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

Left coronary arteriography and left coronary artery injections of Tyrode's solution and glucose solutions were performed in 12 anesthetized dogs. The contrast medium was found to prolong the conduction time through the AV junctional tissue and through the most distal part of the conduction network as verified by His-bundle electrogram and by surface ECG (lead II). The results indicate that for evaluation of the effects on conductivity of various media, it is most reliable to measure the altered conduction velocity in the AV nodal region. The prolongation of conduction time produced by contrast medium explains heart conduction blocks and may contribute to the genesis of ventricular fibrillation, frequent complications to coronary arteriography. The data suggest that anoxemia does not cause this delayed conduction. Hyperosmolarity contributes to the alterations of the conductivity, but the ionic composition and anion toxicity of the contrast medium also may be of importance.
 ...
PMID:Mechanism of production of cardiac conduction abnormalities due to coronary arteriography in dogs. 100 11

1. The ventricular fibrillation threshold (VFT) was measured in the isolated heart of the rabbit perfused via the aorta with McEwen's solution at 37 degrees C by applying a single 10 ms pulse of current during the vulnerable period of late systole. The arrhythmia induced was either fibrillation or a rapid tachycardia. 2. Gassing the McEwen's solution with 5% CO2 in N2 (anoxia) instead of with carbogen caused a negative inotropic and chronotropic effect and significantly lowered the VFT. Although anoxia releases noradrenaline from the heart the effect of anoxia on the VFT was not prevented by beta-adrenoceptor blockade with propranolol or pindolol or by previous treatment with reserpine. 3. Perfusion with adenosine (5 muM) which is released from the heart muscle by anoxia, or with dipyridamole (10 muM) which protects the adenosine from binding or destruction by the tissues, or with both combined failed to alter the VFT significantly. Furthermore neither adenosine nor dipyridamole significantly altered the effect of anoxia on the VFT. 4. Anoxia, adenosine and dipyridamole significantly increased the duration of the induced arrhythmia when compared with that of the controls. 5. Anoxia and adenosine significantly shortened the vulnerable time, i.e., the minimal time after the R-wave of the ECG at which the pulse had to be applied to induce the arrhythmia. 6. Perfusion with the McEwen's solution gassed with 5% CO2 in air (hypoxia) significantly lowered the VFT but the effect was not as great as with anoxia. Isoprenaline when infused lowered the VFT but this effect was not potentiated by hypoxia. 7. The results indicate that (a) anoxia lowers the VFT in the perfused isolated heart of the rabbit and that this effect is not due to adenosine or noradrenaline released by the anoxia and (b) hypoxia does not sensitize the heart to the arrhythmic effect of isoprenaline.
 ...
PMID:The effect of anoxia on the ventricular fibrillation threshold in the rabbit isolated heart. 117 59

In the isolated rat heart, anoxia or ischemia do not induce important ventricular tachyarrhythmias (VTAs). During the 1st min of reperfusion, VTAs are frequent. The frequency and severity of VTAs during reperfusion depend on the duration and the extent of the myocardial damage. Anoxia abolishes reperfusion-induced VTAs as did verapamil (2.5 X 10(-6) M). In isolated guinea pig hearts, beta-methyldigoxin (1.27 X 10(-6) M) provokes VTAs that are progressively increasing in severity. After 26 min of perfusion with an oxygenated beta-methyldigoxin-containing medium, all isolated guinea pig hearts develop ventricular fibrillation. By changing the abnormal rapid ventricular rhythms into progressively slower irregular idioventricular rhythm, anoxia counteracts all types of VTAs exhibited by the intoxicated guinea pig hearts. In conclusion, two conditions seem to be necessary for the development of VTAs during the reperfusion: 1) a sufficient degree of myocardial damage provoked by the preceding ischemic perfusion, and 2) the presence of oxygen during the reperfusion.
 ...
PMID:Inhibitory effect of anoxia on reperfusion- and digitalis-induced ventricular tachyarrhythmias. 723 32