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Aqueous salt solutions containing NaCl, KCl, MgCl2, Na2SO4, CaCl2, NH4Cl, or sodium saccharin are mutagenic in yeast when logarithmic growth of cells is interrupted by exposure to a 0.5-2.0 M salt solution. Stationary-phase cells are not mutated by this treatment. When placed in an enriched medium with the salt, the stationary-phase cells grow after a prolonged lag period. The compounds tested (NaCl, KCl, and sodium saccharin), under conditions in which growth in medium can take place, exhibit an antimutagenic response as measured by the compartmentalization test. The antimutagenic action of salt solutions in yeast is concentration-dependent. Unlike the mutagenic action of these compounds, which approximates an osmolality-dependent response, the antimutagenic action seems to be correlated with toxicity as measured by growth rate reduction at increasing concentrations of the compounds. For example, sodium saccharin and NaCl exhibit almost identical osmolalities; however, 0.3 M sodium saccharin reduces the growth rate much more than does 0.3 M NaCl. At these same molar concentrations, the spontaneous mutation rate for histidine prototrophy is, for the control, 6.2 x 10(-8) mutations/cell/-generation, 3.5 x 10(-8) with 0.3 M NaCl, and 1.7 x 10(-8) with 0.3 M sodium saccharin.
Potassium is one of the most abundant ions in the human body and yet it is difficult to assess potassium balance. Potassium chloride is extensively used as a potassium supplement, both by physicians as a therapeutic modality and by the general public, mostly in the form of salt substitute. Therapeutically, both the oral and intravenous forms of potassium are utilised. Overdose of potassium is not as frequently encountered in clinical practice as hyperkalaemia (excess potassium in the body) due to acute or chronic renal disease. Potassium homeostasis is maintained very delicately and is governed by the daily consumption of potassium and the renal excretion mechanisms. Any change in these or related factors can present as hyperkalaemia. However, potassium overdoses leading to serious consequences do occur. Orally, the dose of potassium has to be large enough so that the normal excretory mechanisms for potassium are overcome and clinical toxicity occurs. It takes a much bigger dose of ingested potassium to produce toxicity in a person with normal renal function than in patients with compromised renal function. Potassium toxicity manifests in significant, characteristic, acute cardiovascular changes with ECG abnormalities. Besides cardiovascular effects, neuromuscular manifestations in the form of general muscular weakness and ascending paralysis occur. Gastrointestinal symptoms manifest as nausea, vomiting, paralytic ileus, and local mucosal necrosis which may lead to perforation. It is imperative when treating hyperkalaemia that the whole clinical picture is taken into account rather than the numerical potassium values. Only the extracellular potassium can be measured in the laboratory, yet 98% of the body potassium is intracellular and cannot be measured. In acute overdose situations due to ingestion of potassium salt, the general principles of treatment for overdoses should be followed. Calcium chloride infusion, dextrose and insulin in water, and correction of acidosis with sodium bicarbonate are helpful in controlling the acute, life-threatening cardiac arrhythmias. These modalities do not remove the excess potassium from the body. That is achieved either by utilising ion-exchange resins or by mechanically removing potassium via haemodialysis. To curtail inadvertent or accidental potassium overdoses, physicians should prescribe any potassium supplements very carefully to their patients and monitor the plasma potassium periodically.
The effects of intravenous infusions of potassium chloride, potassium acetate, potassium aspartate and potassium malate on plasma electrolytes and acid-base balance were investigated in normokalemic or hypokalemic alkalotic rats. Animals who obtained equal volumes of isotonic sodium chloride solution served as controls. All of these potassium solutions increased the plasma potassium concentrations to the same extent. Potassium chloride shifted the acid-base balance to acidotic values in normal rats or corrected metabolic alkalosis in hypokalemic rats. The potassium salts of organic acids, however, caused an increase in alkalosis, acetate acting stronger than aspartate and malate. In potassium deficiency combined with metabolic alkalosis the administration of potassium chloride is preferable to the organic potassium salts since it corrects both the electrolyte disturbances at the same time.
