Potassium Chloride Supplementation Research Articles

Secreted euryarchaeal microhalocins kill hyperthermophilic crenarchaea.

Few antibiotics targeting members of the archaeal domain are currently available for genetic studies. Since bacterial antibiotics are frequently directed against competing and related organisms, archaea by analogy might produce effective antiarchaeal antibiotics. Peptide antibiotic (halocin) preparations from euryarchaeal halophilic strains S8a, GN101, and TuA4 were found to be toxic for members of the hyperthermophilic crenarchaeal genus Sulfolobus. No toxicity was evident against representative bacteria or eukarya. Halocin S8 (strain S8a) and halocin R1 (strain GN101) preparations were cytostatic, while halocin A4 (strain TuA4) preparations were cytocidal. Subsequent studies focused on the use of halocin A4 preparations and Sulfolobus solfataricus. Strain TuA4 cell lysates were not toxic for S. solfataricus, and protease (but not nuclease) treatment of the halocin A4 preparation inactivated toxicity, indicating that the A4 toxic factor must be a secreted protein. Potassium chloride supplementation of the Sulfolobus assay medium potentiated toxicity, implicating use of a salt-dependent mechanism. The utility of halocin A4 preparations for genetic manipulation of S. solfataricus was assessed through the isolation of UV-induced resistant mutants. The mutants exhibited stable phenotypes and were placed into distinct classes based on their levels of resistance.

Suplementação de cloreto de potássio para frangos de corte submetidos a estresse calórico

O experimento foi realizado com objetivo de avaliar os efeitos do estresse calórico e da suplementação de cloreto de potássio (KCl) sobre o desempenho e algumas características fisiológicas de frangos de corte. Quarenta aves, no período de 42 a 49 dias, foram submetidas ao estresse calórico (16 horas a 25 ± 1ºC; duas horas com temperatura crescente; quatro horas a 35 ± 1ºC; e duas horas com temperatura decrescente até a termoneutralidade e com umidade relativa de 63,5 ± 5%), recebendo os seguintes tratamentos: 0,50 e 1,00% KCl na ração; 0,25 e 0,50% KCl na água de bebida. A ração à base de milho e farelo de soja, com 20% de proteína bruta e 3200 kcal EM/kg, foi fornecida ad libitum. A suplementação de KCl na ração ou na água de beber não influiu no ganho de peso, nos consumos de ração e água, na conversão alimentar, na mortalidade, na relação água/ração, no teor de matéria seca das excretas e nas características hematológicas. O estresse calórico aumentou a temperatura retal, o hematócrito, a hemoglobina, o heterófilo e a relação heterófilo/linfócito e reduziu as hemácias, o linfócito, o sódio e o potássio sérico. A suplementação de KCl na água regulou o número de eritrócitos e a hemoglobina em frangos estressados pelo calor. A relação heterófilo:linfócito e a temperatura retal podem ser usadas como índices de estresse.

CHANGING INCIDENCE OF ATRIAL FIBRILLATION FOLLOWING CORONARY ARTERY BYPASS GRAFTING: A RETROSPECTIVE ANALYSIS

SUMMARY The cases of 455 consecutive patients undergoing coronary artery bypass grafting (CABG) in one unit between 1990 and 1993 were retrospectively analysed with particular reference to the incidence of atrial fibrillation (AF), and with reference to any postoperative management that might have influenced this incidence. The recorded incidence of AF fell from 21% in 1990 to 11% in 1993. During this same period: the use of potassium chloride (KCl 20‐40mmol/l) supplements in the intravenous fluid replacement during the Immediate postoperative period increased from 0‐96%; the use of intravenous frusemide decreased from 12‐3%; and the practice of prescribing up to four Frumil (frusemide/amiloride hydrochloride) tablets daily was replaced by a more usual one tablet daily. Although the aetiology of AF post cardiac surgery is multifactorial, these three factors are implicated in the decreasing incidence of this complication in one unit.

Hypergastrinemia, Dysuria-Hematuria and Metabolic Alkalosis: Complications Associated with Gastrocystoplasty

Purpose To help determine the etiology and most appropriate treatment regimen for hypergastrinemia, dysuria-hematuria and metabolic alkalosis following augmentation gastrocystoplasty. Materials and Methods Two patients who presented with refractory metabolic alkalosis (1 with dysuria-hematuria) underwent extensive laboratory evaluation, complete upper gastrointestinal evaluation and intravesical pH probe placement. Results Both patients eventually required high dose oral potassium chloride supplementation. Bladder mucosal pH was not reflected by buffered urinary pH. Both patients demonstrated significant gastroesophageal reflux and diminished overall gastric acid output. Conclusions Outpatient maintenance on potassium chloride supplementation may be warranted in select patients and appears to be preferable to histamine blockade or omeprazole. Postoperative screening esophagogastroscopy and an additional surgical maneuver might be indicated to prevent possible adverse sequelae of reflux esophagitis. Gastrocystoplasty may be an inappropriate operation in children with renal insufficiency who have not had metabolic acidosis.

