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

In isolated perfused rabbit hearts, coronary vasodilation, produced by reduced oxygen tension seems to be independent of myocardial prostaglandin biosynthesis. a) Anoxia (N2: CO2 95: 5 %) produced coronary vasodilation without causing prostaglandin-like substance (PLS) biosynthesis and release; b) the decrease in coronary resistance during hypoxia (N2:02:CO2 - 80:15:5 %) was sustained during myocardial perfusion with the low oxygen media despite the transitory nature of its PLS release; and c) indomathacin, which abolished basal or ADP stimulated myocardial PLS release, did not abolish the coronary vasodilation produced by ischemia, hypoxia, or anoxia.
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PMID:Relationship between oxygen tension, coronary vasodilation and prostaglandin biosynthesis in the isolated rabbit heart. 113 23

The present study provided a model with which the kinetics of CK release in the early phase of reperfusion was investigated. By using Langendroff method the isolated rat heart was first perfused for 10 min for establishing equilibrium, then stopped for 10 min to establish global ischemia, and finally followed by reperfusion for sample collection in every 15 s for the measurement of CK activity (U/L) as an index of cellular damage. A characteristic biphasic release of CK was shown under condition of 3 min reperfusion with Krebs-Henseleit (K-H) solution without glucose. The 1st peak of CK release appeared abruptly in the first 15 s of reperfusion and the 2nd one, during 120-180 s of reperfusion. The appearance of the 2nd peak was shifted to 30-75 s by adding glucose (11.1 mmol/L) into the perfusate. The 1st peak mainly reflects ischemic injury while the 2nd represents reperfusion injury. Anoxia (95% N2 + 5% CO2) or glucose addition may delay or decrease both peaks, but low Ca2+ (0.05 mmol/L) only delays the appearance of the 2nd peak to 3 min. The results suggest that the oxygen paradox rather than calcium paradox is involved in both phases of CK release. As for low Ca2+ decreasing the 2nd peak may be attributed to its effect of reducing Ca2+ inflow and overload injury secondary to oxygen paradox.
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PMID:[The biphasic creatine kinase release from isolated rat heart induced by global ischemia and early period of reperfusion]. 133 13

A vibration technique was used to dislocate the epithelium from the rat small intestine, in order to study the possible regulatory role of the epithelium on intestinal motility. Complete removal of the epithelium led to a slightly potentiated contraction of the longitudinal smooth muscle by the muscarinic agonist methacholine (pD2. 6.5 +/- 0.1 vs. 6.2 +/- 0.2). The maximal beta-adrenergic response expressed relative to the relaxation by 0.5 mM dibutyryl cyclic AMP increased from 55.9 +/- 9.0% to 72.6 +/- 9.1% by this treatment. Efforts were made to relate these observations to the endothelium-dependent relaxation in blood vessels, but no indication was found for a similar mechanism in the small intestine. Not only mechanical dislocation can be employed to affect the mucosal layer, but also intestinal ischemia has been reported to lead to mucosal damage. In this study we mimicked ischemia by applying in vitro anoxia and subsequent reoxygenation to isolated intestinal segments. When intestinal segments are isolated and kept in physiological buffer, xanthine dehydrogenase is converted slowly to xanthine oxidase, irrespective of whether the buffer is oxygenated or not. No evidence was found for oxygen radical damage after anoxia and reoxygenation. However, the intestinal mucosa was damaged both after normoxia, and after anoxia and reoxygenation. Anoxia and subsequent reoxygenation did not affect muscarinic contraction, but slightly increased the beta-adrenergic relaxation, which partly correlates with the effects of mechanical dislocation of the epithelium. The increased sensitivity of the smooth muscle after epithelial damage might be involved in motility changes during intestinal inflammatory diseases.
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PMID:Role of the epithelium in the control of intestinal motility: implications for intestinal damage after anoxia and reoxygenation. 141 84

