Anoxia and Hypoxia

Bickler, P.E. and L.T. Buck (2007). Hypoxia tolerance in reptiles, amphibians, and fishes: life with variable oxygen availability. Annual Review of Physiology 69: 145-170. ISSN: 0066-4278.
Abstract: The ability of fishes, amphibians, and reptiles to survive extremes of oxygen availability derives from a core triad of adaptations: profound metabolic suppression, tolerance of ionic and pH disturbances, and mechanisms for avoiding free-radical injury during reoxygenation. For long-term anoxic survival, enhanced storage of glycogen in critical tissues is also necessary. The diversity of body morphologies and habitats and the utilization of dormancy have resulted in a broad array of adaptations to hypoxia in lower vertebrates. For example, the most anoxia-tolerant vertebrates, painted turtles and crucian carp, meet the challenge of variable oxygen in fundamentally different ways: Turtles undergo near-suspended animation, whereas carp remain active and responsive in the absence of oxygen. Although the mechanisms of survival in both of these cases include large stores of glycogen and drastically decreased metabolism, other mechanisms, such as regulation of ion channels in excitable membranes, are apparently divergent. Common themes in the regulatory adjustments to hypoxia involve control of metabolism and ion channel conductance by protein phosphorylation. Tolerance of decreased energy charge and accumulating anaerobic end products as well as enhanced antioxidant defenses and regenerative capacities are also key to hypoxia survival in lower vertebrates.
Descriptors: amphibians, reptiles, fishes, hypoxia tolerance, variable oxygen availability, adaptations, controlof metabolism, regenerative capacities.

Bobb, V.T. and D.C. Jackson (2005). Effect of graded hypoxic and acidotic stress on contractile force of heart muscle from hypoxia-tolerant and hypoxia-intolerant turtles. Journal of Experimental Zoology. Part A, Comparative Experimental Biology 303(5): 345-353. ISSN: print: 1548-8969; online: 1552-499X.
NAL Call Number: QL1.J854
Descriptors: turtles, hypoxic, acidotic, stress, heart muscle, contractile force, hypoxia tolerant, intolerant, effect.

Crossley, D.A.I. and J. Altimiras (2005). Cardiovascular development in embryos of the American alligator Alligator mississippiensis: effects of chronic and acute hypoxia. Journal of Experimental Biology 208(1): 31-39. ISSN: 0022-0949.
Online: http://dx.doi.org/10.1242/jeb.01355
NAL Call Number: 442.8 B77
Descriptors: reptiles, Alligator mississippiensis, circulatory system, cardiovascular development, acute hypoxia, embryo cardiovascular development, effects of chronic hypoxia, American alligator, North America.

Davis, E.C. and D.C. Jackson (2007). Lactate uptake by skeletal bone in anoxic turtles, Trachemys scripta. Comparative Biochemistry and Physiology. Part A, Molecular and Integrative Physiology 146(3): 299-304. ISSN: 1095-6433.
Abstract: Previous studies have shown that freshwater turtle shells can accumulate lactate during periods of anoxic submergence. Our objective in this study was to determine lactate uptake in other parts of the turtle's skeleton. We measured lactate concentration of 7 skeletal elements and 4 shell samples of red-eared slider turtles, Trachemys scripta, in control animals (N=12) and in animals following submergence for 4-5 days in N(2)-equilibrated water at 10 degrees C (N=8). We also collected blood samples and measured blood pH, PCO(2), and PO(2), and plasma lactate. Contralateral bone samples from 6 control turtles were analyzed for % water and mineral composition; bone from the other 6 were equilibrated with lactate solution in vitro. Anoxic submergence resulted in a combined respiratory/non-respiratory (lactic) acidosis and plasma lactate of 45.6+/-2.5 mmol l(-1). Shell and skeletal lactates all increased significantly in the anoxic animals (30.1-43.9 mmol kg(-1)) with limb bones having the highest levels and skull the least. Skeletal samples equilibrated in lactate solution in vitro for 2 days accumulated lactate in similar fashion with limb bones, except for fibula, higher, and skull significantly less than other bones. We conclude that the entire skeleton of the red-eared slider, like its shell, sequesters lactate and contributes thereby to lactic acid buffering.
Descriptors: reptiles, anoxic turtles, anoxia metabolism, skeletal bone, lactic uptake, lactic acid metabolism, physiology, acidosis, shell, bone, lactic acid buffers.

