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At least 19 recordsLinked to original sources
PubMed2026

Anoxia tolerant DNA replication is supported by ATR kinase in the annual killifish Austrofundulus limnaeus.

Hypoxia and anoxia suppress cell proliferation due to an increase in replication stress and activation of DNA damage checkpoints. Embryos of the annual killifish Austrofundulus limnaeus tolerate prolonged anoxia, indicating improved genomic stability under oxygen starvation. We investigated the cell cycle regulation of the anoxia tolerant killifish embryonic cell line PSU-AL-WS40NE during anoxia. Live-cell imaging confirms continued proliferation of WS40NE cells for the first 24 h of anoxia with minimal cell death. Fluorescence imaging shows that cells accumulate in G1 after the first day in anoxia with a rapid entry into S phase upon reoxygenation. Pharmacological inhibition shows a reliance on ataxia telangiectasia and Rad3 related (ATR) signaling, suggesting that increased γH2AX levels are driven by replication stress instead of DNA damage. This conclusion is supported by a lack of induction of a G2 checkpoint, suggesting minimal DNA damage during anoxic exposure. Maintaining cellular proliferation during anoxia and accumulating cells in the G1 phase for extended anoxic exposure is likely one way that embryos of the killifish can survive prolonged anoxia, which provides insight into mechanisms that enable cells to proliferate under metabolic stress.

Animals↗
PubMed1979

Protein synthesis in rat brain in hypoxia, anoxia and hypoglycemia.

The effect of cerebral hypoxia on protein synthesis was investigated by exposing rats to 5% O2, and examining polypeptide synthesis and size distribution profiles of ribosomes. The findings were compared with the results from cerebral anoxia (decapitation) and hypoglycemia. In cerebral hypoxia there was suppression of polypeptide synthesis, though to a lesser extent than in cerebral anoxia, while no effect was detected in hypoglycemia. Among 4 different ribosomal fractions used for polypeptide synthesis, the microsome was the most sensitive for hypoxia and anoxia, and the polyribosome after short centrifugation was the least sensitive. The size distribution profiles of 3 different ribosomes revealed an increase in the size of the monomere-dimer complex and a decrease of the polysome peak both in cerebral hypoxia and anoxia. Comparison of the energy state and the extent of lactic acidosis in cerebral hypoxia, anoxia and hypoglycemia available in the literature and the functional and structural state of polyribosomes in the present investigation suggests that intracellular acidosis may be the main cause of the suppression of polypeptide synthesis and disaggregation of polyribosomes in hypoxia, and the depletion of energy reserve may be the main cause in anoxia-ischemia.

Animals↗
PubMed1978

Myocardial reactive hyperemia caused by initial myocardial anoxia during aortic valve replacement.

Reactive hyperemic response of individual coronary arteries and of the whole heart to anoxia during coronary cannulation was investigated in 10 patients undergoing aortic valve replacement. Reactive hyperemic response in man is identical to that reported in experimental investigations. The duration of hyperemic response was dependent on the length of the preceding period of anoxia; the longer the period of anoxia, the more prolonged was the hyperemic response. No significant collateral circulation between the coronary arteries could be demonstrated during prolonged anoxia of an individual coronary artery. Blood flow debt was almost always overpaid, but the repayment percentage decreased with the lengthening of the anoxic period, being 460 percent after a short period of anoxia (less than or equal to 2 minutes), 230 percent after an anoxic period of moderate length (3 to 5 minutes), and only 160 percent after a long period of anoxia (greater than or equal to 7 minutes). The total mean repayment of blood flow debt of the whole heart was 195 percent.

Adult↗
PubMed2025

Global maintenance of histone post-translational modifications during the transition into anoxia in embryos of the annual killifish Austrofundulus limnaeus.

