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Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of glucose concentration and anoxia upon the metabolite concentrations and rates of glycolysis and respiration have been investigated in the perfused liver of the fetal guinea pig. In most cases the metabolite concentrations in the perfused liver were similar to those observed in vivo. Between 50 days and term there was a fall in the respiratory rate and in the concentration of ATP and fructose 1,6-diphosphate and an increase in the concentration of glutamate, glycogen and glucose. Reducing the medium glucose concentration from 10 mM to 1 mM or 0.1 mM depressed lactate production and the concentration of most of the phosphorylated intermediates (except 6-phosphogluconate) in the liver of the 50-day fetus. This indicates a fall in glycolytic rate which is not in accord with the known kinetic properties of hexokinase in the fetal liver. Anoxia increased lactate production by, and the concentrations of, the hexose phosphates ADP and AMP in the 50-day to term fetal liver, while the concentration of ribulose 5-phosphate, ATP and some triose phosphates fell. These results are consistent with an activation of glycolysis, particularly at phosphofructokinase and of a reduction in pentose phosphate pathway activity, particularly at 6-phosphogluconate dehydrogenase. The calculated cytosolic NAD+/NADH ratio for the perfused liver was similar to that measured in vivo and evidence is presented to suggest that the dihydroxyacetone phosphate/glycerol 3-phosphate ratio gives a better indication of cytosolic redox than the lactate/pyruvate ratio. The present observations indicate that phosphofructokinase hexokinase and possibly pyruvate kinase control the glycolytic rate and that glyceraldehyde-3-phosphate dehydrogenase is at equilibrium in the perfused liver of the fetal guinea pig.
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PMID:Some effects of glucose concentration and anoxia on glycolysis and metabolite concentrations in the perfused liver of fetal guinea pig. 2 74

Anoxia has been compared with ischaemia. The abrupt restoration of either oxygen of flow may accelerate cardiac damage. Anoxic stimulation of glycolysis (Pasteur effect) is inhibited during ischaemia by lactate and proton accumulation at the levels of phosphofructokinase and glyceraldehyde-3-phosphate dehydrogenase. Anaerobic glycolysis provides lactate and ATP; breakdown of the latter provides protons. During partial respiration thought to occur in partial ischaemia, continued production of CO2 is a factor contributing to intracellular acidosis; mitochondrial ATP when formed by continued respiration also yields protons when ultimately broken down. The endoproducts of aerobic glycolysis (pyruvate and NADH) are transported into the mitochondria by the malate-aspartate cycle and by pyruvate dehydrogenase activity. Adenine nucleotide transferase activity normally transfers the mitochondrially-made ATP to the cytoplasm, but acyl CoA accumulates in ischaemia (or during perfusions with high circulating free fatty acids) to inhibit the transferase. The mitochondrial creatine kinase is thought to transform ATP transported outwards into creatine phosphate which can permeate the outer mitochondrial membrane. Further compartmentation of ATP may be by other creatine kinase isoenzymes or in relation to the cell membrane. The glycogenolytic-sarcoplasmic reticulum complex links a glycogen pool to the sarcoplasmic reticulum. Cyclic AMP may regulate admission of calcium to the cell during the plateau of the action potential and promote calcium uptake by the sarcoplasmic reticulum by phosphorylation of phospholamban. The latter promotes the activity of the calcium-transport ATPase. Calcium and cyclic AMP may also interact at the level of the contractile proteins where cyclic AMP phosphrylates troponin. Cyclic GMP generally has opposite effects to cyclic AMP and undergoes opposite changes in the frog cardiac cycle to those of cyclic AMP. A present it is reasonable to suppose that physiological effects of adrenaline or of cholinergic agents on the myocardium are mediated by cyclic AMP or cyclic GMP, respectively, but this hypothesis still lacks firm support. There is an association between tissue cyclic AMP and ventricular fibrillation after coronary ligation, and direct evidence for a role of cyclic AMP in promoting arrhythmias has been obtained by studies on the ventricular fibrillation threshold in the rat heart. However, there are other mechanisms, involving first the effects of substrates on the action potential duration, and secondly, the fast channel, which can also give rise to the development of malignant arrhythmias.
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PMID:Myocardial metabolism and heart disease. 3 41

Although basal release of cyclic AMP from isolated perfused rat hearts was not measurable, isoprenaline induced substantial release of the nucleotide, suggesting that in vivo the myocardium can contribute to plasma cyclic AMP. Anoxia also increased the amount of cyclic AMP released, but insulin and nicotinate alone or in combination had no effect.
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PMID:The release of adenosine 3':5'-cyclic monophosphate from the isolated perfused rat heart. 17 4

