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Four experiments were conducted to evaluate the effect of heat stress on acid-base status and the birds' response to supplemental KCl and KCO3. The corn-soybean meal fish-meal basal ration (.73% K+) contained more K+ and Cl- than is recommended by the National Academy of Sciences for chicks reared under near optimal conditions (24 C and 55% relative humidity). Chicks reared under continuous thermostress (35 C, 70% relative humidity) exhibited panting phase blood alkalosis (pH of 7.46). Supplementing drinking water with .2% NH4Cl reduced panting phase blood pH to normal values and increased live weight gain (23%) and feed efficiency (7.7%). Supplementing drinking water with .15% KCl also increased (P less than .05) live weight gain (46%) and feed efficiency (15.4%) but did not affect (P less than .46) blood pH. A significant (P less than .01) interaction existed between NH4Cl and KCl for body weight gain. Adding .2% NH4Cl to broiler drinking water reduced the level of KCl required in drinking water to optimize weight gain to .1% KCl. Potassium chloride alone, or with NH4Cl, can alleviate some consequences of heat stress, but supplementing drinking water with a high level of NH4Cl (.5%) decreased (P less than .05) blood pH to acidotic levels and reduced body weight gain. Potassium chloride supplementation exacerbated NH4Cl toxicity. Potassium carbonate reduced (P less than .05) body weight gain indicating that the response may not be attributed to K+ alone. Beneficial effects of NH4Cl therapy for heat stressed broilers are speculative.
Virulence, as determined in a mouse model, and the virulence factor activities of catalase, superoxide dismutase, and listeriolysin O were examined in a parental strain (10403S) and in a nonhemolytic mutant strain (DP-L224) of Listeria monocytogenes. The cells were propagated in media containing various concentrations of sodium chloride or potassium chloride. Strains 10403S and DP-L224 exhibited significant increases in catalase activity and listeriolysin O activity when grown in medium containing either salt at 428 mM. The superoxide dismutase activities for both strains increased when they were grown in medium containing either salt. The superoxide dismutase activity was significantly increased only when cells were propagated in medium containing no salt compared with that when they were propagated in medium containing either salt at 1,112 mM. In addition, the listeriolysin O activity was highest for cells propagated in medium containing KCl at 428 mM, while the activity was significantly less for cells propagated in medium containing NaCl at an equal concentration. Virulence was examined in mouse livers and spleens after intravenous infection, and approximate 50% lethal doses were determined after intragastric and intraperitoneal infection. Each method of infection indicated that listeriolysin O is required for virulence, while growth in salt-containing medium or the production of higher levels of catalase, superoxide dismutase, and listeriolysin O do not appear to enhance the virulence of L. monocytogenes.
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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.
Randomized trials have shown that increasing potassium intake lowers blood pressure. However, most previous trials used potassium chloride, whereas potassium in fruits and vegetables is not a chloride salt. It is unclear whether a nonchloride salt of potassium has a greater or lesser effect on blood pressure compared with potassium chloride. We performed a randomized crossover trial comparing potassium chloride with potassium citrate (96 mmol/d, each for 1 week) in 14 hypertensive individuals. At baseline, blood pressure was 151+/-16/93+/-7 mm Hg with a 24-hour urinary potassium of 81+/-24 mmol. During the randomized crossover part of the study, blood pressure was 140+/-12/88+/-7 mm Hg with potassium chloride (24-hour urinary potassium: 164+/-36 mmol) and 138+/-12/88+/-6 mm Hg with potassium citrate (24-hour urinary potassium: 160+/-33 mmol). These blood pressures were significantly lower compared with that at baseline; however, there was no significant difference in blood pressure between potassium chloride and potassium citrate, mean difference (95% confidence interval): 1.6 (-2.3 to 5.6) mm Hg for systolic and 0.6 (-2.4 to 3.7) mm Hg for diastolic. Our results, in conjunction with the evidence from many previous trials that potassium chloride has a significant blood pressure-lowering effect, suggest that potassium citrate has a similar effect on blood pressure as potassium chloride. These results support other evidence for an increase in potassium intake and indicate that potassium does not need to be given in the form of chloride to lower blood pressure. Increasing the consumption of foods high in potassium is likely to have the same effect on blood pressure as potassium chloride.
