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

Tissue PCO2 (carbon dioxide tension) (PtCO2), interstitial H+ (H+e) and potassium activities (K+e) were monitored in the cerebral cortex of rats during and after 2-3 min of anoxia. Anoxia was associated with systemic hypotension and caused H+e (extracellular hydrogen ion activity) to increase from pH approximately equal to 7.2 to pH approximately equal to 6.5, K+e to rise from approximately equal to 2.4 up to a maximum of approximately equal to 39 mmol/l, and PtCO2 to increase from approximately equal to 52 to approximately equal to 80 mmHg. Lactate increased from 2 to 5 mmol/kg tissue weight during anoxia and did not fall significantly after re-oxygenation for 10 min. A marked relationship existed between changes in PtCO2 and H+e. After re-oxygenation, K+e (extracellular potassium ion activity) and PtCO2 returned to the pre-anoxic level in a few minutes, whereas H+e took approximately equal to 30 min to recover. H+e recovered in a biphasic manner; a rapid decrease lasting approximately equal to 1 min preceded a much slower phase. We propose that the biphasic normalization of H+e after anoxia mainly reflects an initial and rapid washout of CO2 from brain tissue and a subsequent slow elimination of lactic acid occurring via metabolism and removal by the circulation.
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PMID:Simultaneous recording of tissue PCO2, interstitial pH and potassium activity in the rat cerebral cortex during anoxia and the subsequent recovery period. 257 50

By means of in vivo 31P nuclear magnetic resonance (NMR) we measured energy stores and intracellular pH at 10-min intervals in the myotome of unanesthetized carp and goldfish before, during, and after a period of anoxia (1 h for carp and 4 h for goldfish). The fish were mounted in a modified bioprobe, and their gills were irrigated with a constant flow of aerated or anoxic water. Anoxia caused a steep decline of phosphocreatine and intracellular pH in carp muscle. After the phosphocreatine stores had been exhausted by greater than 85%, [ATP] fell, whereas IMP and phosphodiesters accumulated. In goldfish muscle, initial changes followed the same pattern, but after 20 min a steady state of high-energy phosphates was reached and the development of acidosis was dampened. The resistance of goldfish to anoxia is due to metabolic suppression and a switch from lactate to ethanol and CO2 as the anaerobic end products. In both species, recovery was complete within 3 h. The fast pH recovery seems to be mainly caused by H+ and lactic acid efflux.
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PMID:Fish muscle energy metabolism measured by in vivo 31P-NMR during anoxia and recovery. 270 80

The effects of chlorpromazine and trifluoperazine on phosphatidylcholine biosynthesis in the heart were investigated in isolated cardiac cells under normoxic and anoxic conditions. The cells were obtained from 7-day-old chick embryos and were maintained in culture. After 96 hr, cells were maintained either in an incubator with oxygen at room air concentration (normoxia) or in an incubator containing 95% nitrogen and 5% CO2 (anoxia). Pulse chase experiments with [methyl-3H]choline were conducted using a 2-hr incubation with choline. Chlorpromazine and trifluoperazine at 10(-5) M produced a significant (P less than 0.05) increase in the incorporation of choline into both phosphocholine and phospholipid. High concentrations of chlorpromazine or trifluoperazine i.e. 10(-4) M, damaged myocardial cells as reflected in a significant (P less than 0.05) reduction in cellular protein and a further reduction in labelled choline in phosphocholine or phospholipid after adjusting for the lower protein concentrations. Anoxia altered choline metabolism but 6 hr of anoxia was the minimum time needed for the effect to be observable. Anoxia, for 24 hr, produced a significant (P less than 0.05) reduction in labelled choline in phosphocholine without a significant change in incorporation of label in phospholipid or cellular protein. Both chlorpromazine and trifluoperazine at 10(-5) M prevented anoxic-induced changes in phosphocholine metabolism. Thus, chlorpromazine and trifluoperazine affect phospholipid biosynthesis in cardiac cells and prevent anoxia-induced changes in phosphatidylcholine biosynthesis.
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PMID:Effects of chlorpromazine and trifluoperazine on choline metabolism and phosphatidylcholine biosynthesis in cultured chick heart cells under normoxic and anoxic conditions. 275 98

The effect of neuropeptides and their analogs on anoxia-induced amnesia was examined using one-trial passive avoidance task in mice. Anoxia, produced by the exposure to CO2 immediately after the acquisition of avoidance response, induced amnesia which is shown by a short latency to enter from the safety compartment into the shocked compartment in the retention test conducted 24 hr later. In these anoxia-treated animals, thyrotropin-releasing hormone (TRH: 10-20 mg/kg), its analog DN-1417 (10-20 mg/kg) and ACTH 4-10 (66 micrograms/body), which were given sc 15-60 min before the retention test, markedly prolonged the latency in a dose-dependent manner, indicating a reversal of the amnesia. Arginine- and lysine-vasopressin also reversed the amnesia at a dose of 100 micrograms/body. These results suggest that TRH and DN-1417, known to reverse the amnesia produced by the protein synthesis inhibitor cycloheximide, have ameliorating effects on the retrieval process of memory.
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PMID:[Effect of TRH and its analog DN-1417 on anoxia-induced amnesia in mice]. 299 54

