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

Energy coupling for uptake of glycine and alanine in glycerol grown cells of Escherichia coli differs from that of the aromatic amino acids. Respiration and uptake of glycine and alanine show similar inactivations in cells exposed to high intensity violet light or to various concentrations of cyanide. In contrast,uptake of phenylalanine, tyrosine, and tryptophan is resistant to effects of light or cyanide. Anoxia largely inhibits uptake of glycine and alanine while that of the aromatic amino acids is only partially affected. Furthermore, ferricyanide (but not ferrocyanide) completely restores active uptake of aromatic amino acids under anoxic conditions but is without effect on glycine and alanine uptake. Adenosine 5'-triphosphate (ATP) concentration does not increase in anoxic cells exposed to ferricyanide, indicating that ATP cannot be responsible for this restoration. The data suggest that glycine and alanine represent amino acids whose transport shows a complete dependence on energy derived from respiration, while the energy for transport of the aromatic amino acids may be obtained from other sources
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PMID:Coupling of glycine and alanine transport to respiration in cells of Escherichia coli. 109 36

Energy requirements for uptake of 14-C labeled 5-hydroxytryptamine ([14-C]5-HT) were studied in isolated guinea pig lungs, ventilated with 95% O2-5% CO2 and perfused in a recirculating system with Krebs-Ringer-bicarbonate solution containing 4% bovine serum albumin and 5 mM glucose. After 14 min preincubation with various inhibitors, lungs were perfused for 30 min with 0.25 times 10- minus 6 M [14-C]5-HT. Aliquots of perfusate were analyzed for [14-C]5-HT and metabolic products. Control lungs had a fractional serotonin clearance of 0.57 plus or minus 0.04. The rate of removal of [14-C]5-HT was inhibited 96% by imipramine, 88% by chlorpromazine, and 65% by ouabain, but was unaffected by iproniazid. Anoxia and cyanide each inhibited uptake by 68%. Omitting glucose from the perfusate reduced uptake by 30%. 2-Deoxyglucose and iodoacetate decreased the rate of [14-C]5-HT removal by 44 and 70%, respectively. Uptake was not affected by lung weight gain nor by changes in lung mechanical properties produced by [14-C]5-HT. [14-C]5-HT uptake by guinea pig lung requires a metabolic source of energy providing additional evidence for transport by an active process.
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PMID:Depression of pulmonary 5-hydroxytryptamine uptake by metabolic inhibitors. 113 May 33

The accumulation of (-)-3H-adrenaline (3H-A) by rabbit isolated aorta was studied. In all experiments, monoamine oxidase and catechol-O-methyltransferase were inhibited by treatment with pargyline and 3',4'-dihydroxy-2-methyl-propiophenone, respectively. The relationship between the accumulation of 3H derived from 3H-A and the duration of incubation was linear. The 3H-accumulation after 3 h incubation was 22.5 ml/g. In reserpine-treated tissue, the 3H-accumulation levelled off after 30 min and was 8.5 ml/g after 3 h. The concentration of 3H-A or (-)-3H-noradrenaline (3H-NA) and the 3H-accumulation (ml/g) were inversely related. At 10(-8) M, the 1-hour accumulation of 3H derived from 3H-A and 3H-NA was 7.8 and 15.2 ml/g, respectively. With increasing concentrations the accumulation values approached each other. The accumulation of 3H derived from 3H-A by reserpine-treated tissue also showed an inverse relationship with concentration. The accumulation of 3H derived from 3H-A was dependent on the bath temperature. Storage of tissue (0-5 days in salt solution without equilibration with 95% O2/5% CO2; 4 degrees C) did not affect the accumulation of 3H derived from 3H-A. Thereafter (7-14 days), the accumulation decreased. The inhibitory potency (IC50; -log M) of desipramine, cocaine, propranolol, isoprenaline, and normetanephrine on accumulation of 3H derived from 3H-A was found to be 8.26; 6.50; 5.48; 4.88, and 4.02, respectively. The maximal degree of inhibition was almost the same for these drugs, while that of clonidine and corticosterone was 50 and 20%, respectively. In the presence of desipramine, either clonidine, corticosterone or isoprenaline reduces the accumulation of 3H derived from 3H-A. Ouabain and iodoacetic acid, but not sodium cyanide and 2,4-dinitrophenol, reduced the accumulation of 3H derived from 3H-A. Anoxia (95% N2/5% CO2; 37 degrees C; 1-24 h) did not alter the accumulation of 3H derived from 3H-A. Glucose deprivation alone or combined with anoxia markedly reduced the 3H-accumulation. The release of 3H-A from rabbit isolated aorta was studied. This release was compared with that of 3H-NA. The stimulation-evoked 3H-overflow from aorta preloaded with 3H-A decreased with repeated stimulation. In contrast, prestimulation enhanced subsequent stimulation-evoked 3H-overflows. For both 3H-amines, the 3H-overflow increased concomitantly to the same degree with the number of pulses. The time course of 3H-overflows with either 3H-A or 3H-NA was compared.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Accumulation and release of adrenaline, and the modulation by adrenaline of noradrenaline release from rabbit blood vessels in vitro. 176 89