The effect of anoxia and reoxygenation on the synthesis and secretion of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) was studied in primary cultures of human umbilical vein endothelial cells. Sublethal anoxia, determined by trypan blue dye exclusion and lactate dehydrogenase release, was produced by cell culture under a 95% N2, 5% CO2 atmosphere for 2-24 h and was followed by reoxygenation with 95% air, 5% CO2 for 24 or 48 h. Anoxia did not alter the levels of mRNA for t-PA or PAI-1 in the cells or the secretion of t-PA or PAI-1 into the medium. At 24 h, t-PA secreted into conditioned medium was 7.0 +/- 1.4 ng/2 x 10(6) cells (n = 9) and PAI-1 was 300 +/- 13 IU/2 x 10(6) cells (n = 9), whereas the content of t-PA mRNA was 2.2 pg/micrograms of RNA and PAI-1 mRNA was 180 pg/micrograms of RNA. During reoxygenation, however, t-PA antigen and PAI-1 activity as well as mRNA for PAI-1 decreased proportionally to the duration of anoxia, to reach 27 +/- 1.0, 49 +/- 2.0, and 47 +/- 14% of control values, respectively, within 24 h of anoxia. t-PA mRNA also decreased significantly during reoxygenation following anoxia, but the extent could not be accurately quantitated. Addition, during anoxia, of a 200 micrograms/ml concentration of the superoxide anion radical scavenger superoxide dismutase or of a 5 mM concentration of the iron chelator deferoxamine mesylate prevented the subsequent decrease of t-PA antigen during reoxygenation; addition of these compounds during reoxygenation had no effect. Superoxide dismutase, but not deferoxamine mesylate, when added during anoxia prevented the subsequent decrease in PAI-1 activity. These studies suggest that the marked alteration of endothelial cell fibrinolysis during anoxia followed by reoxygenation is most likely mediated by a mechanism dependent on oxygen radicals. Impaired endothelial cell fibrinolysis may contribute to the pathophysiology of ischemia/reperfusion injury.
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PMID:Oxygen radicals generated during anoxia followed by reoxygenation reduce the synthesis of tissue-type plasminogen activator and plasminogen activator inhibitor-1 in human endothelial cell culture. 212 75

Magnetic resonance spectroscopy is able to measure noninvasively a variety of important metabolites involved in cell energetics. These include phosphocreatine, ATP, inorganic phosphate, pH, and lactate. Anoxia, ischemia, and infarction produce rapid loss of high-energy phosphates and accumulation of hydrolysis products. Many animal studies have shown that MRS monitors metabolic changes in various models of human disease. The availability of large, high field magnets and the development of noninvasive localization techniques permits MRS to be performed on selected volumes within the body. It is now clear that MRS in humans will be immediately useful in several areas including studies of malignancy, ischemia, and infarction of various organs and metabolic disorders. It is expected that human MRS will be increasingly used for clinical investigation and eventually for medical diagnosis.
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PMID:NMR spectroscopy for clinical medicine. Animal models and clinical examples. 332 57

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

We investigated the effects of anoxia and ischemia on thallium (201Tl) exchange using isolated rabbit interventricular septa. Anoxia for 20 or 40 min caused a decrease in 201Tl tissue uptake due to an increased efflux of 201Tl with a smaller increase in 201Tl influx. Between 40 and 60 min of anoxia, the increased efflux of 201Tl was reversed and the increase in 201Tl influx was absent. After 60 min of reoxygenation, septa made anoxic for 20-60 min recovered at least 95% of the Tl lost. Mechanical recovery, however, was still significantly depressed. Reperfusion after total ischemia for 20-60 min was followed by resumption of 201Tl uptake despite continued mechanical dysfunction. Efflux rates during reperfusion after ischemia were significantly different from preischemic values but not in a predictable way. This unpredictability complicates interpretation of clinical 201Tl redistribution studies. These results represent important differences from those reported previously using 42K [Am. J. Physiol. 232 (Heart Circ. Physiol. 1): H85-H94 and H564-H570, 1977]. Anoxia did not increase the influx of 42K. Also, 60 min of ischemia resulted in progressive losses of 42K. This implies there are different sensitivities and/or mechanisms for Tl compared with K uptake. Our results are consistent with 201Tl uptake by severely damaged and nonviable cells.
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PMID:Effects of anoxia and ischemia on thallium exchange in rabbit myocardium. 403 8

