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ventricular fibrillation/хипоксия
Линкът е запазен в клипборда
Страница 1 от 195 резултата
Antiarrhythmic agent, MS-551, protects against pinacidil + hypoxia-induced ventricular fibrillation in Langendorff-perfused rabbit isolated heart.
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We studied the electrophysiologic and antifibrillatory effects of the class III agent MS-551 in a rabbit isolated heart model in which ventricular fibrillation (VF) occurs reproducibly under conditions of hypoxia/reoxygenation in the presence of the ATP-dependent potassium channel opener, pinacidil.
Metabolic consequences and predictability of ventricular fibrillation in hypoxia. A 31P- and 23Na-nuclear magnetic resonance study of the isolated rat heart.
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BACKGROUND
Ventricular fibrillation has deleterious metabolic and functional consequences for the heart. This study had two purposes: first, to define the effects of ventricular fibrillation during hypoxia on energy metabolism and accumulation of intracellular Na+ and, second, to test whether the
The protective effect of H2-receptor activation against the duration of myocardial hypoxia/reoxygenation-induced ventricular fibrillation in sensitized guinea-pig hearts.
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Patients with high serum immunoglobulin E levels were reported to be protected against sudden death during acute myocardial infarction. The protection mechanism might be attributed to the facilitation of histamine release from sensitized mast cells; however, this remains to be clarified. In this
Effect of Ado A1- and A2-receptor activation on ventricular fibrillation during hypoxia-reoxygenation.
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We examined the hypothesis that adenosine (Ado)-induced alterations in ventricular electrophysiology may contribute to arrhythmogenesis in a setting of myocardial hypoxia through activation of Ado A1 and A2 receptors in the rabbit isolated perfused heart. There was a 20% incidence of ventricular
The effect of anoxia on the ventricular fibrillation threshold in the rabbit isolated heart.
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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
Physical training increases ventricular fibrillation thresholds of isolated rat hearts during normoxia, hypoxia and regional ischemia.
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The effect of exercise training on cardiovascular mortality is controversial. The purpose of this study was to determine the effect of a period of treadmill training on the ventricular fibrillation threshold of the isolated rat heart. Trained hearts had higher threshold values during standard,
[Histoxic hypoxia as one of the causes of ventricular fibrillation and decreased myocardial contractility].
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Long-lasting infusions of adrenalin were demonstrated to result in histotoxic hypoxy of the myocardium and its decreased contractility. After a preliminary ligation of several branches of the coronary arteries such situations often caused ventricular fibrillation. The restoration of the myocardial
The effect of bupivacaine on myocardial tissue hypoxia and acidosis during ventricular fibrillation.
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Previously we observed that during bupivacaine-induced circulatory collapse, myocardial tissue pH declined more slowly than expected. Here we evaluated the effect of bupivacaine on myocardial acidosis induced by ventricular fibrillation. Sixteen dogs were anesthetized with 1.5% end-tidal isoflurane,
Anoxia and ventricular fibrillation; with a summary of evidence on the cause of fibrillation.
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Experiments are described showing that ventricular fibrillation is more readily produced in isolated rabbit hearts by electrical stimulation when the oxygen supply to the heart is reduced. This evidence completes investigations which have been made into factors affecting the production of
Ventricular fibrillation during uniform myocardial anoxia due to asphyxia.
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Transient ventricular fibrillation; the effects of gradually induced oxygen deficiency on patients with transient ventricular fibrillation and on patients with periodic standstill of the ventricle.
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[The behavior of the intracellular magnesium concentration in the myocardium in insufficiency, hypoxia and ventricular fibrillation].
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Comparison of myocardial anoxia and plasma flow in the etiology of ventricular fibrillation.
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The influence of hyperbaric oxygen and of hypoxia on the ventricular fibrillation threshold.
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Role of acute myocardial hypoxia and ischemic-nonischemic boundaries in ventricular fibrillation.
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