1. The carotid body chemoreceptors are stimulated in situ by hypoxia. We have studied type I cells freshly dissociated from the carotid body of the rabbit. We have used microfluorimetric and patch clamp techniques to examine the responses to hypoxia, to anoxia, and to metabolic inhibition. 2. NADH autofluorescence measured at both 400 and 500 nm increased rapidly and reversibly in response to anoxia or to cyanide (CN-), reflecting a change in mitochondrial metabolism. 3. Indo-1 was used to measure changes in intracellular calcium, [Ca2+]i. Anoxia reversibly increased [Ca2+]i from approximately 50-100 to approximately 200-450 nM in all cells tested. The response showed a striking temperature sensitivity. Responses to hypoxic stimuli were barely detectable at 17-20 degrees C, and were dramatically increased on warming to 36 degrees C. In contrast, responses to K(+)-induced depolarization were only slightly increased in rate of onset and recovery by warming. 4. The rise in [Ca2+]i originated largely from an intracellular store which was slowly depleted by exposure to nominally Ca2(+)-free solutions. Responses were unaffected by blockade of Ca2+ channels with organic (D600, verapamil) or inorganic (Co2+) blockers, by blockade of Na+ channels with tetrodotoxin (TTX), or by increasing action potential duration with tetraethylammonium (TEA). Responses to anoxia were increased by the increased [Ca2+]i loading that follows prior exposure to Ca2(+)-free solutions. 5. Responses to anoxia, to blockade of electron transport by CN-, and to the mitochondrial uncoupler, carbonyl cyanide p-trifluoromethoxy-phenylhydrazone (FCCP), were equivalent in amplitude. The response to anoxia was occluded by concurrent application of FCCP, suggesting that the Ca2+ originates from the same pool in each case. 6. At 35-36 degrees C, responses to graded levels of PO2 were also graded. Thresholds varied between cells, but were typically 30-50 mmHg. Stimulus-responses curves were essentially hyperbolic, increasing dramatically as the PO2 approached 0 mmHg. 7. The sensitivity of cells to hypoxic solutions was increased by acidification of the superfusate over the pH range from 7.3 to 6.85. 8. Cell-attached patch clamp recordings showed depression of spontaneous action potentials associated with a rise in [Ca2+]i during exposure to anoxic solutions. Whole-cell recordings showed that anoxia increased a voltage-gated gK as described previously for CN-, while producing no change in resting conductance. 9. These data suggest that the rise in [Ca2+]i originates largely from Ca2+ efflux from a mitochondrial pool.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Responses of type I cells dissociated from the rabbit carotid body to hypoxia. 223 19

