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

To investigate the etiology of contact lens-induced transient endothelial changes (blebs) in the human cornea, the effects of five different stimuli on corneal thickness and the appearance of the corneal endothelium were assessed. The stimuli included: (1) a silicone contact lens; (2) a silicone contact lens in combination with anoxia; (3) anoxia alone; (4) a thick hydroxyethyl methacrylate (HEMA) contact lens; and (5) a gas mixture of 9.8% carbon dioxide, 20.5% oxygen, and the balance nitrogen. The silicone lens alone produced no significant alteration in endothelial appearance and little change in corneal thickness. However, when nitrogen gas was passed in front of the lens, a typical bleb response was observed. This indicates that the physical presence of a contact lens is insufficient by itself to produce transient endothelial changes. Anoxia alone induced corneal swelling and endothelial bleb formation, indicating a metabolic component in the bleb response. The gas mixture containing 9.8% carbon dioxide also altered the endothelial appearance but had no significant effect on corneal thickness. The thick HEMA lens produced changes in both the appearance of the endothelium and corneal thickness. The only factor common to the stimuli which induced blebs would appear to be their ability to change the pH in or near the corneal endothelial layer.
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PMID:The etiology of transient endothelial changes in the human cornea. 393 Apr 18

In several systems a paradoxical reduction of radiation damage with increasing dose, termed reversion, has been observed. In the fern Osmunda regalis the percentage of cells which does not die but stays alive, although reproductively sterile, increases with dose. The assumed mechanism of this effect is a continuation of cytoplasmic growth during radiation-induced mitotic delay which induces terminal differentiation (early differentiation) thus preventing mitosis and the expression of chromosomal injury. Suppression of cytoplasmic growth after irradiation should abrogate reversion. This was tested using anoxia. Reversion was suppressed by storage of the sporelings in nitrogen for 8 h or more after X-rays, but was not suppressed by storage in 0.27 microM oxygen nor by a 60-min exposure to air after irradiation and before storage in nitrogen. Anoxia before irradiation in air had no effect. Anoxia only during irradiation showed an OER of about 2 for the reversion peak. The partial abrogation of reversion is consistent with the assumed mechanism. Marked reversion also was observed after 14.7 MeV neutrons.
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PMID:The reversion phenomenon in irradiated fern prothalli: effects of acute or chronic anoxia and LET. 397 49

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

Forty-four kinds of organic nitrogen compounds as well as 37 kinds of dyes which contained nitrogen were subjected to TLm test by use of Himedaka (Oryzias latipes) and the results were compared with their partition coefficients between n-octanol and water. Concerning organic nitrogen compounds, such good correlation was observed among them that the larger the partition coefficient was, the smaller was the TLm value. Their acute toxicity to fish was supposed to be revealed after their passage through cell membrane of fish to be accumulated in the body. As far as coal-tar dyes and dyestuffs were concerned, there was a correlation between partition coefficient and TLm value. Methylene blue and rose bengale showed strong acute toxicity to fish and it was assumed that high affinity of these dyes to gill was responsible to depressing the function of gill, to make fish suffer from anoxemia and die.
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PMID:Actual survey on TLm (median tolerance limit) values of environmental pollutants, especially on amines, nitriles, aromatic nitrogen compounds and artificial dyes. 715 31

Previous studies have demonstrated that the mechanism of excitation contraction coupling changes with normal development in rabbit urinary bladder smooth muscle. The present study was designed to determine whether there were any differences in the effects of anoxia and extracellular acidosis in response to field stimulation, bethanechol and KCl between mature (8 weeks) and neonatal (3 days) rabbit bladder smooth muscle. Bladder smooth muscle strips from mature and neonatal New Zealand White rabbits were mounted in organ baths and bathed in oxygenated Tyrode's solution. Anoxia was produced by changing the gas mixture to 95% nitrogen/5% CO2 and the effects on contractility were determined at different times after initiation of anoxia. The extracellular acidosis was produced by decreasing the buffer's NaHCO3 concentration. We conclude that bladder smooth muscle does not exhibit an age-specific ability to counteract the effects of anoxia or acidosis as is seen in the developing rabbit myocardium. Instead it appears that the purinergic mechanisms of contraction are much more sensitive to the effects of anoxia or acidosis. Neonatal bladder smooth muscle exhibits a greater drop in contractility with anoxia or acidosis at low frequency (2 Hz) field stimulation; we attribute this to the fact that neonatal bladder smooth muscle has a greater purinergic component in its response to field stimulation. These differences in the responses to anoxia and pH reflect alternate mechanisms of pharmacologic activation, and not inherent differences in the biochemistry of the maturing smooth muscle.
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PMID:Developmental factors in the contractile response of rabbit urinary bladder: effect of anoxia and extracellular acidosis. 766 16

