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atrioventricular block/hypoxia

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Slices from control C57, mdx, and mdx3cv mice were made hypoxic until both field excitatory postsynaptic potential (fEPSP) and presynaptic afferent volley (AV) disappeared (H1). After reoxygenation and recovery of fEPSP, a second and longer hypoxic test (H2) lasted 3 minutes beyond the time required

Enhanced arrhythmogenicity of Freon 113 by hypoxia in the perfused rat heart.

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The interaction of Freon 113 (1,1,2-trichloro-1,2,2-trifluoroethane) and hypoxia on the heart conduction system was studied using electrocardiogram monitoring of isolated perfused rat hearts. Freon 113 (0.2 mM) alone elicited significant atrioventricular conduction delay (p less than 0.05) and heart
Differentiation between cardiac and neurological origin of syncope may be challenging. Prolonged cerebral hypoxia secondary to cardiac arrhythmias may lead to epileptic seizures. Moreover, partial epileptic seizures by themselves can trigger cardiac arrhythmias. Herein, we present a case of partial

[Patent foramen ovale presented hypoxemia with cardiac sarcoidosis].

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A 53-year-old woman with a double, double, double (DDD) pacemaker due to complete atrioventricular block was admitted to our hospital with a diagnosis of congestive heart failure. At the time of admission, she was in a hypoxic state with cyanosis and clubbed finger. The ultrasonic cardiogram showed
This study examined the effects of quinacrine on the functional and electrophysiological responses of isolated guinea pig hearts and isolated canine papillary muscle and Purkinje fibre preparations. A dose-response relationship for quinacrine (0.01-10.0 micrograms/mL) was studied in isolated guinea

Developmental changes in cardiac recovery from anoxia-reoxygenation.

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The developing cardiovascular system is known to operate normally in a hypoxic environment. However, the functional and ultrastructural recovery of embryonic/fetal hearts subjected to anoxia lasting as long as hypoxia/ischemia performed in adult animal models remains to be investigated. Isolated
Tissue concentrations of adenosine, an endogenous metabolite with negative chronotropic and dromotropic actions, are known to increase when myocardial oxygen supply is reduced. In this study the concentrations of endogenous adenosine released during a period of hypoxic perfusion were measured to
OBJECTIVE The aim was to study the mechanism of global hypoxia induced atrioventricular (AV) nodal conduction block in vivo using a guinea pig model. METHODS Animals subjected to 10 min periods of global hypoxia, induced by decremental changes in O2 content in the inhaled gas mixture, were randomly
Adenosine levels in oxygen-deprived myocardium can rise to 10- 100 microM concentrations known to cause atrioventricular (AV) conduction delay and block. We reported that the AV conduction delay and block caused by hypoxia is markedly attenuated by 10 microM aminophylline, and adenosine competitive
The influence on the cardiac stimulation threshold of changes in the myocardial intra/extracellular potassium ratio induced with ouabain and hypoxia was investigated in 9 dogs with total atrioventricular block. In spite of significant elevations of extracellular potassium and reductions of

Role of aminophylline in atropine resistant atrioventricular block.

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Atrioventricular (AV) block may be induced by ischaemia as a result of production of adenosine, a metabolite that accumulates during hypoxia and ischaemia. Adenosine antagonism has been shown to reverse experimental AV node block in dogs. Recently, theophylline has been shown to be highly effective

Changes in the fetal heart rate and ECG during hypoxia.

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Previous reports on the fetal hypoxic bradycardia in animals have indicated, that there is vagal influence, especially when asphyxia is induced by umbilical cord occlusion. In the present study hypoxia was induced via the mother, thus keeping the fetal circulation intact. The experiments were
Hypoxia and mercury contamination often co-occur in tropical freshwater ecosystems, but the interactive effects of these two stressors on fish populations are poorly known. The effects of mercury (Hg) on recorded changes in the detailed form of the electrocardiogram (ECG) during exposure to
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