Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anoxia has been compared with ischaemia. The abrupt restoration of either oxygen of flow may accelerate cardiac damage. Anoxic stimulation of glycolysis (Pasteur effect) is inhibited during ischaemia by lactate and proton accumulation at the levels of phosphofructokinase and glyceraldehyde-3-phosphate dehydrogenase. Anaerobic glycolysis provides lactate and ATP; breakdown of the latter provides protons. During partial respiration thought to occur in partial ischaemia, continued production of CO2 is a factor contributing to intracellular acidosis; mitochondrial ATP when formed by continued respiration also yields protons when ultimately broken down. The endoproducts of aerobic glycolysis (pyruvate and NADH) are transported into the mitochondria by the malate-aspartate cycle and by pyruvate dehydrogenase activity. Adenine nucleotide transferase activity normally transfers the mitochondrially-made ATP to the cytoplasm, but acyl CoA accumulates in ischaemia (or during perfusions with high circulating free fatty acids) to inhibit the transferase. The mitochondrial creatine kinase is thought to transform ATP transported outwards into creatine phosphate which can permeate the outer mitochondrial membrane. Further compartmentation of ATP may be by other creatine kinase isoenzymes or in relation to the cell membrane. The glycogenolytic-sarcoplasmic reticulum complex links a glycogen pool to the sarcoplasmic reticulum. Cyclic AMP may regulate admission of calcium to the cell during the plateau of the action potential and promote calcium uptake by the sarcoplasmic reticulum by phosphorylation of phospholamban. The latter promotes the activity of the calcium-transport ATPase. Calcium and cyclic AMP may also interact at the level of the contractile proteins where cyclic AMP phosphrylates troponin. Cyclic GMP generally has opposite effects to cyclic AMP and undergoes opposite changes in the frog cardiac cycle to those of cyclic AMP. A present it is reasonable to suppose that physiological effects of adrenaline or of cholinergic agents on the myocardium are mediated by cyclic AMP or cyclic GMP, respectively, but this hypothesis still lacks firm support. There is an association between tissue cyclic AMP and ventricular fibrillation after coronary ligation, and direct evidence for a role of cyclic AMP in promoting arrhythmias has been obtained by studies on the ventricular fibrillation threshold in the rat heart. However, there are other mechanisms, involving first the effects of substrates on the action potential duration, and secondly, the fast channel, which can also give rise to the development of malignant arrhythmias.
 ...
PMID:Myocardial metabolism and heart disease. 3 41

1. The mechanisms responsible for the depolarization of the hepatocytes secondary to anoxia have been studied in isolated perfused dog liver. It was attempted to elucidate the role of the inhibition of the sodium pump following exhaustion of the energy reserves and of the modifications of membrane permeability. Anoxia was compared to ouabain and to a reduction of the cellular ATP level. 2. Membrane potentials were measured with micro-electrodes. Potassium, sodium and chloride were determined in plasma samples and liver tissues. Extracellular space was measured with tritiated inulin or with an electrical impedance method. Adenine nucleotides were also measured in liver biopsies. 3. The fall in membrane potential produced by administration of ouabain (0-1 mM) is greater than the effect of the redistribution of sodium + potassium ions; this suggests that the sodium pump is functioning, at least partially, electrogenically. The administration of dinitrophenol (10 mM), which causes a 74% fall in the ATP level in 15 min, produces, as does ouabain, a depolarization which also corresponds to stopping an electrogenic pump. 4. A partial reduction in the level of ATP brought about by hypoxia, by an inhibitor of cellular respiration, antimycin (10 mM), or by fructose (20 mM) results in a hyperpolarization which may be attributed to an elevation of potassium permeability (PK) since it is concomitant to a loss of K from the liver. The change in membrane permeability could be related to a rise in the free calcium in the cells which has not been documented. Other possible hypothesis include a facilitated transport for potassium. 5. The administration of amobarbitone (10 mM) produces immediately a depolarization which is independent of the progressive reduction in the level of ATP. The depolarization has been attributed to a direct effect of amobarbitone on the membrane reducing the permeability for potassium ions. 6. The depolarization observed in ischaemic anoxia is greater than that produced by ouabain for the same variation in ions concentration. In addition to a likely inhibition of the electrogenic sodium pump, changes in membrane permeability inducing a rise in the PNa/PK ratio must also occur. 7. After ischaemic anoxia for 24 hr at 3 degrees C, the ratio of PNa/PK rises to 0-68 which indicates abolishment of the selective character of membrane permeability. The augmentation in cell volume produced by anoxia might result in an opening of membrane pores, which could entail the augmentation of sodium permeability; the latter would be responsible in part for the depolarization produced by anoxia. 8. According to the severity and length of oxygen deprivation an increase in PK, a cessation of the sodium pump activity and finally an increase in PNa will occur.
 ...
PMID:Effect of anoxia and ATP depletion on the membrane potential and permeability of dog liver. 89 69