Dinkelacker, S.A., J.P. Costanzo, and R.E.J. Lee (2005). Anoxia tolerance and freeze tolerance in hatchling turtles. Journal of Comparative Physiology. B, Biochemical, Systemic, and Environmental Physiology 175(3): 209-217. ISSN: print: 0174-1578; online: 1432-136X.
NAL Call Number: QP33.J681
Abstract: Freezing survival in hatchling turtles may be limited by ischemic anoxia in frozen tissues and the associated accumulation of lactate and reactive oxygen species (ROS). To determine whether mechanisms for coping with anoxia are also important in freeze tolerance, we examined the association between capacities for freezing survival and anoxia tolerance in hatchlings of seven species of turtles. Tolerance to freezing (-2.5 degrees C) was high in Emydoidea blandingii, Chrysemys picta, Terrapene ornata, and Malaclemys terrapin and low in Graptemys geographica, Chelydra serpentina, and Trachemys scripta. Hatchlings survived in a N(2) atmosphere at 4 degrees C for periods ranging from 17 d (M. terrapin) to 50 d (G. geographica), but survival time was not associated with freeze tolerance. Lactate accumulated during both stresses, but plasma levels in frozen/thawed turtles were well below those found in anoxia-exposed animals. Activity of the antioxidant enzyme catalase in liver increased markedly with anoxia exposure in most species, but increased with freezing/thawing only in species with low freeze tolerance. Our results suggest that whereas oxygen deprivation occurs during somatic freezing, freeze tolerance is not limited by anoxia tolerance in hatchling turtles.
Descriptors: turtles, acclimatization, physiology, anoxia, catalase metabolism, freezing, lactates, blood, liver anatomy, histology, enzymology, organ size, oxidative stress.

Jackson, D.C., S.E. Taylor, V.S. Asare, D. Villarnovo, J.M. Gall, and S.A. Reese (2007). Comparative shell buffering properties correlate with anoxia tolerance in freshwater turtles. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology 292(2): R1008-R1015. ISSN: print: 0363-6119; online: 1522-1490.
Online: http://dx.doi.org/10.1152/ajpregu.00519.2006
Abstract: Freshwater turtles as a group are more resistant to anoxia than other vertebrates, but some species, such as painted turtles, for reasons not fully understood, can remain anoxic at winter temperatures far longer than others. Because buffering of lactic acid by the shell of the painted turtle is crucial to its long-term anoxic survival, we have tested the hypothesis that previously described differences in anoxia tolerance of five species of North American freshwater turtles may be explained at least in part by differences in their shell composition and buffering capacity. All species tested have large mineralized shells. Shell comparisons included 1) total shell CO2 concentration, 2) volume of titrated acid required to hold incubating shell powder at pH 7.0 for 3 h (an indication of buffer release from shell), and 3) lactate concentration of shell samples incubated to equilibrium in a standard lactate solution. For each measurement, the more anoxia-tolerant species (painted turtle, Chrysemys picta; snapping turtle, Chelydra serpentina) had higher values than the less anoxia-tolerant species (musk turtle, Sternotherus odoratus; map turtle, Graptemys geographica; red-eared slider, Trachemys scripta). We suggest that greater concentrations of accessible CO2 (as carbonate or bicarbonate) in the more tolerant species enable these species, when acidotic, to release more buffer into the extracellular fluid and to take up more lactic acid into their shells. We conclude that the interspecific differences in shell composition and buffering can contribute to, but cannot explain fully, the variations observed in anoxia tolerance among freshwater turtles.
Descriptors: reptiles, freshwater turtles, shell buffering properties, anoxia tolerence, lactic acid, shell composition, mineralized shells, species comparison.

Jackson, D.C. and J. Liu (2002). The importance of blood flow for lactate uptake into shells of anoxic turtles. FASEB Journal 16(4): A425. ISSN: 0892-6638.
NAL Call Number: QH301.F3
Descriptors: reptiles, turtles, anoxic, lactate uptake, blood flow, importance, meeting.
Notes: Meeting Information: Annual Meeting of the Professional Research Scientists on Experimental Biology, New Orleans, Louisiana, USA; April 20-24, 2002.