Near-infrared (NIR) difference spectra were obtained for oxidized cytochrome c oxidase of isolated mitochondria in vitro and of cerebral tissue in situ observed through scalp and skull. The broad peaks of maximal absorption observed in both were not inconsistent with the customary assignment of an 830 nm peak. However, the ratios of the intensity of the NIR band to that of the visible peak (605 nm), which we found to be identical for in-vitro and in-situ spectra, were consistently and significantly higher than those of the various purified enzyme preparations reported in the literature. In addition the half-band widths of our in-vitro and in-situ preparations were narrower. Haemoglobin spectra in the NIR obtained in clear and in highly light-scattering media showed almost total absence of band distortion in this spectral region, suggesting that the differences observed are not due to scattering effects. Anoxia and the specific oxidase inhibitors, cyanide and carbon monoxide, caused the expected disappearance of the band in both the mitochondria in vitro and the cerebrum in situ. The 830 nm band observed in intact, well-oxygenated animal preparations was therefore identified with the NIR absorption band of oxidized cytochrome c oxidase, notwithstanding the differences with the observations on purified preparations. This points to the possibility of developing instrumentation and techniques for the non-invasive monitoring of the redox state of cytochrome c oxidase as an index to cerebral oxygen sufficiency, i.e. adequate delivery and utilization of oxygen to and by brain tissue.
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PMID:Near-infrared monitoring of cerebral oxygen sufficiency. I. Spectra of cytochrome c oxidase. 289 58

The release of endogenous noradrenaline and its deaminated metabolite dihydroxyphenylglycol in the myocardium have been studied in the isolated perfused heart of the rat subjected to three models of energy depletion: ischemia, anoxia, and cyanide intoxication. Anoxia and cyanide intoxication were combined with substrate deficiency at constant perfusion flow. All three energy-depleting procedures caused a similar overflow of noradrenaline which, following a constant delay of 10 minutes without increased release, amounted to more than 25% of total heart content within 40 minutes. This noradrenaline overflow was not diminished in the absence of extracellular calcium and was inhibited by the uptake1 blocker desipramine in all three experimental models, indicating a common and nonexocytotic release mechanism. In the presence of glucose, neither anoxia nor cyanide intoxication resulted in a measurable noradrenaline overflow. Conversely, blockade of glycolysis or glucose depletion prior to ischemia or cyanide poisoning accelerated the noradrenaline overflow, demonstrating a key role of the sympathetic nerve cells' energy status in causing nonexocytotic catecholamine release. Blockade of energy metabolism in the presence of oxygen (cyanide model) resulted in the overflow of high amounts of dihydroxyphenylglycol that was not inhibited by uptake1 blockade. The release of the lipophilic dihydroxyphenylglycol by diffusion reflects deamination of axoplasmic noradrenaline by monoamine oxidase. Since saturation of the enzyme could be excluded in this model dihydroxyphenylglycol release can be taken as a mirror of cytoplasmic noradrenaline concentration. The results obtained by these studies indicate that nonexocytotic catecholamine release is a two-step process induced by energy deficiency in the sympathetic varicosity. In a first step, noradrenaline is lost from storage vesicles, resulting in increasing axoplasmic concentrations. The second step is the rate-limiting transport of intracellular noradrenaline across the cell membrane by the uptake1 carrier that has reversed its normal net transport direction.
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PMID:Nonexocytotic release of endogenous noradrenaline in the ischemic and anoxic rat heart: mechanism and metabolic requirements. 356 91

1. Using a preparation of rat colon mucosa mounted in vitro in small chambers, some factors which influence the electrical properties of the mucosa have been investigated.2. The mucosa behaved mainly as an ohmic resistance although a very brief transient occurred on first passing current. At 32 degrees C, the fresh preparation had a mean resistance of 108Omega/cm(2) and a mean short circuit current (s.c.c.) of 143 muA/cm(2). Tissues taken from Na-depleted and adrenalectomized rats differed little from normal tissues in electrical resistance but those from Na-depleted rats had higher potential difference (p.d.) and s.c.c.3. Increase of temperature led to a rise of conductance of similar order to that found for ions in aqueous solution. S.c.c. also rose with increase of temperature but the effect was relatively greater consistent with its being dependent on metabolic processes.4. Anoxia or the addition of cyanide, iodoacetate or 2,4-dinitrophenol to the bath fluid caused considerable fall in the p.d. and s.c.c.5. Ouabain decreased the p.d. and s.c.c. when added to the serosal side but had no effect when on the luminal side.6. Aldosterone and acetazolamide had no effect.7. Varying serosal side [K] produced only minor changes in p.d.8. Reducing [Na] of the luminal solution caused a considerable fall of p.d. but similar reduction of [Na] on the serosal side had little effect.9. The frequently employed model which represents the transepithelial p.d. as the sum of diffusion potentials originating at the luminal and serosal sides of the cell layer is not consistent with the present results. The colonic transmucosal p.d. probably originates in the electrogenic transport of Na by a mechanism located on the serosal side of the epithelium.
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PMID:Electrical potential and short circuit current of an in vitro preparation of rat colon mucosa. 563 62

