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Journal of Cardiovascular... Dec 2006The spatio-temporal pattern of arrhythmias in the embryonic/fetal heart subjected to a transient hypoxic or hypothermic stress remains to be established.
INTRODUCTION
The spatio-temporal pattern of arrhythmias in the embryonic/fetal heart subjected to a transient hypoxic or hypothermic stress remains to be established.
METHODS AND RESULTS
Spontaneously beating hearts or isolated atria, ventricles, and conotruncus from 4-day-old chick embryos were subjected in vitro to 30-minute anoxia and 60-minute reoxygenation. Hearts were also submitted to 30-minute hypothermia (0-4 degrees C) and 60-minute rewarming. ECG disturbances and alterations of atrial and ventricular electromechanical delay (EMD) were systematically investigated. Baseline functional parameters were stable during at least 2 hours. Anoxia induced tachycardia, followed by bradycardia, atrial ectopy, first-, second-, and third-degree atrio-ventricular blocks and, finally, transient electromechanical arrest after 6.8 minutes, interquartile ranges (IQR) 3.1-16.2 (n = 8). Reoxygenation triggered also Wenckebach phenomenon and ventricular escape beats. At the onset of reoxygenation QT, PR, and ventricular EMD increased by 68%, 70%, and 250%, respectively, whereas atrial EMD was not altered. No fibrillations, no ventricular ectopic beats, and no electromechanical dissociation were observed. Arrhythmic activity of the isolated atria persisted throughout anoxia and upon reoxygenation, whereas activity of the isolated ventricles abruptly ceased after 5 minutes of anoxia and resumed after 5 minutes of reoxygenation. During hypothermia-rewarming, cardiac activity stopped at 17.9 degrees C, IQR 16.2-20.6 (n = 4) and resumed at the same temperature with no arrhythmias. All preparations fully recovered after 40 minutes of reoxygenation or rewarming.
CONCLUSION
In the embryonic heart, arrhythmias mainly originated in the sinoatrial tissue and resembled those observed in the adult heart. Furthermore, oxygen readmission was by far more arrhythmogenic than rewarming and the chronotropic, dromotropic, and inotropic effects were fully reversible.
Topics: Animals; Arrhythmias, Cardiac; Chick Embryo; Chickens; Disease Models, Animal; Heart; Heart Conduction System; Hypothermia; Hypoxia; In Vitro Techniques; Oxygen; Rewarming
PubMed: 17014683
DOI: 10.1111/j.1540-8167.2006.00637.x -
Journal of Neurochemistry Oct 2005Anoxia in the first week of life can induce neuronal death in vulnerable brain regions usually associated with an impairment of cognitive function that can be detected...
Anoxia in the first week of life can induce neuronal death in vulnerable brain regions usually associated with an impairment of cognitive function that can be detected later in life. We set-up a model of subneurotoxic anoxia based on repeated exposures to 100% nitrogen during the first 7 days of post-natal life. This mild post-natal exposure to anoxia specifically modified the behaviour of the male adult rats, which showed an attention deficit and an increase in anxiety, without any impairment in spatial learning and any detectable brain damage (magnetic resonance imaging and histological analysis). Post-anoxic rats showed a reduction in the expression of group-I metabotropic glutamate receptors (i.e. mGlu1 and mGlu5 receptors) in the hippocampus and cerebral cortex, whereas expression of the mGlu 2/3 receptors, the NR1 subunit of NMDA receptors, and the GluR1 subunit of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors was unchanged. mGlu1 and mGlu5 receptor signalling was also impaired in postanoxic rats, as revealed by a reduced efficacy of the agonist (1S,3R)-1-Aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) to stimulate polyphosphoinositide hydrolysis in hippocampal slices. We conclude that rats subjected to subneurotoxic doses of anoxia during the early post-natal life develop behavioural symptoms that are frequently encountered in the inattentive subtype of the attention deficit hyperactivity disorder, and that group-I mGlu receptors may be involved in the pathophysiology of these symptoms.