Lutz, P.L. and S.L. Milton (2004). Negotiating brain anoxia survival in the turtle. Journal of Experimental Biology 207(Pt 18): 3141-3147. ISSN: 0022-0949.
Online: http://dx.doi.org/10.1242/jeb.01056
NAL Call Number: 442.8 B77
Abstract: The turtle brain's extraordinary ability to tolerate anoxia is based on constitutive and expressed factors. Constitutive factors that predispose for anoxia tolerance include enhanced levels of glycogen stores, increased densities of protective receptors, elevated antioxidant capacities and elevated heat shock protein. However, to survive an anoxic insult, three distinct phases must be negotiated successfully. (1) A coordinated downregulation of ATP demand processes to basal levels. This phase, which takes 1-2 h, includes a reduction in voltage-gated K(+) (Kv) channel transcription and a substantial increase in Hsp72 and Hsc73 levels. During this period, adenosine and K(ATP) channels mediate several key events including channel arrest initiation and a reduction in the release of excitatory amino acids (EAAs). (2) Long-term survival (days) at basal levels of ATP expenditure. Neuronal network integrity is preserved through the continued operation of core activities. These include periodic electrical activity, an increased release of GABA and a continued release of glutamate and dopamine. Adenosine and GABA modulate the glutamate release. There is a further increase in Hsc73, indicating a 'housekeeping' role for this protein during this period. (3) A rapid upregulation of neuronal processes when oxygen becomes available to restore full function, together with the activation of protection mechanisms against reperfusion-generated reactive oxygen species.
Descriptors: reptiles, turtle, anoxia metabolism, brain metabolism, oxygen metabolism, anoxia tolerance, glycogen stores.

Milton, S.L., G. Nayak, P.L. Lutz, and H.M. Prentice (2006). Gene transcription of neuroglobin is upregulated by hypoxia and anoxia in the brain of the anoxia-tolerant turtle Trachemys scripta. Journal of Biomedical Science 13(4): 509-514. ISSN: print: 1021-7770; online: 1423-0127.
NAL Call Number: R850.A1
Abstract: Neuroglobin is a heme protein expressed in the vertebrate brain in mammals, fishes, and birds. The physiological role of neuroglobin is not completely understood but possibilities include serving as an intracellular oxygen-carrier or oxygen-sensor, as a terminal oxidase to regenerate NAD(+) under anaerobic conditions, or involvement in NO or ROS metabolism. As the vertebrate nervous system is particularly sensitive to hypoxia, an intracellular protein that helps sustain cellular respiration would aid hypoxic survival. However, the regulation of Neuroglobin (Ngb) under conditions of varying oxygen is controversial. This study examines the regulation of Ngb in an anoxia-tolerant vertebrate under conditions of hypoxia and anoxia. The freshwater turtle Trachemys scripta can withstand complete anoxia for days, and adaptations that permit neuronal survival have been extensively examined. Turtle neuroglobin specific primers were employed in RT-PCR for determining the regulation of neuroglobin mRNA expression in turtles placed in normoxia, hypoxia (4 h), anoxia (1 and 4 h), and anoxia-reoxygenation. Whole brain expression of neuroglobin is strongly upregulated by hypoxia and post-anoxic-reoxygenation in T. scripta, with a lesser degree of upregulation at 1 and 4 h anoxia. Our data implicate neuroglobin in mediating brain anoxic survival.
Descriptors: anorexia tolerant turtle, Trachemys scripta, gene expression and regulation, hypoxia, nerve tissue proteins, neuroglobin, heme proteins, turtle genetics.