Our objective was to evaluate the response of lactating dairy cows to dietary Na, K, and Cl while holding cation-anion balance constant. Fifteen lactating Holstein cows, blocked according to age and previous milk yield, were assigned randomly to replicated 3 x 3 Latin squares with experimental periods of 3 wk. Diets contained sorghum silage and concentrate in a 40:60 ratio (DM basis) and were formulated to provide +32 meq of [(Na + K) - Cl]/100 g diet DM via one of three variations: 1) basal concentrations of dietary Na, K, and Cl, 2) basal diet with addition of 20 meq of Na and 20 meq of Cl/100 g in the form of 1.17% added NaCl, or 3) basal diet with the addition of 20 meq of K and 20 meq of Cl/100 g in the form of 1.56% added KCl. Free proton concentration in blood was increased by addition of NaCl and KCl; however, this increase did not appear to be physiologically significant, and no other measures of acid-base status were significantly affected. Plasma K was higher and plasma Mg was lower for the diets with supplemental NaCl or KCl than for basal diet. Urine mineral excretion reflected dietary mineral concentration, except Ca and Mg excretion rates were reduced by feeding the KCl diet. Milk yield reflected DM intake, which was lowest with supplemental NaCl. Results of this study indicate that, at a dietary cation-anion balance of +32 meq/100 g of diet DM, the balance of Na and K to Cl in the diet is a more important determinant of dietary impact on systemic acid-base status than actual dietary concentrations of Na, K, and Cl.
The effects of central venous bolus injections of potassium chloride (KCl) on arterial potassium concentration were studied in patients undergoing cardiopulmonary bypass. Ten subjects were studied, and each received a rapid bolus injection of KCl, 33 microEq/kg, both before and after cardiopulmonary bypass. Injections were delivered through the proximal infusion port of a 7.5F pulmonary artery catheter, which was situated in either the superior vena cava or the right atrium. Monitored variables included the electrocardiogram, mean arterial, central venous, and pulmonary artery pressures, end-tidal carbon dioxide and inspired oxygen concentrations, and temperature. Blood was sampled continuously at either the radial artery alone or both the radial artery and aortic root at 2 mL/4.3 s. The difference in magnitude between the maximal potassium concentration achieved and the prebolus baseline potassium concentration (delta K) was correlated with cardiac output, stroke volume, and prebolus baseline potassium concentration (baseline [K+]), using simple linear regression analysis. Although significant hyperkalemia (eg, 7 to 9 mEq/L) developed in both the aortic root and radial artery, this was of no electrocardiographic or hemodynamic consequence, presumably because of the transient nature of the hyperkalemic response, following bolus injection of KCl. There was no significant correlation between delta K and cardiac output or stroke volume; however, delta K did correlate significantly with the Baseline [K+] in a direct linear relationship. It is concluded that central bolus injections of KCl through the proximal infusion port of the pulmonary artery catheter at 33 microEq/kg are safe. This technique should be used cautiously in patients with extremely low cardiac outputs or where intracardiac shunting of blood may exist, as these situations could potentially result in greater hyperkalemic responses than those observed in the current study.
The potassium hydrocarbonate and potassium chloride toxicity was compared in experiments on 113 albino rats. The death following introduction of maximal amounts of potassium chloride was noted to supervene earlier than it did in animals receiving equivalent doses of potassium hydrocarbonate. Simultaneous introduction of sodium hydrocarbonate lowered the toxicity of both potassium hydrocarbonate and chloride. Morphological investigations revealed that toxic doses of potassium hydrocarbonate bring about shifts in the carbohydrate and lipids metabolism. Some mechanisms behind the action produced potassium chloride and hydrocarbonate are discussed.
Clinically relevant doses of potassium chloride (equivalent to 2 mEq/60 kg of body weight) were administered as rapid intravenous (IV) boluses to healthy halothane-anesthetized pigs. Potassium was given either peripherally through a standard IV ear catheter or centrally through the central venous port of a pulmonary artery catheter. Multiple injections were made in each pig, and cardiac output was varied by changing end-tidal halothane concentration. The aortic root potassium concentration was measured every three to six seconds for 90 seconds following potassium administration in each pig. Monitored variables included end-tidal halothane, end-tidal carbon dioxide, pulmonary artery pressure, mean arterial blood pressure, cardiac output, electrocardiogram, and temperature. Following both peripheral and central administration of potassium chloride, aortic root potassium increased significantly. However, the time required to achieve the peak aortic root potassium concentration was significantly less after central administration. In addition, the change in aortic root potassium concentration was greater following central administration compared with peripheral. The change in aortic root potassium concentration correlated inversely with cardiac output only after central, but not peripheral injection. Despite marked transient hyperkalemia in all animals, no electrocardiographic evidence of hyperkalemia could be demonstrated. It is concluded that small bolus doses of potassium chloride (2 mEq/60 kg) can be given safely either peripherally or centrally in normal, hemodynamically stable swine.