Topics: Animals; Animals, Newborn; Behavior, Animal; Brain; Hippocampus; Hydrolysis; Hypoxia; Male; Phosphatidylinositols; Rats; Rats, Wistar; Receptors, Metabotropic Glutamate; Severity of Illness Index
PubMed: 16181418
DOI: 10.1111/j.1471-4159.2005.03349.x -
Acta Psychiatrica Et Neurologica... 1956
Topics: Hypoxia; Hypoxia, Brain
PubMed: 13354415
DOI: No ID Found -
Acta Psychiatrica Et Neurologica... 1956
Topics: Humans; Hypoxia; Hypoxia, Brain
PubMed: 13354414
DOI: No ID Found -
The American Journal of Physiology Jul 1993Hepatocytes from the western painted turtle (Chrysemys picta bellii) display a profound metabolic suppression under anoxia. Fractional rates of protein synthesis fell by...
Hepatocytes from the western painted turtle (Chrysemys picta bellii) display a profound metabolic suppression under anoxia. Fractional rates of protein synthesis fell by 92% during 12 h anoxia at 25 degrees C and were indistinguishable from the rate obtained with cycloheximide. Normoxic recovery saw protein synthesis increase to 160% of control values and return to normal after 2 h. The GTP-to-GDP ratio, implicated in the control of translation, fell threefold during anoxia. Purine nucleotide phosphate profiles suggest that this change occurs through increasing concentrations of ADP and GDP, with concentrations of ATP and GTP and total purines remaining constant. The normoxic cost for protein synthesis was calculated at 47.6 +/- 6.8 mmol ATP/g protein. Normoxic protein synthesis accounted for 36% of overall ATP turnover rates, close to the extent of O2 consumption inhibitable by cycloheximide (28%). Under anoxia, the proportion of ATP turnover utilized by protein synthesis did not change significantly. ATP turnover rates for urea synthesis reflected a similar pattern, falling 72% under anoxia. These results reflect the cell's ability to suppress protein synthesis under anoxia in a manner that is coordinated with the reduction in total metabolic rate.
Topics: Adaptation, Physiological; Adenosine Triphosphate; Animals; Female; Hypoxia; Liver; Oxygen Consumption; Phosphates; Protein Biosynthesis; Purine Nucleotides; Turtles; Urea
PubMed: 8342698
DOI: 10.1152/ajpregu.1993.265.1.R41 -
Canadian Medical Association Journal May 1961
Topics: Brain; Humans; Hypoxia; Hypoxia, Brain
PubMed: 13758570
DOI: No ID Found -
The American Journal of Physiology Aug 1959
Topics: Heart; Humans; Hypoxia; Myocardium
PubMed: 13815443
DOI: 10.1152/ajplegacy.1959.197.2.449 -
Biochimica Et Biophysica Acta Oct 2014ChREBP (carbohydrate response element binding protein) is a glucose-responsive transcription factor that is known to be an important regulator of glycolytic and...
BACKGROUND
ChREBP (carbohydrate response element binding protein) is a glucose-responsive transcription factor that is known to be an important regulator of glycolytic and lipogenic genes in response to glucose. We hypothesized that activation of ChREBP could be relevant to anoxia survival by the anoxia-tolerant turtle, Trachemys scripta elegans.
METHODS
Expression of ChREBP in response to 5 and 20h of anoxia was examined using RT-PCR and Western immunoblotting. In addition, subcellular localization and DNA-binding activity of ChREBP protein were assessed and transcript levels of liver pyruvate kinase (LPK), a downstream gene under ChREBP control were quantified using RT-PCR.
RESULTS
ChREBP was anoxia-responsive in kidney and liver, with transcript levels increasing by 1.2-1.8 fold in response to anoxia and protein levels increasing by 1.8-1.9 fold. Enhanced nuclear presence under anoxia was also observed in both tissues by 2.2-2.8 fold. A 4.2 fold increase in DNA binding activity of ChREBP was also observed in liver in response to 5h of anoxia. In addition, transcript levels of LPK increased by 2.1 fold in response to 5h of anoxia in the liver.
