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

The effect of severe anoxia produced by gassing with 100% nitrogen on gastric mucosal permeability and hydrogen ion back diffusion was investigated using an in vitro preparation of rabbit fundic gastric mucosa mounted in an Ussing chamber. Permeability was estimated by determination of the flux of the water soluble, nonlipidsoluble molecule erythritol from the mucosal to serosal solution. The flux rate across normal tissue was 2.80 plus or minus 0.41 pmoles/cm-2/sec, and rose to 3.32 plus or minus 0.57 pmoles/cm-2/sec after 2 hr of severe anoxia. Hydrogen ion ack diffusion was measured by determining with a pH stat the amount of hydrogen required to maintain the [H+] of the mucosal solution at 0.1, 1.0, 2.0 and 3.2 mEq/L in both normal and anoxic tissues. One hour of anoxia increased the back diffusion of H+, but the changes only became statistically significant at all pH values after 1.5 hr. Anoxia did however cause an immediate fall in potential difference to zero, and a rise in resistance which after 30 min fell progressively to preanoxic levels. Anoxia produces a small increase in gastric mucosal, permeability, an effect which may be enhanced by other factors.
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PMID:Effect of severe anoxia on the permeability of gastric mucosa (38517). 23 69

The characteristics of normal thiamine transport across the intestine were studied in rats using intact intestinal loops and everted jejunal segments. In vivo studies with [35-S]-thiamine hydrochloride revealed, in all segments of small intestine, saturation kinetics for low thiamine concentrations (0.06 to 1.5 muM), but a linear relationship between high concentrations (2 to 560 muM) and absorption. Moreover, in vitro studies of net transmural flux using everted jejunal sacs demonstrated movement of [14-C]-thiamine hydrochloride against a concentration gradient only when low, but not when high, thiamine concentration was used, so that the serosal to mucosal ratio became significantly greater than the initial value of one. Pyrithiamine, 2 muM, dinitrophenol, 200 muM, norethylmaleimide, 100 muM, and ouabain, 10 muM, reduced the net transmural flux of 0.2 muM thiamine. In contrast, these inhibitors had no effect on 20 muM thiamine. When unidirectional flux across the jejunum was measured, saturation kinetics was again demonstrated for low thiamine concentrations. This phenomenon, however, was abolished by the addition of pyrithiamine, which exerted competitive inhibition on thiamine absorption. Anoxia and sodium lack reduced intestinal uptake of 0.5 muM thiamine to 58% and 74% of normal, respectively, but did not affect uptake of 50 muM thiamine. Lowering the marked with low thiamine concentrations (O10, 1.648) than with high concentration (Q10, 1.127). Stirring of the water layer reduced Km to 59% of unstirred value, while Vmax and permeability coefficient remained unchanged. Finally, movement of low concentration thiamine against an electrical gradient was observed under conditions of electrical short circuiting and zero potential difference. In contrast, no such effect was seen with high concentrations. These studies suggest that there exists in the rat a dual system of intestinal thiamine transport. At low concentrations, thiamine is absorbed by an active process; at high concentrations, transport across the intestine is largely a passive movement.
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PMID:Thiamine transport across the rat intestine. I. Normal characteristics. 112 98

Sheets of mucosa from the jejunum of healthy horses were mounted in incubation chambers and bathed with Krebs-Ringer bicarbonate solution. Changes in tissue function and histologic appearance were compared after the following conditions: (1) control conditions for 30 minutes with 95% O2/5% CO2 in the gas phase; (2) same conditions as control, except incubation with superoxide dismutase (300 U/ml) during the last 18 minutes; (3) anoxia for 15 minutes with 95% N2/5% CO2, followed by reoxygenation for 15 minutes; (4) same conditions as 3, except incubation with superoxide dismutase during reoxygenation; and (5) anoxia for 30 minutes. Anoxia reduced the accumulation of radiolabeled L-alanine and caused cell swelling, as indicated by an increase in tissue water and tissue Na contents. Reoxygenation improved the tissue's ability to accumulate L-alanine, but tissue swelling continued after this treatment. Tissue Na content and L-alanine accumulation were restored to control values by reoxygenation with superoxide dismutase in the bathing medium. The grade of structural damage, as indicated by separation of epithelial cells from villi, was equally severe after all, but control, conditions. Superoxide dismutase had no effect on the tissue control conditions. Results of this study suggest that superoxide radicals are involved in the pathogenesis of reperfusion injury in equine jejunal mucosa and that this may be of clinical importance in cases of small intestinal strangulation obstruction.
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PMID:Effects of superoxide dismutase on injury induced by anoxia and reoxygenation in equine small intestine in vitro. 178 22