Milton, S.L. and H.M. Prentice (2007). Beyond anoxia: The physiology of metabolic downregulation and recovery in the anoxia-tolerant turtle. Comparative Biochemistry and Physiology. Part A, Molecular and Integrative Physiology 147(2): 277-290. ISSN: 1095-6433.
Abstract: The freshwater turtle Trachemys scripta is among the most anoxia-tolerant of vertebrates, a true facultative anaerobe able to survive without oxygen for days at room temperature to weeks or months during winter hibernation. Our good friend and colleague Peter Lutz devoted nearly 25 years to the study of the physiology of anoxia tolerance in these and other model organisms, promoting not just the basic science but also the idea that understanding the physiology and molecular mechanisms behind anoxia tolerance provides insights into critical survival pathways that may be applicable to the hypoxic/ischemic mammalian brain. Work by Peter and his colleagues focused on the factors which enable the turtle to enter a deep hypometabolic state, including decreases in ion flux ("channel arrest"), increases in inhibitory neuromodulators like adenosine and GABA, and the maintenance of low extracellular levels of excitatory compounds such as dopamine and glutamate. Our attention has recently turned to molecular mechanisms of anoxia tolerance, including the upregulation of such protective factors as heat shock proteins (Hsp72, Hsc73), the reversible downregulation of voltage gated potassium channels, and the modulation of MAP kinase pathways. In this review we discuss three phases of anoxia tolerance, including the initial metabolic downregulation over the first several hours, the long-term maintenance of neuronal function over days to weeks of anoxia, and finally recovery upon reoxygenation, with necessary defenses against reactive oxygen stress.
Descriptors: reptiles, freshwater turtle, Trachemys scripta, metabolic downregulation, anoxia tolerant turtle, anoxia tolerance physiology, molecular mechanisms, oxygen stress.

Overgaard, J., T. Wang, O.B. Nielsen, and H. Gesser (2005). Extracellular determinants of cardiac contractility in the cold anoxic turtle. Physiological and Biochemical Zoology 78(6): 976-995. ISSN: 1522-2152.
NAL Call Number: QL1.P52
Abstract: Painted turtles (Chrysemys picta) survive months of anoxic submergence, which is associated with large changes in the extracellular milieu where pH falls by 1, while extracellular K+, Ca++, and adrenaline levels all increase massively. While the effect of each of these changes in the extracellular environment on the heart has been previously characterized in isolation, little is known about their interactions and combined effects. Here we examine the isolated and combined effects of hyperkalemia, acidosis, hypercalcemia, high adrenergic stimulation, and anoxia on twitch force during isometric contractions in isolated ventricular strip preparations from turtles. Experiments were performed on turtles that had been previously acclimated to warm (25 degrees C), cold (5 degrees C), or cold anoxia (submerged in anoxic water at 5 degrees C). The differences between acclimation groups suggest that cold acclimation, but not anoxic acclimation per se, results in a downregulation of processes in the excitation-contraction coupling. Hyperkalemia (10 mmol L(-1) K+) exerted a strong negative inotropic effect and caused irregular contractions; the effect was most pronounced at low temperature (57%-97% reductions in twitch force). Anoxia reduced twitch force at both temperatures (14%-38%), while acidosis reduced force only at 5 degrees C (15%-50%). Adrenergic stimulation (10 micromol L(-1)) increased twitch force by 5%-19%, but increasing extracellular [Ca++] from 2 to 6 mmol L(-1) had only small effects. When all treatments were combined with anoxia, twitch force was higher at 5 degrees C than at 25 degrees C, whereas in normoxia twitch force was higher at 25 degrees C. We propose that hyperkalemia may account for a large part of the depressed cardiac contractility during long-term anoxic submergence.
Descriptors: painted turtles, Chrysemys picta, anoxic, cold, cardiac contractility, extracellular determinants, long term anoxic submergence.