Many organisms have adapted to survive anoxic or hypoxic environments, but the epigenetic responses involved in this successful stress response are not well described in most species. Embryos of the annual killifish Austrofundulus limnaeus have the greatest tolerance to anoxia of all vertebrates, making them a powerful model to study the cellular mechanisms necessary for anoxia tolerance. However, the global histone landscape of this species has never been quantified or explored in relation to stress tolerance. Liquid chromatography-mass spectrometry and a Python bioinformatics workflow were used to identify histones and their post-translational modifications. This pipeline resulted in the detection of 252 unique biologically relevant histone post-translational modifications (hPTMs) (unimod + residue). These PTMs represent 16 types of biologically relevant hPTMs present during both anoxia and normoxia in Wourms' stage 36 embryos. This hPTM library presents an exciting opportunity to study histone modifications across development and in response to environmental stressors. No significant changes in PTM or histone abundance were observed between anoxic and normoxic embryos, suggesting that 24 h of anoxia is not sufficient to induce epigenetic or histone isoform changes at the organismal level. This result is inconsistent with data presented for similar stresses in mammalian cells and thus stabilization of the hPTM landscape may be an adaptation that supports anoxia tolerance.

anoxia↗
PubMed1977

Effect of anoxia, 2,4-dinitrophenol and salicylate on xylose transport by isolated rat soleus muscle.

1. These studies examined the theory that ATP served to regulate muscle sugar transport by a feedback mechanism. Xylose uptake by isolated rat soleus muscle was determined over a 5-min period following preincubation at 37 degrees C for various times in the presence of insulin (0.1 unit/ml), 2,4-dinitrophenol (0.5 or 0.05 mM) or salicylate (5 mM) or under anaerobic conditions. 2. Xylose uptake, measured in freshly isolated soleus muscles, was approximately 3.5--4.0 mumol/g per h. When the muscles were preincubated at 37 degrees C, this rate fell by 50% during the first 30 min and then slowly increased. 3. The stimulatory effect of insulin was evident within 2 min in freshly isolated soleus muscle and increased on preincubation, reaching a maximum value (approx. 14 mumol/g per h) after 20 min. 4. There was a 10-min lag period before xylose uptake was stimulated by anoxia. This lag period was approximately doubled when the incubation temperature was lowered from 37 degrees C. The stimulatory effect of anoxia was promptly reversed when muscles were transferred from anaerobic to aerobic conditions. 5. There was a 5-min lag period before xylose uptake was stimulated by 2,4-dinitrophenol (0.05 mM) or by sodium salicylate (mM). At a concentration of 0.5 mM, 2,4-dinitrophenol stimulated xylose uptake in freshly isolated muscle. Whereas the stimulatory effects of insulin, anoxia and salicylate all tended to plateau with time, the effect of 2,4-dinitrophenol tended to peak and then decline. 6. There was no obvious relationship between total muscle ATP levels and xylose uptake. The stimulatory effect of anoxia, 2,4-dinitrophenol or salicylate on xylose uptake was not preceded by the fall in muscle ATP. Similarly, ATP levels did not change when xylose uptake was stimulated by anoxia at 27 degrees C, or when xylose uptake was restored to basal values by transferring muscles from anaerobic to aerobic conditions. 7. It was argued that the presence of the myofibrils could act as a permeability barrier, which would limit the access of ATP produced within the interior of the cell to a regulatory site on, or close to, the sarcolemma. On the other hand, it is conceivable that the ATP produced on the periphery of the fibre by the subsarcolemmal mitochondria could play a more specific role in the feedback regulation of sugar transport. 8. Insulin stimulated xylose uptake in the presence of 2,4-dinitrophenol (0.5 mM) when this was measured in freshly isolated muscle, but not after a period of preincubation. This suggested that there may be some ATP-dependent process involved in the stimulatory effect of insulin.

Adenosine Triphosphate↗
PubMed1979

Visualization of the distance between perfusion and anoxia along an ischemic border.

The distance between perfusion and anoxia was measured on the border of an experimental ischemic area in the rabbit heart. Reduced nicotinamide adenine dinucleotide (NADH) fluorescence photography was used to detect myocardial anoxia. Fluorescein angiography marked areas of myocardial perfusion. The hearts were isolated, perfused with a hemoglobin-free solution and performed no external work. In all hearts there was a narrow band between areas of perfusion and anoxia that measured 329 +/- 42 mu (mean +/- SD). The transition from minimal to full NADH fluorescence was abrupt, less than 80 mu. We conclude that the normoxic/anoxic transition is sharp, and the gap between perfusion and anoxia is narrow along an ischemic border in the isolated heart performing no external work. These data suggest that in the vivo working heart the gap between perfusion and anoxia would be even narrower.