Potassium loss may cause arrhythmias and cardiac injury in patients undergoing heart surgery with cardiopulmonary bypass (CPB). In a prospective, randomized trial two different methods of potassium substitution were investigated regarding their influence on cardiac rhythm following reperfusion. Patients received either potassium chloride (Group I, n = 102) or potassium magnesium aspartate (Inzolen, group II, n = 105) to achieve intraoperative serum potassium concentrations of 4.5 mmol/l. St. Thomas cardioplegic solution was used. CPB was performed in moderate hypothermia (28-32 degrees C) with a non-pulsatile pump flow, a membrane oxygenator and a single two-stage venous catheter. The two study groups were comparable with regard to biometric data, preoperative state, duration of operation, ischemia and clinical outcome. In 6 patients in group I and in 3 patients in group II perioperative myocardial infarction was diagnosed based on ECG and CK-MB findings. One patient in each group died during the postoperative hospital stay. At the time of declamping mean serum potassium concentration was 4.9 +/- 0.7 mmol/l in group I and 4.8 +/- 0.5 mmol/l in group II (n.s.). The concentration of magnesium was significantly lower in the potassium chloride substitution group (1.48 mmol/l) compared to the other group (2.33 mmol/l) (p < 0.05). No significant differences in cardiac electric activity were observed between the two groups. The incidence of ventricular fibrillation in the early reperfusion period was 37% versus 45% (n. s.). In both groups patients with a potassium value of < 4.5 mmol/l showed a significantly higher incidence of ventricular fibrillation. Five percent of the patients had bradycardia requiring temporary pacing.(ABSTRACT TRUNCATED AT 250 WORDS)
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.
During the spring of 2004, in the Calgary Health Region (CHR) two critical incidents occurred involving patients receiving continuous renal replacement therapy (CRRT) in the intensive care unit (ICU). The outcome of these events resulted in the sudden death of both patients. The Department of Critical Care Medicine's Patient Safety and Adverse Events Team (PSAT), utilized the Healthcare Failure Mode and Effect Analysis (HFMEA) tool to review the process and conditions surrounding the ordering and administration of potassium chloride (KCI) and potassium phosphate (KPO4) in our ICUs. The HFMEA tool and the multidisciplinary team structure provided a solid framework for systematic analysis and prioritization of areas for improvement regarding the use of intravenous, high-concentration KCL and KPO4 in the ICU.
Sodium chloride (NaCl) and potassium chloride (KCl) are both capable of inducing lethality and mutations when each is administered at a molarity of two for different lengths of time to logarithmic phase cells of the yeast Saccharomyces cerevisiae. Analysis of the revertants indicates that the reversions can be base substitutions, of both the transition and the transversion type, as well as frameshift mutations. At equal molarity, with the frequency of mutations as the criterion, KCl and NaCl are equally efficient in inducing all types of mutations.
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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.
Ninety four children aged less than 5 years with diarrhoeal dehydration and acidosis were treated randomly with either World Health Organisation (WHO) oral rehydration solution containing sodium chloride, potassium chloride, sodium bicarbonate and glucose or an oral solution with tripotassium citrate monohydrate replacing the sodium bicarbonate and potassium chloride in the WHO solution. Fifty five children (58%) were hypokalaemic (potassium less than 3.5 mmol/l) on admission. All but two in the citrate group were successfully treated. There were no significant differences in rehydration solution intake, stool output, gain in body weight, and fall in plasma specific gravity and haematocrit between the two treatment groups after 48 hours' treatment. Significant improvement in the serum potassium concentration was observed in the hypokalaemic children receiving potassium citrate solution compared with children receiving WHO solution after 24 and 48 hours' treatment. None developed hyperkalaemia. Although children receiving potassium citrate solution corrected their acidosis at a slower rate than the WHO solution group during the first 24 hours, by 48 hours satisfactory correction was observed in all. Tripotassium citrate can safely replace sodium bicarbonate and potassium chloride and may be the most useful and beneficial treatment for diarrhoea and associated hypokalaemia.
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The selectivity of glass electrodes suitable for potassium-ion measurements depends on the age of electrodes and the composition of the solution. An empirical equation describing the electrode potential as a function of solution composition is given for practical application in solutions containing both sodium and potassium.
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Prevention of erythrocyte dehydration is a potential therapeutic strategy for sickle cell disease. Increasing erythrocyte magnesium (Mg) could inhibit sickle cell dehydration by increasing chloride (CI) and water content and by inhibiting potassium chloride (K-CI) cotransport. In transgenic SAD 1 and (control) C57BL/6 normal mice, we investigated the effect of 2 weeks of diet with either low Mg (6 +/- 2 mg/kg body weight/d) or high Mg (1,000 +/- 20 mg/kg body weight/ d), in comparison with a diet of standard Mg (400 +/- 20 mg/ kg body weight/d). The high-Mg diet increased SAD 1 erythrocyte Mg and K contents and reduced K-CI cotransport activity, mean corpuscular hemoglobin concentration (MCHC), cell density, and reticulocyte count. SAD 1 mice treated with low-Mg diet showed a significant reduction in erythrocyte Mg and K contents and increases in K-CI cotransport, MCHC, cell density, and reticulocyte counts. In SAD 1 mice, hematocrit (Hct) and hemoglobin (Hb) decreased significantly with low Mg diet and increased significantly with high-Mg diet. The C57BL/6 controls showed significant changes only in erythrocyte Mg and K content, and K-CI cotransport activities, similar to those observed in SAD 1 mice. Thus, in the SAD 1 mouse, changes in dietary Mg modulate K-CI cotransport, modify erythrocyte dehydration, and ultimately affect Hb levels.