Pamenter, M.E., M.D. Richards, and L.T. Buck (2007). Anoxia-induced changes in reactive oxygen species and cyclic nucleotides in the painted turtle. Journal of Comparative Physiology. B, Biochemical, Systemic, and Environmental Physiology 177(4): 473-481. ISSN: print: 0174-1578; online: 1432-136X.
NAL Call Number: QP33.J681
Abstract: The Western painted turtle survives months without oxygen. A key adaptation is a coordinated reduction of cellular ATP production and utilization that may be signaled by changes in the concentrations of reactive oxygen species (ROS) and cyclic nucleotides (cAMP and cGMP). Little is known about the involvement of cyclic nucleotides in the turtle's metabolic arrest and ROS have not been previously measured in any facultative anaerobes. The present study was designed to measure changes in these second messengers in the anoxic turtle. ROS were measured in isolated turtle brain sheets during a 40-min normoxic to anoxic transition. Changes in cAMP and cGMP were determined in turtle brain, pectoralis muscle, heart and liver throughout 4 h of forced submergence at 20-22 degrees C. Turtle brain ROS production decreased 25% within 10 min of cyanide or N(2)-induced anoxia and returned to control levels upon reoxygenation. Inhibition of electron transfer from ubiquinol to complex III caused a smaller decrease in [ROS]. Conversely, inhibition of complex I increased [ROS] 15% above controls. In brain [cAMP] decreased 63%. In liver [cAMP] doubled after 2 h of anoxia before returning to control levels with prolonged anoxia. Conversely, skeletal muscle and heart [cAMP] remained unchanged; however, skeletal muscle [cGMP] became elevated sixfold after 4 h of submergence. In liver and heart [cGMP] rose 41 and 127%, respectively, after 2 h of anoxia. Brain [cGMP] did not change significantly during 4 h of submergence. We conclude that turtle brain ROS production occurs primarily between mitochondrial complexes I and III and decreases during anoxia. Also, cyclic nucleotide concentrations change in a manner suggestive of a role in metabolic suppression in the brain and a role in increasing liver glycogenolysis.
Descriptors: reptiles, anoxic induced changes, western painted turtle, cyclic nucleotides, reactive oxygen species, ATP production, brain.

Price, E.R., F.V. Paladino, K.P. Strohl, Santidrian T P, K. Klann, and J.R. Spotila (2007). Respiration in neonate sea turtles. Comparative Biochemistry and Physiology. Part A, Molecular and Integrative Physiology 146(3): 422-428. ISSN: 1095-6433.
Abstract: The pattern and control of respiration is virtually unknown in hatchling sea turtles. Using incubator-raised turtles, we measured oxygen consumption, frequency, tidal volume, and minute volume for leatherback (Dermochelys coriacea) and olive ridley (Lepidochelys olivacea) turtle hatchlings for the first six days after pipping. In addition, we tested the hatchlings' response to hypercapnic, hyperoxic, and hypoxic challenges over this time period. Hatchling sea turtles generally showed resting ventilation characteristics that are similar to those of adults: a single breath followed by a long respiratory pause, slow frequency, and high metabolic rate. With hypercapnic challenge, both species responded primarily by elevating respiratory frequency via a decrease in the non-ventilatory period. Leatherback resting tidal volume increased with age but otherwise, neither species' resting respiratory pattern nor response to gas challenge changed significantly over the first few days after hatching. At the time of nest emergence, sea turtles have achieved a respiratory pattern that is similar to that of actively diving adults.
Descriptors: reptiles, neonate sea turtles, leatherback, Dermochelys coriacea, olive ridley, Lepidochelys olivacea, respiration, pattern, control, hatchling, oxygen consumption, tidal volume.

Rial, R.V., M.C. Nicolau, A. Gamundi, T. Ortega, and M. Akaarir (2002). Periodic breathing and apnoeas in reptiles. Journal of Sleep Research 11(Suppl. 1): 191-192. ISSN: 0962-1105.
Descriptors: reptiles, periodic breathing, sleep apnea.
Notes: Meeting Information: 16th Congress of the European Sleep Research Society, Reykjavik, Iceland; June 3-7, 2002.