Animals↗
PubMed1975

Effect of severe anoxia on the permeability of gastric mucosa (38517).

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.

Animals↗
PubMed1978

[Influence of age on the modifications of cerebral electrogenesis in the curarized rat induced by acute and repeated asphyxic anoxia].

In curarized rats, acute and iterative asphyxic anoxia produced large modifications of the cerebral electrogenesis, whose intensity could be evaluated, during each anoxia, by measurements of three parameters : the resistance to anoxia, the post-asphyxic recuperation and the cerebral electric silence. Comparative trials, carried out on animals of the same stock, showed that the cerebral sensibility towards anoxia was very different according to their age : maximal sensibility in 2 or 28 months old rats, minimal sensibility between 8 to 15 months. These results are discussed in terms of choice of animal material and specially of the age of rats used for study of the cerebral anoxia, as well as for the study of cerebral anti- hypoxic drugs.

Aging↗
PubMed1979

Effects of anoxia and depolarization on the movement of carbon atoms derived from glucose into macromolecular fractions in rat brain slices.

Incorporation of U-14C-glucose into macromolecules (lipid, protein and nucleic acid fractions) of rat brain cortex slices was studied in vitro under conditions of anoxia and reoxygenation. Additionally, the influence of depolarization on control and postanoxic U-14C-glucose metabolism was investigated. Postassium-induced depolarization of the slices lowered their capacity to incorporate 14 from U-14C glucose into proteins and nucleic acids without any changes in the labeling the lipids. Fifteen and 30 minutes of anoxia depressed the rate of 14C incorporation into each of the above macromolecules was partly restored compared to the control. Excess of potassium in the medium during the reoxygenation period inhibited restoration of the synthetic capacity of the slices execpt lipids, into which incorporation of 14C was even stimulated under depolarizing conditions. The influence of anoxia and depolarization were investigated also in different classes of lipids and proteins. 14C incorporation into SDS-extractable and residual proteins and phospholipid fraction containing phosphoinositol was closest to the control during reoxygenation which suggests the relatively highest resistance of these fractions of anoxia.

Acetates↗
PubMed1978

Neuronal-vascular relationship in experimental ischaemic anoxia.

The concept of temporal and spatial relationship between neuronal and vascular changes in the central nervous system following different kinds of anoxia still remains debatable, in that it is uncertain if anoxia-ischaemia primarily produces vascular changes in the brain or it initially damages the cerebral neurons. The present investigation has been undertaken to denote the sequential relationship between neuronal and vascular changes following experimental cerebral ischaemic anoxia. Adult healthy albino rats were subjected to ischaemic anoxia by bilateral clamping of their common carotid arteries for varying intervals of 5, 10 and 15 min. The animals of each group were subsequently sacrificed on days 1, 3, 5, 7 and 10 after the clamping procedure, for light-microscopic study of their brains. Our findings are characterized by initial vascular changes, which appear to have resulted in 'no-reflow' leading subsequently to neuronal damage. The latter, in turn, secondarily caused damage to the microvasculature.

Animals↗
PubMedDate not supplied

Some observations on negative endocochlear potential during anoxia.

The effects of anoxia on the endocochlear potential (EP) and +K and +Na concentrations in the endolymph were studied in three groups of guinea pigs: kanamycin-treated guinea pigs, waltzing guinea pigs and normal guinea pigs. The magnitude of the EP in kanamycin-treated guinea pigs and waltzing guinea pigs did not show marked deviation from that observed in normal animals. The +K and +Na concentrations in the endolymph in those animals with severe suppression of sound-evoked cochlear potentials were also within the normal range. The changes in +K and +Na concentrations in the endolymph in anoxic condition were similar in the three groups of animals. However, the rate of decline of the EP was slower in kanamycin-treated guinea pigs and old waltzing guinea pigs. In young waltzing guinea pigs showing moderate suppression on the cochlear microphonics, the decline of the EP during anoxia was comparable to that observed in normal guinea pigs. The results indicate that anoxia decreases +K and increases +Na concentrations in the endolymph in a similar fashion in kanamycin-treated guinea pigs, waltzing guinea pigs and normal guinea pigs. It is suggested that the decline of the EP during anoxia is correlated with the +K conductance of the organ of Corti.