Potassium chloride (KCl) given subcutaneously in high concentrations causes necrosis of skin, possibly from vasoconstriction around the injection site. The authors studied guinea pigs given subcutaneous injections of various volumes and concentrations of KCl and observed the severity of the cutaneous lesions. In further experiments, therapeutic agents were injected subcutaneously 10 minutes after KCl infiltration. The severity of cutaneous lesions was not affected by various volumes of KCl of the same concentration, but was correlated positively with increasing concentrations of the salt when concentration was varied. Dextrose, 5%, and sodium bicarbonate, 1 M, had no effect on the cutaneous lesions caused by KCl, while hyaluronidase, 150 U/ml, lessened them. Lidocaine, 1%, a vasodilator, eliminated cutaneous lesions caused by KCl. Kcl-induced lesions may be due to vasocontriction, which can be relieved by lidocaine.
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NuLYTELY (PEG 3350, Sodium Chloride, Sodium Bicarbonate, and Potassium Chloride for Oral Solution), a product from Braintree Laboratories, Inc. is a modification of GoLYTELY (PEG 3350 and Electrolytes for Oral Solution) that has been found to have the same therapeutic advantages in terms of safety, efficacy, speed and patient acceptance. This product was developed to improve upon the taste of GoLYTELY. NuLYTELY represents an effective alternative for bowel cleansing prior to colonoscopy that may be more acceptable to some patients.
A single blind placebo controlled, cross-over study comparing a new microencapsulated potassium chloride tablet (MET) with two reference formulations of oral potassium, potassium chloride solution (PS) and potassium chloride wax-matrix tablets (WMT), was performed in 12 normal healthy volunteers. Urinary potassium excretion was the main criterion of comparison. Results showed that all three formulations have excellent bioavailability. This indicates that potassium absorption in the stomach is similar to that in more distant portions of the gut. The slow-release characteristics of both MET and WMT were confirmed. Clinical and pharmacological tolerance was excellent and no side-effects were reported with any of the potassium formulations studied.
The release of potassium chloride incorporated into hydrogenated vegetable oil and hydroxypropyl methylcellulose matrix tablets was studied in vitro. The formulations containing 20% hydrogenated vegetable oil and hydroxypropyl methylcellulose showed a sustained-release profile comparable to that of a standard commercially available sustained-release preparation, containing 8 mEq potassium chloride embedded in a wax material. The formulated and standard sustained-release potassium chloride tablets were compared to a conventional enteric-coated potassium chloride tablet in 10 healthy subjects. Mean recoveries in 24-hr urine potassium levels from four dosage forms (after subtracting normal urine potassium excretion levels) were 76 +/- 32% from hydroxypropyl methylcellulose, 95 +/- 22% from hydrogenated vegetable oil-incorporated matrix tablets, 91 +/- 29% from commercially available sustained-release tablets, and 97 +/- 13% from enteric-coated tablets. There was no significant difference (P greater than 0.05) in the time to reach maximum excretion rates among the three sustained-release tablets. No significant adverse effect was experienced with any of the preparations.
1. Urinary kallikrein excretion in the anaesthetized rat was measured during intravenous KCl infusion in control and in K+-adapted rats. 2. The infusion of 0.1 mol/l KCl at 3.0 ml/h for 60 min in control rats resulted in a significant increase in urinary kallikrein excretion, associated with diuresis, natriuresis and kaliuresis. 3. When rats were offered 0.1 mol/l KCl to drink ad libitum for 14 days (K+-adaptation), the basal excretion of kallikrein was higher than in the control rats. In K+-adapted rats, intravenous infusion of 0.1 mol/l KCl resulted in significantly greater increase in urinary kallikrein excretion than in the control rats. 4. The Na+-channel blocker, amiloride (8.5 mg/kg body weight), significantly increased urinary kallikrein excretion immediately after injection in control and K+-adapted rats. However, in the subsequent 60 min, kallikrein excretion decreased markedly to values lower than those before injection of amiloride. 5. When amiloride was superimposed on a continuous 0.1 mol/l KCl infusion in K+-adapted rats, there was an immediate increase in kallikrein excretion. In the subsequent 20 min, kallikrein excretion decreased only to increase again in the next 40 min of KCl infusion. 6. Since amiloride injection reduces urinary kallikrein excretion in control and K+-adapted rats, the results suggest that urinary kallikrein excretion in the rat is through a mechanism(s) affected by amiloride. The high urinary kallikrein excretion and the greater response to KCl infusion in K+-adapted rats suggest that the K+-transport mechanism is more important than the mechanism affected by amiloride.