An inventory of hemodynamic and respiratory measurements was obtained in two patients with acute respiratory failure syndrome prior to and during venoarterial extracorporeal membrane oxygenation for study of oxygen transport. As the inspired oxygen concentration fraction was reduced from 1.0 to 0.5 and paO2 was increased from less than 50 to physiologic ranges during extracorporeal membrane oxygenation, tachycardia and pulmonary hypertension were reversed. Total oxygen transport was reduced rather than increased. Oxygen consumption and oxygen extraction were not altered during extracorporeal membrane oxygenation. However, a striking reduction was observed in cardiac output. After reversal of anoxemia, the total of the cardiac output of the patient and the extracorporeal membrane oxygenation flow were less than the cardiac output of the patient prior to extracorporeal membrane oxygenation. These observations provide evidence that the beneficial effects of extracorporeal membrane oxygenation stem, at least in part, from a reduction of the work load on the heart. Since high cardiac output failure is observed during progression of adult respiratory distress syndrome, mechanical support of circulation during extracorporeal membrane oxygenation may be of primary therapeutic benefit.
 ...
PMID:Oxygen transport during extracorporeal oxygenation for the treatment of adult respiratory distress syndrome. 98 47

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.
 ...
PMID:Relationship between oxygen tension, coronary vasodilation and prostaglandin biosynthesis in the isolated rabbit heart. 113 23

The effect of temporary glucose and oxygen deprivation on isometric tension as well as content of glycogen, creatine phosphate (CP), adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), and adenylate pool (AP) were studied in potassium-contracted guinea pig isolated taenia coli. Under aerobic conditions glucose removal caused a decrease in tension, glycogen, CP, ATP, and energy charge; ADP and AMP increased, keeping the adenylate pool size unchanged. During rigor caused by additional anoxia, there was an increase in tension associated with further decrease in ATP and marked reduction of adenylate pool. Restoration of oxygen supply caused only a small increase in ATP that, though sufficient for abolishing rigor, was insufficient to support potassium contraction. Restoration of both glucose and oxygen did not restore tension even though ATP stores were increased further. Elevation of extracellular calcium caused partial restoration of tension, suggesting that the defect was in calcium metabolism rather than energy metabolism. During recovery AP remained low, possibly due to deamination of AMP. Anoxia in the presence of glucose reduced ATP to a concentration similar to that due to aerobic glucose deprivation but tension decreased much less. This result is consistent with different degrees of ATP depletion in various functional (Ca pump vs. contractile mechanism) compartments.
 ...
PMID:Reversibility of mechanical and biochemical changes in smooth muscle due to anoxia and substrate depletion. 116 61