Action Potentials↗
PubMed1979

Cerebral anoxia: effect of deep hypothermia and pH.

Deep hypothermic circulatory arrest facilitates repair of congenital cardiac anomalies in infants. It is known empirically that hypothermia protects against central nervous system (CNS) ischemic damage. The Q10O2 is only 2.2 for brain and thus a decrease in metabolic rate does not fully account for protective effects of hypothermia. Since enthalpy of dissociation of H2O is high (approximately 7 kcal/mole), its pH is temperature dependent (7.0 at 25 degrees C, 7.4 at 20 degrees C) and hypothermia may in part protect by its influence on hydrogen ion concentration. A manifestation of CNS susceptibility to ischemia is an obstruction of the microcirculation [no-reflow lesion (NRL)] demonstrated by infusion of carbon black into the cerebral circulation after a period of circulatory arrest. White lesions (NRL) against a gray background on cut section of brain increase in size with increasing time of arrest. The effect of anoxia versus circulatory arrest, brain temperature, and extracellular brain pH on NRL was studied in 45 mongrel dogs, subjected to varying periods of N2-induced anoxia on cardiopulmonary bypass (CPB) at 37 degrees C or 20 degrees C. In some studies jugular venous pH was adjusted by infusion of NaHCO3 or HCl. Control groups included normothermic CPB without anoxic and normothermic CPB, anoxia, and equimolar NaCl infusion. NRL was quantified by planimetry of photographs of cut sections of brain. These results confirm that NRL is abated by hypothermia and suggest that (1) NRL is a function of anoxia and not arrested circulation since perfusion with N2 at 37 degrees C does not protect the brain (i.e., NRL is not solely related to "critical reopening pressure") and (2) NRL is in part a function of extracellular pH.

Animals↗
PubMed1978

Protective effect of a novel imidazole derivative against cerebral anoxia.

The protective effect of 1-[2-(2-chlorobenzoyl)-4-nitrophenyl]-2-(diethylaminomethyl) imidazole fumarate (Y-9179) against cerebral anoxia was investigated with a variety of experimental models in mice and rats. Y-9179, at doses lower than 1 mg/kg, showed a consistent protective action against the cerebral anoxia in all of the models studied: hypoxia, ischemia, histotoxic and asphyxic anoxia. The antianoxic activity of Y-9179 was found to be about 100 times greater than that of pentobarbital. This anti-anoxic effect was observed at very small doses at which neither sedation nor motor depression was induced. There was no decrease in the protective effect or no adverse effect even at as high a dose as 30 mg/kg, which corresponded to about 150 times the effective dose. The universal anti-anoxic properties of Y-9179 may be useful both clinically and as a pharmacological tool to elucidate the physiological significance of cerebral anoxia.

Animals↗
PubMedDate not supplied

Disturbances of extracellular pK, pNa and pH during no-flow anoxia.

The initial period of no-flow anoxia can be divided in at least two parts. During the first period lasting approximately 1 min., the O2 available in tissue gives rise to CO2 which increases hydrogen ion activity and may lead to Na+ influx2 (presumably due to increased membrane permeability to Na+). In the second period, starting after the first minute, the increase in lactate content leads to further decrease in pH and is accompanied by extensive sodium influx and a distinct potassium efflux. However, it is striking that the isolated perfused rat liver is able to tolerate 1 hour of norm-flow anoxia without severe cellular damage, whereas two minutes of no-flow anoxia lead to a decrease in cellular ATP content by 28%.

Adenosine Triphosphate↗
PubMed1979

Intermembrane inclusions induced by anoxia in heart and skeletal muscle mitochondria.

