Preliminary experience in the treatment of hyperthyroidism with potassium perchlorate.
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Among patients receiving thiazides for hypertension, there was no reliable predictor of those who would develop significant hypokalemia (a decrease in serum potassium of at least 0.5 mEq. per L). Eighty percent of patients required 60 mEq. of potassium chloride 10 percent elixir daily for successful treatment of thiazide-induced hypokalemia. Foods containing potassium or organic anion compounds of potassium are not useful in this potentially dangerous situation.
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In KOH, the Mg(II)-bromopyrogallol red (BPR) complex produced a very sensitive polarographic wave at -1.30 V. The wave height was linear with the concentration of Mg(II) in the range of 0.05 to 2 microg/mL. The detection limit was 0.01 microg/mL. The electrochemical behavior of Mg(II)-BPR was studied by electrochemical and spectrophotometric methods. Experiments proved that the polarographic wave of Mg(II)-BPR was due to the reduction of BPR in the Mg(II)-BPR complex. The method, which was sensitive, selective, and simple to perform, was used to determine magnesium in foods, and the results were consistent with those obtained by atomic absorption spectroscopy.
Passive uptake of potassium acetate into the mitochondrial matrix can be induced by nigericin, a K+/H+ antiporter, or by A23187, a Mg2+/2H+ antiporter. The latter process is thought to reflect operation of the Mg2+-dependent, endogenous K+/H+ antiporter, but there is ambiguity with respect to the mechanism of K+ transport in this assay (Nakashima, R.A., and Garlid, K.D. (1982) J. Biol. Chem. 257, 9252-9254). Kinetic analysis of potassium acetate transport provides verification that Mg2+ depletion 1) unmasks the K+/H+ antiporter, 2) opens up an intrinsic anion uniporter, 3) has no effect on acetic acid transport, and 4) does not induce high K+ uniport conductance. Mg2+-dependent uptake of potassium acetate is thereby shown to be mediated specifically by operation of the endogenous K+/H+ antiporter, as previously proposed. An extension of this analysis confirms that N,N'-dicyclohexylcarbodiimide and quinine block potassium acetate uptake via specific action on the K+/H+ antiporter. These findings support those of a previous study (Martin, W.H., Beavis, A.D., and Garlid, K.D. (1984) J. Biol. Chem. 259, 2062-2065) in which binding of [14C]N,N'-dicyclohexylcarbodiimide to membrane proteins under selective conditions was used to identify an 82,000-dalton band as the protein responsible for K+/H+ antiport in mitochondria.
We developed a method for the simultaneous determination of monomethyl mercury (MMHg), inorganic mercury [Hg(II)], and total mercury (THg) in biological materials. A variety of biological materials can be digested in methanolic KOH solution. The MMHg and Hg(II) present are converted to volatile ethyl derivatives, methylethyl mercury and diethyl mercury, by an aqueous-phase ethylation reaction with sodium tetraethylborate. The ethyl derivatives are precollected onto a trapping column at room temperature, in case of disconnection with the separation/detection system, and then thermally desorbed into a packed isothermal gas chromatography (GC) column. Eluted organo-Hg compounds from the GC column are decomposed into Hg0, and detection is completed by cold vapor atomic fluorescence spectrometry (CVAFS). Pure standard solutions can be used for calibration. The sum of MMHg and Hg(II) obtained by this method equals the THg value obtained by digestion with HNO3 and H2SO4, reduction with SnCl2, and single-stage amalgamation/CVAFS for all biological materials studied. Absolute detection limits are 0.6 pg and 1.3 pg of Hg as MMHg and Hg(II), respectively, corresponding to 0.3 ng and 0.6 ng/g (wet) of sample.
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The exchange of potassium between cells and plasma of heparinized human blood has been studied in vitro using the radioactive isotope K(42). The changes in cell and plasma specific activity are characteristic of a simple two-compartment system. The mean of seven determinations of the exchange rate at 38 degrees C. is 1.8 per cent of the cellular potassium per hour. The results indicate that at 38 degrees C. the rate is relatively insensitive to oxygenation or reduction of the hemoglobin, and to 1200 r of gamma radiation. With varying temperature the rate follows pseudo first order kinetics with a Q(10) of 2.35. Below 15 degrees C. the rate of loss of potassium exceeds the rate of uptake.
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