Canine vein strips were mounted for isometric tension recording. Anoxia did not affect basal tension of saphenous and pulmonary strips mounted in standard Krebs-Ringer solution or after 30 min of incubation in glucose-free solution. Anoxia depressed the strength of spontaneous contractions of mesenteric veins; in glucose-free solution (30 min), anoxia relaxed the strips. Veins placed in glucose-free solution for more than 60 min contracted with anoxia; this contraction was not inhibited by iproveratril. When the vein strips were contracted by norepinephrine or KCl, anoxia depressed the contractions, most in mesenteric and least in saphenous preparations; this depression was greater in the absence of glucose. When oxygen was present, the absence of glucose had little effect on the response to vasoactive agents. Contractions with acetylcholine were depressed by anoxia in mesenteric and pulmonary strips but were augmented in saphenous veins; the latter potentiation was inhibited by iproveratril and by incubation in glucose-free solution. Thus, especially in the saphenous vein, anaerobic glycolysis can provide most of the energy requirements, and intracellular substrates are available for oxidative metabolism.
 ...
PMID:Effects of anoxia and glucose depletion on isolated veins of the dog. 127 67

The effects were studied of hypoxia on intracellular ion activities in sheep heart Purkinje fibres. The intracellular pH (pHi), surface pH (pHs), intracellular potassium activity (aki), and intracellular sodium activity (aNai) of the cells were recorded using liquid ion exchanger-filled microelectrodes. Various methods of inhibiting oxidative phosphorylation were compared for their effect on pHi. These methods were the use of hypoxia, anoxia or NaCN (2 mM). Hypoxia was produced by degassing solutions under reduced pressure then bubbling with 100% nitrogen gas. Anoxia was produced in a similar manner but with the addition of the reducing agent sodium dithionite (0.5 mM) to remove all traces of oxygen from the solutions. Anoxia caused the most marked changes. Concentration of sodium dithionite between 0.1 and 1 mM produced similar maximum rates of acidification. High concentrations (5 or 20 mM) could produce larger intracellular acidifications apparently unrelated to anoxia. The effects of hypoxia and NaCN were similar. Inhibition of Na(+)-H+ exchange with amiloride (1 mM) had little effect on the pH changes produced by hypoxia. Periods of hypoxia exceeding 1 h still resulted in rapid, readily reversible changes in pHi. Hypoxia caused a rise in aNai, the effect being larger in anoxic conditions. The intracellular K+ activity decreased in hypoxia with further decreases in anoxic conditions. The intracellular ion changes produced during hypoxia are discussed in terms of the production of lactic acid by the cells and changes in the ATP supply to the Na(+)-K+ pump.
 ...
PMID:Intracellular pH changes induced by hypoxia and anoxia in isolated sheep heart Purkinje fibres. 131 38

Effect of the cessation of oxygen supply on cAMP content and neuronal spike activity (NSA) in the cortex brain was studied. The interruption of oxygen supply during in first decades of seconds evoked changes in the pattern of NSA, followed with the decrease of cAMP content (to 56 +/- 10%). Then the phase of neuronal hyperactivity and increase of cAMP level (to 198 +/- 26%) took place. The content of cAMP approximated the basal one in 2.5 min anoxia. Anoxia during 5 min resulted in direct opposite shifts of cAMP content in two groups of cats (an increase up to 223 +/- 11%, and decrease up to 75 +/- 8%, respectively, which correlated with individual features of NSA recovery in postanoxic period and values of cAMP basal level in the cortex of different animals. Upon 30 min reoxygenation after 2.5 min anoxia a decline of the content of cAMP (to 63 +/- 12%) accompanied enhance of NSA. This period of reoxygenation after 5 min anoxia demonstrated two types of reactions, observed in different groups of cats: the first type--NSA tended to normalization with the level of cAMP 44 +/- 8% below basal level, and the second type--insufficient recovery of NSA attended by value of cAMP 90 +/- 13% above basal level.
 ...
PMID:[Anoxia-induced changes in cAMP contents in the cat cerebral cortex]. 133 96

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.
 ...
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.
 ...
PMID:Role of the epithelium in the control of intestinal motility: implications for intestinal damage after anoxia and reoxygenation. 141 84


1 2 3 4 5 6 7 8 9 10 Next >>