The borderline hypertensive rat is the first filial offspring of the spontaneously hypertensive rat and the Wistar-Kyoto rat. With increased dietary sodium chloride intake, the borderline hypertensive rat develops hypertension and exaggerated cardiovascular and renal responses to acute environmental stress, similar to those observed in the hypertensive spontaneously hypertensive rat parent. In other models of sodium chloride-sensitive hypertension with different genetic background (Dahl rat), dietary potassium chloride supplementation protects against the development of hypertension, increased sympathetic nervous system activity, and exaggerated responses to acute environmental stress. This investigation sought to determine whether the dietary sodium chloride-induced development of both the hypertension and the exaggerated responses to acute environmental stress could be reversed or prevented by increased dietary potassium chloride intake. Dietary potassium chloride intake was increased with a 1% potassium chloride drinking solution either after 12 wk of 8% sodium chloride intake (reversal) or concomitant with the onset of 12 wk of 8% sodium chloride intake (prevention). An increase in dietary potassium chloride intake did not reverse or prevent the development of either the hypertension or the exaggerated cardiovascular and renal responses to acute environmental stress in borderline hypertensive rats fed 8% sodium chloride. It is concluded that the difference in genetic background between borderline hypertensive rats and other models of sodium chloride-sensitive hypertension is an important determinant of the protective effect of dietary potassium chloride supplementation.
The palatability of various commercially available potassium chloride preparations was studies. Twenty potassium chloride samples were tested by 152 people from February 1975 to April 1975. Nine samples were placed into a "most preferred" group and divided into 36 possible pairs, each to be tested four times. Twenty-four volunteers tested six pairs of samples and chose the preferred sample in each pair. The three samples, which finished with the highest scores (K-Lyte/Cl Packets, Kato Powder Packets and Kaochlor 10%), although not significantly different from the rest of the subgroup of nine, were all highly flavored and among the most expensive. It is suggested that when selecting a potassium chloride preparation, cost, convenience, palatability, and most importantly, long-term compliance with the prescribed regimen, must be considered.
Potassium chloride was subjected to various kinds of pretreatments and irradiated in a nuclear reactor. Irradiated potassium chloride was dissolved in deaerated aqueous solution of several sulfur-salts. A portion of the solution was chromatographed on a thin layer chromatographic plate and the distribution of 35S-chemical species was determined. Irradiation of potassium chloride degassed at 3x10(-4)Torr resulted in the formation of about 60% of 35S in the form of thiosulfate and remainder was distributed among sulfide, sulfate and elementary sulfur. Thiosulfate[35S] was converted to elementary sulfur[35S] first by reducing to hydrogen sulfide [35S] with nascent hydrogen and then by oxidizing the latter to elementary sulfur[35S] with hexacyanoferrate(III). Elementary sulfur[35S] was finally extracted into benzene. Radiochemically pure elementary sulfur[35S] could be produced by simple procedures with a yield of about 60%. Thiosulfate[35S] was decomposed with acid to elementary sulfur[35S] and sulfur[35S] dioxide. The former was separated by centrifuging and dispersed in boiling water to form colloidal suspension of elementary sulfur[35S]. Approximately 40% of 35S was recovered as colloid.
The diffusivity of potassium chloride in composite agar slab/microporous membrane structures loaded with various amounts of Escherichia coli whole cells was determined using both time-lag and steady-state methods. The diffusion coefficient of KCl decreased linearly with the logarithm of the immobilized-cell content. The effect exerted by bacterial growth inside the immobilization matrices on KCl diffusivity was then investigated. The diffusion coefficient of KCl obtained by time-lag analysis decreased during incubation of the immobilized-cell structures, whereas less consistent results arose from the steady-state method. An apparent doubling time for immobilized E. coli, increasing with the initial cell content of the gel, was obtained from the calibration relationship between KCl diffusivity and the number of organisms in agar.