Stecyk, J.A. and A.P. Farrell (2007). Effects of extracellular changes on spontaneous heart rate of normoxia- and anoxia-acclimated turtles (Trachemys scripta). Journal of Experimental Biology 210(Pt 3): 421-431. ISSN: 0022-0949.
Online: http://dx.doi.org/10.1242/jeb.02653
NAL Call Number: 442.8 B77
Abstract: Heart rate (f(H)) of the anoxia-tolerant freshwater turtle (Trachemys scripta) during prolonged anoxia exposure is 2.5- to 5-times lower than the normoxic rate, but whether alterations in blood composition that accompany prolonged anoxia contribute to this bradycardia is unknown. We examined how temperature acclimation, oxygen deprivation, acidosis, hyperkalemia, hypercalcemia and adrenaline affect chronotropy in the turtle myocardium. We monitored spontaneous contraction rates of right-atrial preparations obtained from 21 degrees C- and 5 degrees C-acclimated turtles that had been exposed to either normoxia or anoxia (6 h at 21 degrees C; 2 weeks at 5 degrees C). Sequential exposures to saline solutions were designed to mimic, in a step-wise manner, the shift from a normoxic to anoxic extracellular condition (for normoxia-acclimated preparations) or the reverse (for anoxia-acclimated preparations). Our results clearly show that prolonged anoxia exposure re-sets the intrinsic f(H) of turtles at both temperatures, with reductions in intrinsic f(H) in the range of 25%-53% compared with normoxia. This intrinsic change would contribute to the bradycardia observed with prolonged anoxia. Further, we found negative chronotropic effects of extracellular anoxia, acidosis and hyperkalemia, and positive chronotropic effects of hypercalcemia and adrenaline. The exact nature of these extracellular effects depended, however, on the acclimation temperature and the prior exposure of the animal to anoxia. With normoxia-acclimated preparations at 21 degrees C, combined anoxia and acidosis (pH reduced from approximately 7.8 to approximately 7.2) significantly reduced spontaneous f(H) by 22% and subsequent exposure to hyperkalemia (3.5 mmol l(-1)K(+)) further decreased f(H). These negative chronotropic effects were ameliorated by increasing the adrenaline concentration from the tonic level of 1 nmol l(-1) to 60 nmol l(-1). However, in anoxia-acclimated preparations at 21 degrees C, anoxia alone inhibited f(H) (by approximately 30%). This negative chronotropic effect was counteracted by both hypercalcemia (6 mmol l(-1) Ca(2+)) and adrenaline (60 nmol l(-1)). At 5 degrees C, only the combination of anoxia, acidosis (pH reduced from approximately 8.0 to approximately 7.5) and hyperkalemia (3.5 mmol l(-1) K(+)) significantly reduced spontaneous f(H) (by 23%) with preparations from normoxia-acclimated turtles. This negative chronotropic effect was fully reversed by hypercalcemia (10 mmol l(-1) Ca(2+)). By contrast, spontaneous f(H) of anoxia-acclimated preparations at 5 degrees C was not affected by any of the extracellular changes. We conclude that prior temperature and anoxia experiences are central to determining f(H) during prolonged anoxia in Trachemys scripta both as a result of the re-setting of pacemaker rhythm and through the potential influence of extracellular changes.
Descriptors: reptiles, freshwater turtle, Trachemys scripta, extracellular changes, effect, spontaneous heart rate, normoxia, anoxia, bradycardia.

Storey, K.B. (2007). Anoxia tolerance in turtles: Metabolic regulation and gene expression. Comparative Biochemistry and Physiology. Part A, Molecular and Integrative Physiology 147(2): 263-276. ISSN: 1095-6433.
Abstract: Freshwater turtles of the Trachemys and Chrysemys genera are champion facultative anaerobes able to survive for several months without oxygen during winter hibernation in cold water. They have been widely used as models to identify and understand the molecular mechanisms of natural anoxia tolerance and the molecular basis of the hypoxic/ischemic injuries that occur in oxygen-sensitive systems and underlie medical problems such as heart attack and stroke. Peter L. Lutz spent much of his career investigating turtle anaerobiosis with a particular focus on the mechanisms of brain ion homeostasis and neurotransmitter responses to anoxia exposure and the mechanisms that suppress brain ion channel function and neuronal excitability during anaerobiosis. Our interests intersected over the mechanisms of metabolic rate depression which is key to long term anoxia survival. Studies in my lab have shown that a key mechanism of metabolic arrest is reversible protein phosphorylation which provides coordinated suppression of the rates of multiple ATP-producing, ATP-utilizing and related cellular processes to allow organisms to enter a stable hypometabolic state. Anoxia tolerance is also supported by selective gene expression as revealed by recent studies using cDNA library and DNA array screening. New studies with both adult T. scripta elegans and hatchling C. picta marginata have identified prominent groups of genes that are up-regulated under anoxia in turtle organs, in several cases suggesting aspects of cell function and metabolic regulation that have not previously been associated with anaerobiosis. These groups of anoxia-responsive genes include mitochondrially-encoded subunits of electron transport chain proteins, iron storage proteins, antioxidant enzymes, serine protease inhibitors, transmembrane solute carriers, neurotransmitter receptors and transporters, and shock proteins.
Descriptors: reptiles, turtles, T. scripta elegans, C. picta marginata, anoxia tolerence, metabolic regulation, gene expression, anaerobes, winter, cold, hibernation, anoxia responsive genes.

