cesium/infarction

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[Comparative 131-cesium scintigraphic and electrocardiographic studies of patients following the acute phase of myocardial infarct].

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The determination of the extent and site of morphological changes in heart muscle, while still living, after a healed myocardial infarction is of a doubtless theoretical and practical interest. Certain possibilities, in that respect, are revealed by the myocardium scintigraphy with131 cesium. The

[Effect of the diethylamine analog of etmozin and cesium chloride on the idioventricular rhythm in dogs in the late stages of experimental myocardial infarct].

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Atrioventricular block was produced by infusion of 0.1-0.2 ml of 40% formaline into the A-V node or the bundle of His. Effect of diethylamine analog of etmozin (1 mg/kg) and cesium chloride (20 mg/kg) on the idioventricular rate was studied in control and experimental dogs 24 hours after the

Cesium-129 myocardial scintigraphy to quantify myocardial infarction in dogs.

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The sizes of surgically induced acute myocardial infarctions were quantified in a study of 28 dogs. Four projections (right and left anterior oblique, anterior, and left lateral) were obtained with 129Cs myocardial scintigraphy. Control images, taken before surgery, were compared with images taken

[Heart scintigraphy by means of Cesium 131 in myocardial infarct and in ischemic heart disease].

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[Evaluation of cesium-131 myocardial scintiphotography in the detection of myocardial infarction].

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THE DIRECT DIAGNOSIS OF MYOCARDIAL INFARCTION BY PHOTOSCANNING AFTER ADMINISTRATION OF CESIUM-131.

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Cesium-129 myocardial scintigraphy to detect myocardial infarction.

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Cesium 131 photoscan: aid in the diagnosis of myocardial infarction.

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Studies on slow cardiac action potentials occurring in potassium-rich media as a simulation of the early phase of myocardial infarction. Influence of potassium-conductance blockers and antiarrhythmic drugs.

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In the acute phase of myocardial infarction, a marked intracellular potassium loss and the lack of intact coronary circulation are known to result in extracellular hyperpotassemia partially depolarizing the damaged cells. To simulate these conditions, isolated guinea pig papillary muscles were

Cardiac TRPV1-afferent signaling promotes arrhythmogenic ventricular remodeling after myocardial infarction.

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Chronic sympathoexcitation is implicated in ventricular arrhythmogenesis (VAs) following myocardial infarction (MI), but the critical neural pathways involved are not well understood. Cardiac adrenergic function is partly regulated by sympathetic afferent reflexes, transduced by spinal afferent

Modulation of drug effects by regional sympathetic denervation and supersensitivity.

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BACKGROUND Regional sympathetic denervation, such as that produced by a myocardial infarction, causes electrophysiological heterogeneity in the ventricles. The purpose of this study was to test the hypothesis that such denervation could cause drugs to exert heterogeneous myocardial

Myocardial images in nonacute coronary and noncoronary heart diseases.

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To determine the variables that might affect interpretability of myocardial perfusion images in patients with acute myocardial infarctions, images obtained following intravenous administration of potassium-43 or cesium-129 were evaluated in 68 patients with nonacute coronary or noncoronary heart

Thrombin modulates phosphoinositide metabolism, cytosolic calcium, and impulse initiation in the heart.

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Thrombin stimulates phosphoinositide hydrolysis and increases cytosolic calcium in several types of cells. To determine whether thrombin exerts similar stimulatory actions in the heart and whether this mechanism is linked to changes in cardiac electrical activity, the effects of thrombin on several

The interference of uptake of thallium-201 in cultured rat myocardial cells with existence of potassium related pharmaceuticals--a preliminary report.

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Thallium-201 myocardial perfusion imaging is wildly used to detect and assess the extent of jeopardized myocardial ischemia in the coronary artery disease and the viability of myocardium post infarction. In recent years, there has been a great deal of pharmacological development of blockers and

Mechanisms of triggered activity induction at the border zone of normal and abnormal cardiac tissue.

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Ionic mechanisms that may be involved in inducing triggered activations at the border zone (BZTAs) of normal and abnormal Purkinje fiber segments were investigated. In a two-chamber bath, fibers were divided into a normal segment and segment treated with ethylenediaminetetraacetic acid to stimulate

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