Anoxia has been shown to potentiate the constrictor effects of 5-hydroxytryptamine (5HT) in isolated vascular tissue. In the present study, canine coronary arterial rings were incubated with various treatments and exposed to 5HT (4 X 10(-7) M) and anoxia (95% N2 and 5% CO2). Developed tension was increased by 250 +/- 40 mg by 5HT alone and 2,000 +/- 90 mg by 5HT and anoxia. Calcium (5 mM) potentiated, while inorganic (lanthanum, 10(-2) M) and organic calcium antagonists (nifedipine, verapamil and diltiazem; IC50 = 7 X 10(-9), 7.3 X 10(-8) and 2.4 X 10(-7) M, respectively) blocked the anoxic potentiation. Anoxia alone decreased resting tension (RT). Methysergide 3 X 10(-5) M inhibited both the 5HT- and anoxia-potentiated responses. Nitroglycerin decreased RT and inhibited the anoxic response (IC50 = 7.6 X 10(-6) M), while dipyridamole decreased RT and did not affect the anoxic response. These data suggest that the potentiation of 5HT contraction by anoxia is dependent upon extracellular calcium influx and is linked to a 5HT receptor. In addition, inhibition of the anoxic response can be achieved at other sites and is not a property common to all coronary vasodilators.
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PMID:Effects of nitroglycerin, dipyridamole, nifedipine, verapamil and diltiazem on canine coronary arterial rings contracted with 5-hydroxytryptamine and anoxia. 309 50

Neurons grown in cultures of dissociated brain cells degenerate when exposed to anoxia and deprived of glucose. We have developed culture systems in which neurons can be grown in the presence or absence of astrocytes and have used them to study the influence of astrocytes on the neuronal degeneration induced by anoxia and glucopenia. Cultures were prepared from fetal rat forebrains. Mixed cultures contained neurons (identified by immunocytochemical staining of neuron-specific enolase, NSE) and about an equal number of non-neuronal cells (identified by glial fibrillary acid protein). Pure neuronal cultures were prepared by adding a cytostatic compound (cytosine arabinoside) to the medium. Treated cultures were exposed for 4 h to glucose-free medium and an atmosphere of 95% N2 and 5% CO2, whereas control cultures were left in the usual medium containing glucose and in an atmosphere composed of 95% air and 5% CO2. After an interval of 24 h, cultures were fixed, taken for NSE staining, and the number of surviving neurons was counted. Exposure to anoxia and glucopenia reduced the number of surviving neurons in pure neuronal cultures to 5-10% of control levels. In contrast, in mixed cultures 40-60% of the neurons survived these conditions. Anoxia without glucose deprivation reduced the number of surviving neurons in both types of cultures to the same extent as anoxia combined with glucopenia. Glucose deprivation alone was ineffective. The findings suggest a protective influence of astrocytes on neurons under anoxic conditions. gamma-D-Glutamylglycine protected neurons in both types of cultures from anoxia-induced degeneration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Astrocytes protect cultured neurons from degeneration induced by anoxia. 367 91

The isolated rat heart was perfused by Langendorff's technique with either an oxygenated (95% O2 and 5% CO2) or an anoxic (95% N2 and 5% CO2) solution. Anoxia increased coronary flow and effluent adenosine concentration, but the time course of these changes was discordant; coronary flow increased transiently (the maximum increase in flow was observed within 1-2 min after the onset of anoxia), whereas the effluent adenosine concentration increased as a function of the time during anoxia. The concentration of effluent adenosine reached 3 microM 10 min after anoxia. The tissue (myocardial) adenosine content changed in parallel with the effluent adenosine concentration. An infusion of adenosine increased coronary flow dose-dependently, and the maximum increase was obtained when 0.27 microM of adenosine was infused. Effluent adenosine concentration was 0.05-0.3 microM in both anoxia and adenosine infusion experiments at the time when the maximum increase in coronary flow occurred. An increase in concentrations of adenosine above 0.05-0.03 microM in the effluent was not accompanied by an increase in coronary flow. These results raise a question about the role of adenosine in regulating coronary circulation during anoxic perfusion, though there is a possibility of vasodilatory function of adenosine in early period of anoxic perfusion.
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PMID:Difference in the time course between increases in coronary flow and in effluent adenosine concentration during anoxia in the perfused rat heart. 408 39

