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Side 1 fra 16 resultater
Lack of effect of treatment with human recombinant-tumour necrosis factor (HrTNF) on the binding of quinidine to alpha 1-acid glycoprotein (AGP).
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Tumour necrosis factor (TNF) is known to be a key mediator in the acute phase response and its administration has been shown to cause a five fold increase in serum alpha 1-acid glycoprotein (AGP) concentration in the rat. Since, in man, plasma AGP level determines the protein binding of many
Quinidine hepatotoxicity. A report of a case and review of the literature.
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A case is described of presumed quinidine hepatotoxicity, characterized by the development of fever, abnormal serum transaminase values, which improved after cessation of the drug but recurred after a challenge dose, and centrizonal hepatocellular necrosis detected on liver biopsy. Morphological
Quinidine and procainamide inhibit murine macrophage uptake of apoptotic and necrotic cells: a novel contributing mechanism of drug-induced-lupus.
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A number of mechanisms have been proposed to explain the etiology of drug-induced lupus (DIL) but the effect of apoptotic and necrotic cell handling has not been previously examined.
OBJECTIVE
To evaluate the effect of quinidine and procainamide at therapeutic range concentrations, on the uptake of
Problems in assessing infarction size by epicardial mapping: preliminary studies with quinidine.
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Some of the laboratory difficulties in assessing infarction size produced by intermittent coronary artery occlusion were demonstrated by using an epicardial mapping technique in anesthetized open-chest dogs. Intermittent occlusion of a left anterior descending coronary artery branch resulted in a
Quinidine prevents paraoxon-induced necrotizing myopathy in rats.
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Acute organophosphorus anticholinesterase poisoning induces a necrotizing end-plate myopathy in rats and patients. Acetylcholine (ACh) excess leads to prolonged synaptic currents and increased influx of cations including calcium through the postsynaptic ACh receptor channels with prolonged muscle
Amiodarone inhibits production of tumor necrosis factor-alpha by human mononuclear cells: a possible mechanism for its effect in heart failure.
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BACKGROUND
Recent studies suggest that cytokines such as tumor necrosis factor (TNF)-alpha and interleukins (ILs) are capable of modulating cardiovascular function and that drugs used in the treatment of heart failure have various modulatory effects on the production of cytokines. This study was
Quinidine photosensitivity.
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Two patients with quinidine photosensitivity had an eczematous dermatitis in a photosensitivity distribution on the face, neck, hands, and forearms. Histologically, both patients showed a bandlike dermal lymphohistiocytic infiltrate with overlying vacuolar changes and necrosis in keratinocytes at
The anti-necrosis role of hypoxic preconditioning after acute anoxia is mediated by aldose reductase and sorbitol pathway in PC12 cells.
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It has been demonstrated that hypoxic preconditioning (HP) enhances the survival ability of the organism against the subsequent acute anoxia (AA). However, it is not yet clear whether necrosis induced by AA can be prevented by HP, and what are the underlying mechanisms. In this study, we examined
Drug-induced lupus erythematosus: incidence, management and prevention.
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The generation of autoantibodies and autoimmune diseases such as systemic lupus erythematosus has been associated with the use of certain drugs in humans. Early reports suggested that procainamide and hydralazine were associated with the highest risk of developing lupus, quinidine with a moderate
Drug-induced lupus.
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Drug-induced lupus is a syndrome resembling mild systemic lupus erythematosus which can complicate treatment with certain apparently unrelated therapies. The most common individual agents are procainamide and hydralazine. Drugs less frequently associated with the disease are chlorpromazine,
A status report on drug-associated acne and acneiform eruptions.
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Several drugs have been associated with the development of eruptions that may simulate acne vulgaris. These drugs include corticosteroids, epidermal growth factor receptor inhibitors, cyclosporine, anticonvulsants, antipsychotics, antidepressants, tumor necrosis factor-alpha (TNF-alpha) inhibitors,
Effects of CYP inhibitors on precocene I metabolism and toxicity in rat liver slices.
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We present a comprehensive in vitro approach to assessing metabolism-mediated hepatotoxicity using male Sprague-Dawley rat liver slices incubated with the well characterized hepatotoxicant, precocene I, and inhibitors of cytochrome P450 (CYP) enzymes. This approach combines liquid chromatography
Reentrant tachyarrhythmias in right atria of cardiomyopathic versus healthy Syrian hamster.
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We studied the role of acetylcholine (ACh) and calcium overload in the induction of atrial flutter or atrial fibrillation (AF) in right atria from 34 normal male Syrian hamsters (F1B) and 33 cardiomyopathic Syrian hamsters (BIO 14.6) associated with focal myocardial necrosis. Action potential (AP)
Involvement of human cytochrome P450 2D6 in the bioactivation of acetaminophen.
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Acetaminophen (APAP), a widely used analgesic and antipyretic agent, can cause acute hepatic necrosis in both humans and experimental animals when consumed in large doses. It is generally accepted that N-acetyl-p-benzoquinone imine (NAPQI) is the toxic, reactive intermediate whose formation from
Bretylium tosylate: a review.
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The chemistry, pharmacology, pharmacokinetics, clinical uses, adverse effects, drug interactions and dosage of bretylium tosylate, a recently approved antiarrhythmic agent, are reviewed. Bretylium tosylate is used to treat life-threatening ventricular arrhythmias, principally ventricular
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