The effect of anoxia and ischemia on the release of amino acid transmitters from cerebellar slices induced by veratridine or high [K+] was studied. Synaptic specificity was tested by examining the tetradotoxin (TTX)-sensitive and the Ca2+-dependent components of stimulated release. Evoked release of endogenous amino acids was investigated in addition to more detailed studies on the stimulated efflux of preloaded [14C]GABA and D-[3H]aspartate (a metabolically more stable anologue of acidic amino acids). [14C]GABA release evoked by either method of stimulation was unaffected by periods of up to 35 min of anoxia and declined moderately by 45 min. In contrast, induced release of D-[3H]Asp increased markedly during anoxia to a peak at about 25 min, followed by a decline when anoxia was prolonged to 45 min. Evidence was obtained that the increased evoked efflux of D'[3H]Asp from anoxic slices was not due to impaired reuptake of the released amino acid and that it was completely reversible by reoxygenation of the slices. Results of experiments examining the evoked release of endogenous amino acids in anoxia were consistent with those obtained with the exogenous amino acids. Only 4 of the 10 endogenous amino acids studied exhibited TTX-sensitive veratridine-induced release under aerobic conditions (glutamate, aspartate, GABA, and glycine). Anoxia for 25 min did not affect the stimulated efflux of these amino acids with the exception of glutamate, which showed a significant increase. Compared with anoxia, effects of ischemia on synaptic function appeared to be more severe. Veratridine-evoked release of [14C]GABA was already depressed by 10 min and that of D-[3H[Asp showed a modest elevation only a 5 min. Stimulated release of D-Asp and labelled GABA declined progressively after 5 min. These findings were compared with changes in tissue ATP concentrations and histology. The latter studies indicated that in anoxia the earliest alterations are detectable in glia and that nerve terminals were the structures by far the most resistant to anoxic damage. The results thus indicated that evoked release of amino acid transmitters in the cerebellum is compromised only by prolonged anoxia in vitro. In addition, it would appear that the stimulated release of glutamate is selectively accentuated during anoxia. This effect may have a bearing on some hypoxic behavioral changes and, perhaps, also on the well-known selective vulnerability of certain neurons during hypoxia.
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PMID:Effects of anoxia on the stimulated release of amino acid neurotransmitters in the cerebellum in vitro. 612 87

The early stages of anoxemia and ischemia are associated with highly selective, reversible defects in sarcolemmal ionic exchange of potassium not necessarily the result of impaired sodium pump function. At a later stage structural defects in the membrane led to irreversible loss of intracellular potassium and creatine kinase. Similar stages can be demonstrated in the sarcolemmal selectivity for divalent cations. The degree of sarcolemmal injury from ischemia can be significantly influenced by the conditions of reperfusion. Reduced calcium content of blood reperfused for only 5 minutes can improve the mechanical recovery of ischemic rabbit ventricle. The influx of calcium during reperfusion impairs those processes required for restoration of sarcolemmal integrity.
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PMID:Myocardial ischemia: ionic events in ischemia and anoxia. 625 41

We investigated differences between ischemic and anoxic myocardium with respect to early mechanical and metabolic changes. Ischemia and anoxia were induced in the area perfused by the distal left anterior descending artery in 32 mongrel dogs. Since both the ischemia and the anoxia in this preparation resulted in very little change in global cardiac hemodynamics, indirect mechanical and metabolic effects on the involved myocardium were minimal. However, regional anoxia caused a later development of a myocardial systolic bulge than did regional ischemia (44.8 +/- 13.6 vs 26.8 +/- 9.9 sec). Myocardial ATP content was reduced to the same level 5 min after the onset of ischemia and anoxia. Anoxia with high K+ did not result in an earlier myocardial systolic bulge time, but myocardial ATP was maintained at a higher level than during ischemia. Anoxia with low pH also did not affect the time for development of a myocardial systolic bulge. We concluded that neither acidosis nor hyperpotassemia are more causally related to the earlier development of a myocardial systolic bulge during regional ischemia than during regional anoxia. Also the absolute value of myocardial ATP content is unlikely to be causally related to the determination of myocardial contraction, as reflected by the development of a myocardial systolic bulge.
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PMID:Different effects of acute ischemia and anoxia on the canine myocardium. 651 94


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