Endocytosis in the renal tubular cell is a permanent process serving the role of saving nitrogen from plasma peptides that are continuously cleared away by kidney glomerulus. Since small proteins appear in urine after strenuous exercise, it was hypothesized that renal ischemia impairs the tubular endocytic reabsorption of proteins. The aim of this paper is to describe a simple in vitro model of renal endocytosis and to use it in studies of endocytic metabolic requirements. The results show that rabbit renal proximal tubules in suspension are able to take up 125I-lysozyme, as well as RITC-lactalbumin. The fluorescent protein was taken up only by the ends of the everted tubule fragments, and accumulated into intracellular vesicles, demonstrating the luminal pathway of endocytosis. The amount of 125I-lysozyme taken up was equivalent to that taken up by isolated perfused tubules (Nielsen et al. (1986) Am. J. Physiol. 251, F822-F830). Anoxia decreased 12-fold the intracellular accumulation of 125I-lysozyme; however, the time-course of inhibition shows that only the late steps of endocytic accumulation are energy-dependent. Substrate deprivation studies suggest a specific role of glucose to sustain endocytosis. Lastly, renal uptake of 125I-lysozyme was shown to be strongly depressed by chloroquine, an alkalinizing agent of endosomes and lysosomes. We conclude that (1) renal tubules in suspension are a satisfactory model for endocytic studies in kidney; (2) suppressing oxygen and substrate supplies to kidney impairs endocytic tubular reabsorption of proteins.
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PMID:Protein endocytosis by a kidney tubule suspension: metabolic requirements. 829 19

We evaluated the effects of magnesium on extracellular dopamine (DA) and its metabolites in the striatum of 5-d-old rats submitted to 16 min of anoxia using microdialysis and HPLC. Rat pups were divided into three groups and received either 1) intrastriatal perfusion (IS) of MgSO4, 2) intraperitoneal injection (IP) of MgSO4, and 3) NaCl and Ringer's solution, respectively in place of MgSO4. After stabilization, Mg2+, saline, and Ringer's solution were administered; then, 114 animals were exposed to 100% nitrogen for 16 min. Anoxia induced a DA surge, an acutely marked increase of DA, in both the control and the IP group. In contrast, the DA surge was significantly suppressed in the IS group (p < 0.01, analysis of variance). During anoxia, the plasma Mg2+ in the IP group, but not in the IS group, maintained a significantly higher level compared with the basal level. On the other hand, Mg2+ in the perfusates in the IS group, but not in the IP group, maintained a significantly high level during anoxia. Alterations induced by anoxia in other metabolites, 3,4-dihydroxyphenylacetic acid, homovanillic acid, norepinephrine, and 5-hydroxyindole-3-acetic acid, did not significantly differ among the three groups. We propose that elevated levels of Mg2+ in the striatum had inhibitory effects on the DA surge during anoxia.
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PMID:Magnesium attenuates a striatal dopamine increase induced by anoxia in the neonatal rat brain: an in vivo microdialysis study. 916 93

In a previous communication we reported that glucose deprivation from KHRB medium resulted in a marked stimulation of Ca2+ uptake by brain tissue, suggesting a relationship between glucose and Ca2+ homeostasis in brain tissue. Experiments were carried out to investigate the significance of glucose in Ca2+ transport in brain cells. The replacement of glucose with either D-methylglucoside or 2-deoxyglucose, non-metabolizable analogues of glucose, resulted in stimulation of Ca2+ uptake just as by glucose deprivation. These data show that glucose metabolism rather than glucose transfer was necessary to stimulate Ca2+ uptake in brain tissue. Inhibition of glucose metabolism with either NaF, NaCN, or iodoacetate resulted in stimulation of Ca2+ uptake similar to that produced by glucose deprivation. These results lend further support for the concept that glucose metabolism is essential for Ca2+ homeostasis in brain. Anoxia promotes glucose metabolism through glycolytic pathway to keep up with the demand for ATP by cellular processes (the Pasteur effect). Incubation of brain slices under nitrogen gas did not alter Ca2+ uptake by brain tissue, as did glucose deprivation and the inhibitors of glucose metabolism. We conclude that glucose metabolism resulting in the synthesis of ATP is essential for Ca2+ homeostasis in brain. Verapamil and nifedipine which block voltage-gated Ca2+ channels, did not alter Ca2+ uptake stimulated by glucose deprivation, indicating that glucose deprivation-enhanced Ca2+ uptake was not mediated by Ca2+ channels. Tetrodotoxin which specifically blocks Na2+ channels, abolished Ca2+ uptake enhanced by glucose deprivation, but had no effect on Ca2+ uptake in presence of glucose (controls). These results suggest that stimulation of Ca2+ uptake by glucose deprivation may be related to Na2+ transfer via NaCa exchange in brain.
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PMID:Regulation of Ca2+ homeostasis by glucose metabolism in rat brain. 940 77