Storey, K.B. (2003). Anoxia and hypoxia: oysters, turtles and beyond. SICB Annual Meeting and Exhibition Final Program and Abstracts 2003: 315-316. ISSN: print: 1540-7063; online: 1557-7023.
Descriptors: reptiles, turtles, anoxia, hypoxia, oysters, meeting abstracts.
Notes: Meeting Information: Annual Meeting and Exhibition of the SICB (Society for Integrative and Comparative Biology), Toronto, ON, Canada; January 04-08, 2003.

Toney, V.I. and D.C. Jackson (2003). Cardiovascular effects of graded hypoxia and graded acidosis on the myocardium of the western painted turtle. FASEB Journal 17(4-5): Abstract No. 313.5. ISSN: 0892-6638.
NAL Call Number: QH301.F3
Descriptors: reptiles, painted turtle, graded hypoxia, acidosis myocardium, cardiovascular, effects, meeting.
Notes: Meeting Information: FASEB Meeting on Experimental Biology: Translating the Genome, San Diego, CA, USA; April 11-15, 2003.

Toney, V.I. and D.C. Jackson (2002). Cardiovascular effects of graded hypoxia on the myocardium of the western painted turtle. FASEB Journal 16(5): A887. ISSN: 0892-6638.
NAL Call Number: QH301.F3
Descriptors: reptiles, painted turtle, graded hypoxia, effects, myocardium, cardiovascular, effects, meeting abstracts.
Notes: Meeting Information: Annual Meeting of Professional Research Scientists on Experimental Biology, New Orleans, Louisiana, USA; April 20-24, 2002.

Warren, D.E., S.A. Reese, and D.C. Jackson (2006). Tissue glycogen and extracellular buffering limit the survival of red-eared slider turtles during anoxic submergence at 3 degrees C. Physiological and Biochemical Zoology 79(4): 736-744. ISSN: 1522-2152.
NAL Call Number: QL1.P52
Abstract: The goal of this study was to identify the factors that limit the survival of the red-eared slider turtle Trachemys scripta during long-term anoxic submergence at 3 degrees C. We measured blood acid-base status and tissue lactate and glycogen contents after 13, 29, and 44 d of submergence from ventricle, liver, carapace (lactate only), and four skeletal muscles. We also measured plasma Ca(2+), Mg(2+), Na(+), K(+), Cl(-), inorganic phosphate (P(i)), lactate, and glucose. After 44 d, one of the six remaining turtles died, while the other turtles were in poor condition and suffered from a severe acidemia (blood pH = 7.09 from 7.77) caused by lactic acidosis (plasma lactate 91.5 mmol L(-1)). An initial respiratory acidosis attenuated after 28 d. Lactate rose to similar concentrations in ventricle and skeletal muscle (39.3-46.1 micromol g(-1)). Liver accumulated the least lactate (21.8 micromol g(-1)), and carapace accumulated the most lactate (68.9 micromol g(-1)). Plasma Ca(2+) and Mg(2+) increased significantly throughout submergence to levels comparable to painted turtles at a similar estimated lactate load. Glycogen depletion was extensive in all tissues tested: by 83% in liver, by 90% in ventricle, and by 62%-88% in muscle. We estimate that the shell buffered 69.1% of the total lactate load, which is comparable to painted turtles. Compared with painted turtles, predive tissue glycogen contents and plasma HCO(-)(3) concentrations were low. We believe these differences contribute to the poorer tolerance to long-term anoxic submergence in red-eared slider turtles compared with painted turtles.
Descriptors: reptiles, painted turtles, red-eared slider turtle, Trachemys scripta, anoxic submergence, 3 degrees centigrade, tissue glycogen, extracellular buffering, survival.