Heart and skeletal muscle from rats of different ages were incubated in vitro in an oxygen-free medium supplied with substrates in order to investigate the effect of anoxia on muscle fine structure, particulary on the mitochondria. In skeletal muscle fibers anoxia has been found to induce changes similar to those previously described in ischemic muscles in vivo namely giant mitochondria, apparently derived by mitochondrial fusion, and intermembrane inclusions with a paracrystalline structure. The plate-like inclusions are mostly located in the intracristal spaces and are closely associated to cristal membranes even in markedly swollen mitochondria. Identical inclusions have been observed in cardiac muscle cells following anoxic injury, whereas they are never found in non-muscle cells such as endothelia, fibroblasts and nerve fibers. Cardiac and skeletal muscle fibers from newborn rats maintained in an oxygen-free medium show mitochondrial swelling but no intermembrane inclusions. The different response of mitochondria from developing vs adult striated muscle to anoxia may be due to changes during postnatal development in the quality or quantity of the protein component(s) involved in paracrystal formation.

Animals↗
PubMed1975

Cerebrospinal-fluid acid-base and electrolyte changes resulting from cerebral anoxia in man.

To study metabolic changes in the central nervous system after profound anoxia, we measured changes in cisternal and lumbar cerebrospinal fluid. Acid-base values and electrolyte concentrations were determined in cisternal and lumbar fluid from 12 severely anoxic patients (cardiac arrest), and from 15 within 24 hours after cardiac resuscitation. In the severely anoxia patients the normal cisternal-lumbar pH gradient was reversed, cisternal fluid was more acid (pH 6.815 vs. 6.953), and cisternal potassium concentration was twice that of lumbar (6.7 vs 3.5 mEq per liter). These findings indicate that during anoxia potassium and hydrogen ion flow from brain cells into the brain extracellular fluid, and that acute changes are reflected more accurately by cisternal than by lumbar fluid. In resuscitated patients cisternal fluid was normal, and normal cisternal-lumbar differences were found; thus, the normal milieu of brain cells is rapidly reestablished after resuscitation.

Adolescent↗
PubMed1979

Release of alpha hydroxybutyrate from neonatal rat heart cell cultures exposed to anoxia and reoxygenation: comparison with impairment of structure and function of damaged cardiac cells.

Spontaneously beating monolayer cultures of neonatal rat heart cells first exposed to depletion of oxygen and metabolic substrates for 1 to 7 h (anoxia). Subsequently the cultures were resupplied with oxygen and substrates (reoxygenation). The release of alpha-hydroxybutyrate dehydrogenase (HBDH) from the cells, the extent of necrosis, and the changes in spontaneous contractile activity were measured. HBDH release was observed to start after 1 h of anoxia and to increase to 84% of intracellular HBDH activity after 7 h of anoxia. Reoxygenation of anoxic heart cells is associated with accelerated HBDH release (oxygen paradox). The activity of HBDH released by cardiac cells, the number of necrotic cells and the impairment of beating capacity of the cells depend on the duration of the anoxic period in a similar way. This study demonstrates that cardiac cell death can be assessed quantitatively and reliably by the measurement of the activity of HBDH released by the cells.

Animals↗
PubMed1979

The nature of the negative endocochlear potentials produced by anoxia and ethacrynic acid in the rat and guinea-pig.

1. The alterations in the Na+ and K+ concentrations of the cochlear endolymph and in the endocochlear potential were followed simultaneously by means of ion-sensitive and conventional micro-electrodes during simple anoxia, during anoxia after i.v. ethacrynic acid and after i.v. ethacrynic acid alone. The endolymphatic pH changes were measured separately and the effect of perilymphatic ethacrynic acid upon the endocochlear potential was investigated. 2. The over-all Na+:K+ permeability ratio for the endolymph system was determined in individual animals for the first time using an indirect method. The normal mean values of 0.27 (rat) and 0.38 (guinea-pig) were increased after ethacrynic acid. Permeability changes occurred during anoxia but were delayed in onset. 3. The negative endocochlear potentials in each situation behaved quantitatively like modified K+ diffusion potentials largely dependent upon the K+ and Na+ gradients between endolymph and perilymph.

Animals↗