The transport of K+ and H+ (both expressed as mueq/h) by in vitro chambered bullfrog (Rana catesbeiana) gastric mucosa have been studied under a variety of conditions such as anoxia, addition of p-chloromercuribenzene sulfonic acid (PCMBS) into the secretory solution, inclusion of ouabain in the nutrient solution, addition of thiocyanate (SCN-) into the mucosal solution, and replacement of nutrient chloride (Cl-) with sulfate (SO4(2-)), or gluconate (Gl). Anoxia reversibly reduced the H+ transport close to zero within 15 min and gradually reduces the K+ transport throughout the 2-h period of anoxia. The presence of 2.5 X 10(-4) M mucosal PCMBS in the histamine-stimulated mucosa increases the K+ transport, which is promptly reduced by changing the gas phase to 95% N2-5% CO2. Addition of ouabain to the nutrient solution of the histamine-stimulated mucosa with PCMBS on the mucosal side significantly (P < 0.05) reduces the K+ transport within 60 min. Addition of SCN- to the mucosal solution of a histamine-stimulated mucosa with regular nutrient or O, K+ nutrient and 10, K+ mucosal solution reduces the H+ transport to near zero within 60 min. This SCN- inhibition can be reversed by elevating secretory K+. Substitution of nutrient Cl- with SO4(2-) or Gl in the histamine-stimulated mucosa reversibly inhibits H+ transport and reduces K+ transport to a low level (0.7 +/- 0.05). Our data suggest that the K+ transport across the apical membranes of gastric cells is to a large extent a passive carrier-mediated process, and the transport of both K+ and Cl- are coupled at the apical membrane.
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PMID:Secretion of H+ and K+ by bullfrog gastric mucosa: characterization of K+ transport pathway. 625 8

Stripped, proximal bullfrog duodenum was mounted in an Ussing chamber between HCO3--buffered nutrient (serosal) and unbuffered secretory (luminal) solutions. This preparation showed stable electrical parameters and caused alkalinization of the secretory solution at a rate of 0.95 +/- 0.03 mueq.cm-2.h-1 (mean +/- SE; n = 100). Anoxia and 2,4-dinitrophenol each reduced alkalinization by 50-60%, but acetazolamide (5 X 10(-4)M) had no effect. Removal of nutrient HCO3- and CO2 reduced alkalinization by over 90%, whereas increasing nutrient [HCO3-] at constant partial pressure of CO2 (PCO2) or increasing nutrient PCO2 at constant [HCO3-] each caused saturable increases in alkalinization, despite opposite effects on nutrient pH. Dibutyryl adenosine 3',5'-cyclic monophosphoric acid, but not dibutyryl guanosine 3',5'-cyclic monophosphoric acid, increased luminal alkalinization to 167 +/- 21% of control. Removal of nutrient, but not secretory, Na+ reduced alkalinization by 74%. Changes in the rate of alkalinization were accompanied by corresponding changes in potential difference and short-circuit current. Removal of Cl- or nutrient K+ or addition of histamine, thiocyanate, or catecholamines had no effect on electrical or secretory characteristics. We conclude that a) the amphibian duodenum transports alkali from nutrient to secretory solutions by both active and passive processes, b) there is a small secretion of endogenous HCO3-, c) alkaline secretion is electrogenic, d) Cl- does not contribute to the short-circuit current, e) alkaline secretion is partially dependent on nutrient Na+ that acts in a facilitatory, not cotransport, role, f) there is no Cl--HCO3- exchange, and g) alkaline secretion is independent of nutrient pH.
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PMID:Alkaline secretion by amphibian duodenum. I. General characteristics. 626 7

Previous investigations have demonstrated impairment of hepatic gluconeogenic activity during both hypovolemia and sepsis, but the mechanisms responsible remain unclear. The present study was designed to determine the influence of lack of oxygen on gluconeogenesis independent of humoral factors, products of ischemic peripheral tissues or pH changes. Livers obtained from Sprague-Dawley rats fasted 24 hours were perfused with Krebs-Henseleit buffer containing 5 mM lactate for 30 minutes. In the control group (n = 8) perfusion was continued; in others, anoxia was induced by perfusing with buffer equilibrated with 95% N2 and 5% CO2 for periods of 15, 30, or 60 minutes (n = 4, 5, and 5, respectively). The initial conditions were then reinstituted for an additional 45 minutes. Anoxia caused hepatic release of K+, indicative of disordered hepatic cellular ionic gradients and an abrupt cessation of gluconeogenesis. Reoxygenation partially reversed these alterations but some impairment of gluconeogenesis persisted and the degree of uptake of K+ from the perfusion media was decreased as the duration of anoxia increased. The degree of restoration of gluconeogenesis after a period of anoxia was closely associated with restoration of cellular uptake of K+. By comparison, livers taken from hypovolemic animals maintained at a mean arterial blood pressure of 40 mm Hg until the beginning of the decompensatory stage of shock exhibited a gluconeogenic capacity of only 41% of control animals and was comparable to the compromise induced by between 30 and 60 minutes of anoxia. These results suggest that the abilities to restore hepatic electrolyte balance and gluconeogenesis after oxygen deprivation are affected in parallel and may reflect a common dependence on the restoration of ATP stores after the insult.
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PMID:Effect of hemorrhage and anoxia on hepatic gluconeogenesis and potassium balance in the rat. 684 34


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