We studied the relationships between the positive inotropic effects of isoproterenol, increased frequency of contraction or paired electrical stimulation, and cyclic AMP concentration and phosphorylase activity in isolated guinea pig papillary muscles. The minimum concentration of isoproterenol (10 nM) that augmented isometric force development increased cyclic AMP concentration. However 100 nM isoproterenol was required to increase the phosphorylase activity ratio (-AMP/+AMP) from 0.15 +/- 0.03 to 0.25 +/- 0.03. After addition of 1 muM isoproterenol to the bath, cyclic AMP increased within 0.5 minute from 0.58 +/- 0.03 to 1.04 +/- 0.13 mol/kg (wet weight), peak contractile force was elevated 2-fold at 1 minute, and the phosphorylase activity ratio rose to 0.40 +/- 0.02 in 4 minutes. Although an increase in contraction frequency (6/min to 36/ min) and paired stimulation produced more than a 3-fold increase in peak contractile force, there were no changes in cyclic AMP and phosphorylase activity. The cyclic AMP concentration during diastole was 0.60 +/- 0.04 and in midsystole, 0.55 +/- 0.03 mumol/kg. Anoxia increased the phosphorylase activity ratio from 0.19 +/-0.02 to 0.41 +/- 0.04 without elevation of cyclic AMP concentration. Removal of Ca2+ from the bathing medium prevented active force development and the anoxic increase in phosphorylase activity, but did not prevent the isoproterenol-induced increase in cyclic AMP and phosphorylase. These results suggest that cyclic AMP is a factor in the catecholamine-induced enhancement of inotropic state. However, it does not appear to play a role in the maintained augmentation of inotropic state produced by increased contraction frequency and paired stimulation, nor does the concentration of the cycle nucleotide appear to vary during the contraction cycle or during anoxia. Extracellular Ca2+ is required for contraction, the positive inotropic aciton of catecholamines and phosphorylase b to a conversion by anoxia.
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PMID:The role of cyclic adenosine 3', 5'-monophosphate and calcium in the regulation of contractility and glycogen phosphorylase activity in guinea pig papillary muscle. 18 12

Renal cortex slices from newborn, 2-week, and 4-week-old Sprague-Dawley rats had reduced initial rates of taurine uptake compared to adult slices after short (less than 30 min) incubation periods. From birth onward, steady-state accumulation occurred by at least two sodium-dependent uptake systems. The first system had an "apparent Km1" = 0.1 mM and a Vmax varying from 1.8 to 5.1 mumoles/ml ICF/120 min at four ages. The second uptake mode had an apparent Km2 = 12-16 mM and a Vmax of 45 mumoles/ml ICF/120 min. Efflux of taurine was reduced in slices from younger animals possibly accounting for taurinuria. Only other beta-amino acids inhibited accumulation. Anoxia inhibited uptake at high concentration ( greater than 1.0 mM) at each age, but taurine accumulation at low concentrations ( less than 0.4 mM) was relatively protected from anoxia in neonatal ( less than 36 hr of age) tissue. Preincubation in taurine-free medium for 120 min enhanced low concentration, but not high concentration uptake in neonatal and 2-week slices. After preincubation in dibutyryl cyclic AMP (dbcAMP) enhanced uptake of taurine was found in adult cortex, but not in neonatal cortex. The ontogeny of renal taurine transport in cortex slices appeared to involve faster initial uptake rates and faster efflux as well as greater dependence on aerobic metabolism with maturation. Age-related differences in the response to preincubation and cyclic nucleotides were also indicative of maturation events in renal tubular amino acid transport.
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PMID:Development aspects of renal beta-amino acid transport II. Ontogeny of uptake and efflux processes and effect of anoxia. 22 17