1. The metabolic requirements for catecholamine secretion elicited by acetylcholine or by calcium plus high K(+) were studied on acutely denervated perfused cat adrenal glands.2. Glucose-deprivation plus anoxia caused an increase in the spontaneous catecholamine output from adrenal glands perfused with normal Locke solution, which was abolished by the removal of calcium from the perfusion medium.3. Anoxia plus glucose-deprivation did not depress the secretory response to repeated exposures of a low concentration of acetylcholine, but did depress the response to a higher concentration of acetylcholine. Glucose-deprivation and nitrogen, when imposed either separately or together, did not inhibit total catecholamine output in response to calcium. Differential analysis of the calcium-evoked secretion showed that during anoxia, catecholamine output was maintained primarily by adrenaline secretion.4. Cyanide (0.2 mM) potentiated the secretory response to calcium in the presence of glucose, but when glucose was omitted from the perfusion medium, cyanide caused a gradual decline in calcium-evoked secretion. Iodoacetic acid (IAA) (0.2 mM) depressed the response to calcium by about 50% under aerobic conditions and by 90% under anaerobic conditions.5. The glycogen content of medullae was profoundly depleted under anoxic conditions.6. It is concluded that energy is required for the secretory action of calcium on medullary chromaffin cells. The energy may be derived from glycolysis or oxidative metabolism. A possible interaction between calcium and adenosine triphosphate acid (ATP) in eliciting catecholamine secretion is discussed.7. The alteration in the percent adrenaline and noradrenaline secreted during anoxia indicates that anoxia may regulate medullary catecholamine secretion through a peripheral, as well as a central mechanism.
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PMID:The metabolic requirements from catecholamine release from the adrenal medulla. 577 Aug 85

Measurement of cytosolic free calcium (Cai) in small mammalian cells has been achieved by incorporating into cells the photoprotein aequorin by hypoosmotic shock treatment (HOST). The method and the instrumentation necessary for monitoring Cai are described in detail. We present evidence that the aequorin-Ca light signal originates in the cytosol and that the cells subjected to the HOST procedure have a normal viability and functional integrity with respect to growth, respiration, membrane transport calcium metabolism, and hormone responsiveness. From 36 measurements made at 25 degrees C, the cytosolic free calcium of cultured kidney cells is estimated to be 60 nM assuming an intracellular free magnesium of 1 mM. Anoxia and metabolic inhibitors (10 mM cyanide) dramatically increase the cytosolic free calcium, and both effects are fully reversible.
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PMID:Measurement of cytosolic free calcium in mammalian cells with aequorin. 609 70

Oxygen tensions in the major venous inputs to the systemic and portal-vein hearts of normoxic Atlantic hagfish (12.3 +/- 1.7 and 11.0 +/- 1.6 mmHg, respectively) are low compared with typical vertebrate values. Anoxia and poisoning with cyanide and azide do not significantly affect in situ performance of the systemic heart. Idoacetate poisoning, however, results in a significant decrease in cardiac performance of the systemic heart to 12% of the initial value after 3 h. Activities of mitochondrial enzymes of hagfish ventricle suggest a small potential for aerobic metabolism compared with those in the aerobic ventricle of Atlantic cod. Activities of enzymes of carbohydrate metabolism indicate similar anaerobic capacity in hagfish and cod ventricle. The ratio of pyruvate kinase to cytochrome c oxidase, an index of anaerobic to aerobic capacity, is 5.6 times greater in hagfish than cod ventricle. Metabolite concentrations in freeze-clamped ventricles of normoxic and hypoxic hagfish indicate hypoxia-induced activation of glycogenolysis, enhanced substrate flow across 6-phosphofructokinase, and an apparent secondary constriction of glycolysis at the level of glyceraldehyde-phosphate dehydrogenase. Carbohydrate utilization via the glycolytic pathway appears essential for maintenance of cardiac performance in both normoxic and anoxic hagfish. Under conditions of severe hypoxia, ATP provision is probably met by anaerobic glycolysis.
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PMID:Atlantic hagfish cardiac muscle: metabolic basis of tolerance to anoxia. 629 22


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