CONCLUSIONS
The results suggest that activation of ChREBP in response to anoxia might be a crucial factor for anoxia survival in turtle liver by contributing to elevated glycolytic flux in the initial phases of oxygen limitation.
GENERAL SIGNIFICANCE
This study provides the first demonstration of activation of ChREBP in response to anoxia in a natural model of anoxia tolerance, further improving our understanding of the molecular nature of anoxia tolerance.
Topics: Animals; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; Gene Expression Regulation, Developmental; Hypoxia; Liver; Pyruvate Kinase; Time Factors; Turtles
PubMed: 24931694
DOI: 10.1016/j.bbagen.2014.06.001 -
Journal of the Royal Society of Medicine Aug 1991The investigation of commercial diving accidents has indicated that the danger of anoxia, from the inhalation of gases not containing oxygen, is not fully recognized.... (Review)
Review
The investigation of commercial diving accidents has indicated that the danger of anoxia, from the inhalation of gases not containing oxygen, is not fully recognized. The problem is more common in a variety of general industrial situations and is an occasional cause of death in anaesthesia. It is a particular hazard with inert gases, which, because they are recognized to be non-toxic, give a false sense of security. The pathological findings consist of pulmonary oedema and petechial haemorrhages, mainly in the brain, lungs and myocardium. Whenever possible, a minimum oxygen content should be included in all gases liable to be respired, but where this is not possible, oxygen analysers and alarms should be provided. Where a general hazard exists, personnel must be warned of the danger.
Topics: Acute Disease; Anesthesia, General; Asphyxia; Brain; Diving; Humans; Hypoxia; Metallurgy; Occupational Diseases
PubMed: 1886120
DOI: 10.1177/014107689108400815 -
The American Journal of Physiology Sep 1993The garter snake Thamnophis sirtalis parietalis can readily tolerate several hours of freezing or anoxia exposure. Both stresses halt oxygen availability to tissues and...
The garter snake Thamnophis sirtalis parietalis can readily tolerate several hours of freezing or anoxia exposure. Both stresses halt oxygen availability to tissues and to endure these stresses snakes must cope with potential oxidative stress arising as a result of the ischemic/anoxic condition followed by reperfusion of aerated blood during recovery. To determine whether antioxidant defenses are important for freezing and anoxia survival, we monitored the activities of antioxidant enzymes and the levels of glutathione (GSH and GSSG) during freezing (5 h at -2.5 degrees C) and anoxia (10 h under N2 gas at 5 degrees C) exposures in three organs (muscle, liver, and lung) of snakes. Freezing resulted in a significant rise in the activity of muscle and lung catalase (by 183 and 63%) and in muscle glutathione peroxidase (52%). Anoxia enhanced muscle and liver superoxide dismutase activities (by 59 and 118%) and also caused a 57% increase in muscle GSH levels. The increase in muscle GSH concentration in anoxia (from 0.45 to 0.71 mM) could also stimulate muscle glutathione peroxidase activity in vivo by 1.5-fold because of its low affinity for GSH (Km = 11 mM). The ratio of GSSG/GSH was not affected by experimental state in any tissue, suggesting that oxidative stress did not occur during the freezing or anoxic exposure. Rather, H2O2- and O2(-)-detoxification systems may be activated in preparation for possible oxygen free radical overgeneration during thawing or reoxygenation. Antioxidant defenses appear to be part of the adaptive machinery for reptilian tolerance of freezing and anoxia.
Topics: Adaptation, Physiological; Animals; Enzymes; Freezing; Glutathione; Hypoxia; Liver; Lung; Muscles; Oxygen; Snakes; Tissue Distribution
PubMed: 8214160
DOI: 10.1152/ajpregu.1993.265.3.R646