Crucian carp (Carassius carassius L.), which are extremely anoxia-tolerant, were exposed to 17 days of anoxia at 8 degrees C. One group of fish was transferred to normoxic water for 1-8 h immediately after the anoxic period. All the eight amino acids measured in brain (including four putative neurotransmitters) were more or less strongly affected by anoxia. Gamma-aminobutyric acid (GABA) displayed a nearly fivefold increase during anoxia. It is hypothesized that the increased level of this inhibitory transmitter, maybe in combination with the decrease seen in excitatory amino acids (glutamate and aspartate), causes a lowered brain activity and, hence, is a key factor behind the decrease in physical activity and systemic energy metabolism seen in anoxic Carassius. The brain levels of serotonin, dopamine and norepinephrine were remarkably well preserved after anoxia (although their synthesis is oxygen-dependent), suggesting adaptive mechanisms. However, anoxia reduced the norepinephrine level in kidney (chromaffin tissue) by 92% and, in contrast to previous results on shorter anoxic periods (3-7 days), the peripheral catecholamine store showed little sign of recovery during the subsequent normoxia. Anoxia was found to deplete the liver glycogen store severely, and the few fish that died after 15-17 days of anoxia contained no detectable liver glycogen.
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PMID:Long-term anoxia in crucian carp: changes in the levels of amino acid and monoamine neurotransmitters in the brain, catecholamines in chromaffin tissue, and liver glycogen. 197 85

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

1. The effect of hypoxia on synaptic transmission between hair cells and afferent fibers was examined in the sacculus of goldfish. For this, we recorded potentials, intracellularly, from large afferent fibers. Anoxia was introduced by perfusing the gill with water deprived of oxygen or by halting the water flow to the gill. 2. The ear of the goldfish is most sensitive to hypoxia. Sound-evoked afferent activities were profoundly depressed within several minutes after the introduction of hypoxia. 3. The depressed afferent activity was attributed to a reduction in the amplitude of sound-evoked excitatory postsynaptic potentials (EPSPs) generated at afferent fiber terminals, since no significant change was detected in the resting and action potentials of afferent fibers or in intensity of the threshold current required to set up an action potential. Also, there was no marked change in the electrical activity of hair cells, determined by the finding that the amplitude of intramacularly recorded microphonic potentials and that of the coupling potentials was not altered. 4. A statistical analysis of the amplitude of sound-evoked EPSPs revealed that the binomial parameter n decreased during hypoxia, in parallel with a reduction in the amplitude of EPSPs, while the binomial parameter p either remained unaltered or was augmented. No change was found in the quantal size, thereby indicating that the sensitivity of the postsynaptic membrane remained unchanged. These results indicate that presynaptic mechanisms within hair cells, especially those playing a role in transmitter release or in replenishment of the latter, are suppressed during hypoxia.
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PMID:High susceptibility to hypoxia of afferent synaptic transmission in the goldfish sacculus. 282 17