The effect of severe anoxia produced by gassing with 100% nitrogen on gastric mucosal permeability and hydrogen ion back diffusion was investigated using an in vitro preparation of rabbit fundic gastric mucosa mounted in an Ussing chamber. Permeability was estimated by determination of the flux of the water soluble, nonlipidsoluble molecule erythritol from the mucosal to serosal solution. The flux rate across normal tissue was 2.80 plus or minus 0.41 pmoles/cm-2/sec, and rose to 3.32 plus or minus 0.57 pmoles/cm-2/sec after 2 hr of severe anoxia. Hydrogen ion ack diffusion was measured by determining with a pH stat the amount of hydrogen required to maintain the [H+] of the mucosal solution at 0.1, 1.0, 2.0 and 3.2 mEq/L in both normal and anoxic tissues. One hour of anoxia increased the back diffusion of H+, but the changes only became statistically significant at all pH values after 1.5 hr. Anoxia did however cause an immediate fall in potential difference to zero, and a rise in resistance which after 30 min fell progressively to preanoxic levels. Anoxia produces a small increase in gastric mucosal, permeability, an effect which may be enhanced by other factors.
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PMID:Effect of severe anoxia on the permeability of gastric mucosa (38517). 23 69

A detailed analysis of the lipid content of guinea-pig lung following anaphylaxis in vivo induced by aerosolized antigen showed a significant reduction in all fractions. Anoxia induced by nitrogen produced reductions in the partial glycerides and ethanolamine phospholipid. Exposure to an aerosol of histamine caused a reduction in all but the choline phospholipid and sphingolipid fractions. It was concluded that the losses of choline phospholipid and sphingolipid result from the anaphylactic reaction and not from subsequent changes.
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PMID:Investigation of changes in the lipid content of guinea-pig lung after anaphylaxis. 23 17

Myocardial levels of ammonia, glutamate, and glutamine and the release of glutamate and glutamine were studied in the isolated perfused rat heart during perfusion with ammonium chloride, epinephrine, and conditions of anoxia or ischaemia. Perfusion for 15 min with effective ammonium chloride concentrations of 0.53, 0.71, and 2.06 mmol/l resulted in glutamine production of 1.34, 0.95, and 4.41 mmol with 15 min-1/200 dry weight compatible with the presence of glutamine synthetase in rat myocardium. Myocardial ammonium content was unchanged by perfusion with 0.53 and 0.71 mmol/l ammonium chloride, but was increased by 1.36 mumol with 15 min-1/200 mg dry weight by perfusion with 2.06 mmol/l ammonium chloride. Increased myocardial contents of ammonia and glutamine were not accompanied by depression of left ventricular pressure. Perfusion with epinephrine (0.20 mug/ml) resulted in an increased myocardial content of glutamine. Anoxia or ischaemia resulted in no changes in ammonia content, and no changes in glutamine or glutamate production. The net release of glutamine into the perfusate was about 10 times the net release of glutamate.
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PMID:Glutamine production by the isolated perfused rat heart during ammonium chloride perfusion. 24 May 5

The authors present four new born with severe anoxemia after congenital diaphragmatic hernia repair. In three babies' hypoxemia was present from birth. Cardiac catheterization revealed pulmonary hypertension, resulting in a state of fetal circulation. Tolazoline produced an improvement in oxygenation, but became secondary ineffective. In one case ductus arteriosus was occluded during cardiac catheterization, after which immediate improvement in peripheral oxygenation was seen. Ligation of the patient ductus arteriosus was proposed in that case. In the fourth infant, hypoxemia developed secondary and was successfully treated with tolazoline. It is suggested that ligation of the patient ductus arteriosus and administration of pulmonary vasodilatators are both effective in improving oxygenation, in patients who may die an anoxic death after repair of a severe congenital diaphragmatic hernia.
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PMID:[Pulmonary hypertension and fetal circulation after severe congenital diaphragmatic hernia (author's transl)]. 43 90

Groups of 4 Wistar rat littermates of matched sex and weight received the following daily treatment between the ages of 2 and 11 days: handling (untreated controls, UC), succinylcholine paralysis and ventilation with 100% O2 (respirator control, RC), electroconvulsive seizures (ECS) and ECS while paralyzed and ventilated with O2 (respirator seizures, RS). Analysis of heart blood O2 content showed that mechanical ventilation with 100% O2 effectively prevented the anoxemia observed during convulsive seizures. In the ECS and RS groups, several behavioral milestones (e.g. swimming) matured later than they did in either control group (UC, RC). No difference was observed between the two groups of seizure-treated rats. At the age of 30 days, both ECS and RS groups had smaller brains with a reduced DNA, RNA, protein and cholesterol content in both forebrain and hindbrain, suggesting that seizures curtailed the number of brain cells. The lack of any difference between the two seizure groups suggests that at least part of the adverse effects of experimental neonatal seizures on brain and behaviour are independent of anoxemia.
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PMID:Does anoxemia play a role in the effects of neonatal seizures on brain growth? An experimental study in the rat. 48 39


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