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Pàgina 1 des de 45 resultats
Intestinal Necrosis due to Digitalis.
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Intestinal hemmorrhagic necrosis as a complication of digitalis intoxication.
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Hemorrhagic necrosis of the intestine: its occurrence with digitalis intoxication.
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[An unusual case of "catecholamine necrosis" caused by accidental digitalis poisoning].
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Toxic manifestations of digitalis are one of the most prevalent adverse drug reactions encountered in clinical practice. The estimated incidence is about 20% in hospitalized patients in the USA. The authors describe a rare case of myocardial "catecholamine necrosis" (anteroseptal myocardial
Hemorrhagic bowel necrosis associated with acute digitalis poisoning in an infant.
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Reversal of digitalis-induced mesenteric vasospasm by sodium nitroprusside.
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Digitalis constricts the peripheral vasculature. When digitalis is administered to patients whose mesenteric blood flow is reduced secondary to heart failure, the vasoconstrictor action coupled to reduced mesenteric flow may result in mesenteric ischemia or hemorrhagic bowel necrosis. The clinical
[Haemorrhagic necrosis of the digestive tract consecutive to massive digitalis intoxication (author's transl)].
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A 60-year-old man under digitalis treatment for hypertensive heart tried to commit suicide by absorbing a 15 mg dose of digitoxin. Severe intestinal bleeding occurred 12 hours later, followed by pseudo-occlusive syndrome and ischaemia of the distal lower limbs. On abdominal incision the whole gut
High doses of digitalis increase the myocardial production of proinflammatory cytokines and worsen myocardial injury in viral myocarditis: a possible mechanism of digitalis toxicity.
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Results of recent studies suggest that proinflammatory cytokines cause myocardial contractile dysfunction, and that the drugs used to treat heart failure modulate the production of cytokines. This study was designed to examine the effects of digoxin in a murine model of heart failure induced by
The effect of digitalis on experimental myocardial infarct size and hemodynamics.
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Early studies suggested that digitalis exacerbated ischemia (ST segment data); however, there are no studies assessing the effect of this agent on anatomic infarct size with the use of a risk zone technique. Therefore, the aim of this study was to assess quantitatively whether digitalis extends
Canine cardiac digitalis receptors are preserved in congestive heart failure induced by rapid ventricular pacing.
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In dogs, it has been reported that acute ischemia or severe and terminal heart failure results in a selective reduction of myocardial alpha 3 isoform of Na, K-ATPase activity. The aim of this study was to evaluate if a similar change in the two canine digitalis receptor isoforms occurs following 4
High doses of digoxin increase the myocardial nuclear factor-kB and CaV1.2 channels in healthy mice. A possible mechanism of digitalis toxicity.
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BACKGROUND
Toxic effects of digoxin may occur with normal therapeutic serum level. However, the underlying mechanisms are not fully understood. Nuclear factor kappa-B (NF-kB) is an important transcription factor in most organ systems and is often implicated in the harmful effects of cardiac injury.
Nonocclusive hemorrhagic necrosis of the intestine.
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Hemorrhagic intestinal necrosis occurs without demonstrable mechanical obstruction of the mesenteric vascular supply. The etiologic factors include (1) congestive heart failure, (2) cardiac arrhythmia, (3) dehydration, and (4) digitalis therapy with or without digitalis toxicity. All of these
[Extensive intestinal necrosis without obstruction caused by so-called low flow state].
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Medical history of a 36 year old woman with severe combined valvular deformities and frequent failure of the circulation inspite of the treatment with digitalis is reported. Impairment of the circulation gradually lead to the so called "low flow state" which resulted in infarction of the small
[Necrosis of the terminal ileum after drug poisoning. Case report].
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In an attempt to commit suicide, a 32-year-old women swallowed a vast amount of psychiatric drugs, i.e. tranquilizers, amphetamines, hynotic and antidepressant agents. By intensive care, using high doses of catecholamines and appropriate antidota, satisfactory circulation and oxygenation could be
Na+/K+ pump and endothelial cell survival: [Na+]i/[K+]i-independent necrosis triggered by ouabain, and protection against apoptosis mediated by elevation of [Na+]i.
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Recent studies have demonstrated the tissue-specific effect of Na+/K+ pump inhibition by ouabain and other cardiac glycosides on cell viability. The vascular endothelium is an initial target of cardiac glycosides employed for the management of congestive heart failure as well as circulating
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