Abstract
Acute fluoride poisoning is associated with sudden cardiac death by an unknown mechanism. Because F- binds to Ca2+ to cause marked hypocalcemia, lowered serum Ca2+ concentrations have been thought to be a major underlying factor in the ventricular irritability of F(-)-toxic patients. However, correction of the hypocalcemia does not prevent sudden death. Paradoxically, while decreasing extracellular Ca2+ levels, in vitro studies have shown F- increases intracellular Ca2+, which is thought to trigger Ca2+-dependent K+ channels and produce a K+ efflux. The K+ efflux may be important clinically, as patients with F- overdose can exhibit hyperkalemia shortly before cardiovascular collapse. In erythrocyte suspensions, we found that propranolol, which increases the sensitivity of the Ca2+-dependent K+ channels, exacerbates the efflux, and quinidine, which blocks the channel, prevents the efflux. In six dogs, 35 mg/kg of sodium fluoride given intravenously produced intractable ventricular fibrillation within 140 minutes. Four dogs given 200 mg of quinidine sulfate with the sodium fluoride developed no ventricular arrhythmias. The data indicate that F–induced hyperkalemia is important in sudden cardiac death following acute fluoride toxicity and that this hyperkalemia is mediated by Ca2+-dependent K+ channels.
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On the Physiological and Medicinal Action of Hydrofluoric Acid and the Fluorides.
EXCERPTS: General Summary. 1. On account of the corrosive action of these substances on glass vessels their use in ordinary therapeutics seems beset by many difficulties. But by attending to a few precautions these obstacles can be so minimized as to be practically overcome. 2. The topical action of strong hydrofluoric acid differs
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Acute fluoride poisoning.
Fluoride poisoning is a potentially severe environmental hazard for children. A case of fluoride poisoning is presented which was manifested by severe hypocalcemia, ventricular arrhythmias, and respiratory failure. Treatment of this poisoning, including peritoneal dialysis, is discussed. The kinetics of fluoride distribution as measured in this patient suggest a rapid
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Fluorosis in Aden
The cases to be described here occurred in the Aden Protectorate where for the last 12 years mass screening of the chest to exclude pulmonary tuberculosis has been carried out. The patients had all drunk the brackish water from the wells, and the analysis of the water from a well
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Buffalo (Bubalus bubalis) epiphyseal proteins give protection from arsenic and fluoride-induced adverse changes in acetylcholinesterase activity in rats
The objective of this study was to determine the effect of fluoride (F) and arsenic (As) on the activity of acetylcholinesterase (AChE), a critically important nervous system enzyme, and to test the protective role of buffalo epiphyseal (pineal) proteins (BEP) in rats. Arsenic (20 mg/kg BW, intraperitoneally) and F (150
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Fluoride in Drinking Water: A Scientific Review of EPA’s Standards.
Excerpts: Summary Under the Safe Drinking Water Act, the U.S. Environmental Protection Agency (EPA) is required to establish exposure standards for contaminants in public drinking-water systems that might cause any adverse effects on human health. These standards include the maximum contaminant level goal (MCLG), the maximum contaminant level (MCL), and the secondary
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