1. A system is described for simultaneously measuring the respiration and the reflectance of a tissue slice and is applied to a study of guinea-pig cerebral cortical slices.2. Reducing bathing medium osmolarity led to a reversible decrease in reflectance of these slices (as well as slices from liver and kidney cortex). In half isotonic solutions reflectance was reduced by 31%.3. Anoxia led to a decreased reflectance which was eliminated if all the Cl was substituted by the larger glucuronate anion.4. It is concluded that slice reflectance is lowered when cellular volumes are increased by water or isotonic solution influx.5. Membrane depolarization effected by ouabain, high (60 mM) K bathing medium, veratridine or repeated electrical pulses led to rapid decreases in reflectance of 25, 27, 31 and 7.5% respectively. Turning off the electrical pulses caused reflectance to return to control values. Reversibility of the chemical effectors was not tested.6. Substitution of Cl by glucuronate abolished the reflectance changes, although it did not inhibit the increased respiration induced by the depolarizing stimuli.7. Tetrodotoxin abolished both the respiratory and reflectance effects of veratridine and electrical pulses but had no effect upon those of high K or ouabain.8. The decrease in reflectance began about 1 sec after initiation of the pulses and was half maximal by 8 sec.9. Titrating reflectance against [K] showed that an increase of 5 mM-K led to a 4% decrease in reflectance and that reflectance became minimal between 60 and 80 mM-K(+).10. It is concluded that membrane depolarization in excitable cells of the cerebral cortex (and also, possibly, in the glia) causes rapid increases in cell volume due to influx of isotonic solution.11. The results indicate, more specifically, that changes in intercellular K concentrations of size and duration thought to occur following nervous activity in the C.N.S. cause cell volume changes large enough to drastically reduce the intercellular volumes and so, transiently, increase extracellular molecular and ionic concentrations. Increases of extracellular [K] and [Ca] have significant effects upon synaptic transmission and upon spontaneous nervous activity. It is suggested that nervous activity in one cell (or portion of it) might, in this way, strongly influence function in neighbouring elements.
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PMID:Effects of membrane depolarization on light scattering by cerebral cortical slices. 435 67

The effects of medium K+ concentration on the tissue uptake of p-aminohippurate (PAH) were investigated in rat kidney cortex slices. K+ concentration in the incubation medium was changed in the absence of Na+. Increase in K+ concentration up to 145 mM revealed an augmenting effect on PAH uptake when tissue water content was controlled at about 72% by elevating medium osmolarity with mannitol. The K+-induced enhancement of PAH uptake was almost completely abolished by the simultaneous presence of extremely high concentration of hippurate. Anoxia reduced this augmenting effect. Pyruvate added to the medium scarcely affected this augmenting effect. The uptake rate during the initial 10-min incubation increased linearly in proportion to the increase in log [K]o/[K]i. The results suggest that high medium K+ concentration stimulates PAH transport by a carrier-mediated process which is dependent on oxidative metabolism. However, the mode of action of K+ on PAH uptake seems to be different from that of Na+. It seems likely that K+ exerts its effect on PAH transport by the alteration of the peritubular membrane potential.
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PMID:Effect of potassium on p-aminohippurate transport in rat kidney cortex slices. 707 54

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

1. Ion and water content of goldfish intestinal mucosa, stripped free from muscular layers were measured under various incubation conditions. 2. Ouabain induces an increase in cation content that is electrically compensated for by chloride. The increase in solute content is accompanied by an increase in water content. 3. When extracellular chloride is partially replaced by sulphate, ouabain does induce cell shrinkage. 4. Anoxia induces a rapid increase in cell volume that is restored by oxygenation of the incubation solution. Ouabain prevents the restoration of volume. 5. It is concluded that the classical ouabain-sensitive Na/K pump participates in the maintenance of cellular volume. We suggest that the constancy in volume after ouabain poisoning as is reported for many tissues might be due to a low chloride conductance of its membranes. 6. Anisotonic media (range: 0.6-1.2 isotonicity), made by variation on mannitol concentration, induce changes in cell water content that deviates from the simplified van't Hoff equation by about 10%. No change in water content after the initial increase was found. 7. We conclude that goldfish enterocytes do not possess a mechanism for rapid volume readjustment.
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PMID:Cell volume regulation in goldfish intestinal mucosa. 732 33


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