental conditions.

Adult↗