According to the anoxemia theory of atherosclerosis, an imbalance between the demand for and supply of oxygen and nutrients in the arterial wall is a key factor in atherogenesis. However, the energy metabolic state of the arterial tissue in vivo is largely unknown. We applied a bioluminescence method, metabolic imaging, to study local ATP concentrations in cryosections of normal pig and atherosclerotic and normal rabbit aorta. Some vessels were subjected to energy metabolic restrictions by incubation at different oxygen and glucose concentrations and others were rapidly frozen in liquid nitrogen to reflect the in vivo situation. Local ATP concentrations and the ATP distribution at a microscale was dependent on oxygen as well as glucose concentrations during incubation. ATP depletion was seen in the mid media of pig aorta in all incubations, but only at low oxygen concentration without glucose in the media of the thinner rabbit aorta. ATP-depleted zones were seen deep in pig media (>750 microm from the lumen) and in rabbit plaques (>300 micrometer+ from the lumen) even at high oxygen (pig 75% O2 and rabbit 21% O2) and glucose concentrations (5.6 mmol/L glucose). This observation probably illustrates an insufficient diffusion of glucose, which highlights the importance of studying the conditions for diffusion not only of oxygen but also of other metabolites in the arterial wall. In rapidly frozen vessels the medial ATP concentration was shown to be 0.6 to 0.8 micromol/g wet weight (both pig and rabbit aorta) and in pig aorta a gradient could be seen indicating higher ATP concentrations at the lumenal side. We propose that metabolic imaging, as applied to snap-frozen tissue, may be used to assess the energy metabolic situation in the arterial wall in vivo. The spatial resolution allows the detection of local variations within the arterial tree. However, steep concentration gradients (eg, near the border of the tissue) will be underestimated. The method may be extended to include determinations of glucose and lactate concentrations and will be used in parallel with an established method to assess hypoxia in the arterial wall in vivo.
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PMID:A bioluminescence method for the mapping of local ATP concentrations within the arterial wall, with potential to assess the in vivo situation. 1019 22

The role of ATP in anoxic activation of ATP-sensitive K+ (KATP) channels was studied in dorsal vagal neurons of mouse brainstem slices. In the whole-cell configuration, cyanide-induced chemical anoxia evoked within 10 s a 300-pA outward current that gave rise to a hyperpolarization of 24 mV. These responses were mimicked by nitrogen-aerated saline, rotenone or diazoxide and abolished by tolbutamide. The cyanide-induced hyperpolarization was due to activation of 70 pS K(ATP) channels that were half-maximally blocked by 5 microM internal ATP. Dialyzing the cells with either 1, 20 or 0 mM ATP did not, however, affect the time to onset, the kinetics or the magnitude of the cyanide-induced hyperpolarization. Impairment of ATP consumption by ouabain, vanadate or reduced temperature had no effect either. Thus, anoxia-induced activation of these KATP channels cannot be explained by a fall of cellular ATP or a concomitant rise of ADP. Anoxia-related changes of the actin cytoskeleton or the composition of the plasma membrane are also not likely to be involved, as cytochalasin D did not affect the cyanide-evoked hyperpolarization and phosphatidylinositol 4,5-bisphosphate failed to decrease the ATP sensitivity of single KATP channels. Finally, because of a lack of effects of reduced/oxidized glutathione and the oxidase blocker diphenyliodonium on the cyanide-induced hyperpolarization, cellular redox state does not appear to be involved. Our results indicate that despite a high sensitivity to ATP in excised patches, anoxic activation of KATP channels is independent of cellular ATP. Rather the ATP block seems to be removed as a consequence of impaired mitochondrial function.
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PMID:ATP-independent anoxic activation of ATP-sensitive K+ channels in dorsal vagal neurons of juvenile mice in situ. 1180 67


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