Acute Muscular Paralysis in an Adult With Subclinical Bartter's Syndrome Associated With Gentamicin Administration

We report an adult case of asymptomatic Bartter's syndrome with the first presentation of hypokalemic paralysis triggered by gentamicin injection. Marked hypokalemia and hypomagnesemia associated with excessive kaliuresis and magnesiuria were found. Plasma renin activity and aldosterone concentration were high, but blood pressure was normal. Renal biopsy revealed hypercellularity of the renin-producing cell of the juxtaglomerular apparatus. Muscular paralysis subsided after potassium chloride supplementation. Hypokalemia was corrected with potassium and magnesium supplements and the use of diclofenac. To the best of our knowledge, there have been no reports of muscular paralysis associated with gentamicin in Bartter's syndrome.

Potassium Level and Wintering Cow Performance: Study Two

Ninety-six crossbred gestating cows were randomly assigned to one of three treatments that provided the following levels of supplemental K: 1) 7, 2) 47, and 3) 78g/h/d, respectively, in a cottonseed meal (CSM)-based range cube. Treatments 2 and 3 included potassium chloride as the source of additional K. A CSM-based range cube was fed to provide .18kg crude protein/h/d. Cows were gathered from the same dormant winter pasture three times per week, individually stalled, and fed their respective supplements.During the 93- to 96-d gestation period, cows fed supplemental K (treatments 2 and 3) tended to lose less weight than those not supplemented with potassium chloride. Supplementing K during the 23-d lactation period at the 94g/h/d K level tended to reduce weight loss compared to the control or 156gK level. Condition score change through calving was significantly improved with potassium chloride supplementation. Calf daily gain from birth to mid-April tended to be improved when cows were supplemented with 94gK. The K requirement for dry gestating beef cows appears to be approximately .65% on a dietary dry matter basis.

Drinking Water Temperature and Potassium Chloride Supplementation Effects on Broiler Body Temperature and Performance During Heat Stress

Four experiments were conducted to evaluate the effect of drinking water temperature and KCl supplementation on broiler performance during cycling temperature heat stress. Drenching birds with 12.8°C water reduced body temperature at a6 min post-drenching for 37°C (43 vs. 43.5), but not 24°C (43.5 vs. 43.5) exposed birds. Feed consumption and body weight gain improved as drinking water temperature declined from 43.3 to 10°C. Potassium chloride supplementation increased feed consumption and weight gain of birds offered cold water (P < .05). However, KCl supplementation of warm drinking water had no beneficial effect on feed consumption or weight gain. Body temperature rise during heat stress exposure was less (P < .05) for 10 vs. 43.3°C drinking water temperature and drinking water heat sink potential was positively correlated (P < .09) with gain, feed consumption, and gain/feed ratio.

Renal Papillary Cytoplasmic Granularity and Potassium Depletion Induced by Carbonic Anhydrase Inhibitors in Rats

Renal papillary cytoplasmic granularity (RPCG) induced by carbonic anhydrase inhibitors (CAIs) in rats is characterized by the accumulation of dense secondary lysosomes in epithelial, endothelial, and interstitial cells and may be related to drug-induced potassium depletion. Female Sprague-Dawley rats were given the CAI, acetazolamide, by gavage. Half were supplemented with 1% potassium chloride in the drinking water. Two treated groups were allowed to recover for 1 or 2 mo. Potassium supplementation inhibited RPCG by 80% but produced little amelioration of the mild 13% decrease in serum potassium induced by 200 mg/kg/day acetazolamide for 28 days. Acetazolamide-induced RPCG is reversible because 1- and 2-mo recovery periods decreased the incidence by 75% and 80%, respectively. The results support the hypothesis that RPCG is related to potassium depletion secondary to carbonic anhydrase inhibition. Because supplementation of potassium chloride had little effect on serum potassium, these data suggest that depletion of renal medullary potassium content is important in the pathogenesis of RPCG as previously suggested by others. Other types of diuretics that produce hypokalemia as a side effect may not deplete medullary potassium since RPCG has not been reported in humans or animals given these drugs.

Effect of low sodium diet or potassium supplementation on adolescent blood pressure.

The roots of essential hypertension extend back into the first two decades of life, suggesting that effective intervention during those years may lead to a reduction in the incidence of adult hypertension. Decreasing the dietary sodium/potassium ratio offers a potentially effective approach to blood pressure reduction. This study tested the feasibility of 3-year sodium reduction or potassium supplementation in adolescents and the effect of these interventions on the rate of rise of blood pressure during adolescence. After 19,452 5th to 8th grade students were screened, 210 from the upper 15 percentiles of blood pressure distribution (105 boys, 105 girls) were randomly assigned to one of three groups: low sodium diet (70 mmol sodium intake per day), potassium chloride supplementation (normal diet plus 1 mmol/kg potassium chloride per day), or placebo (normal diet plus placebo capsule). Capsules for the potassium chloride and placebo groups were administered in a double blind protocol. Blood pressure was measured every 3 months for 3 years. The effect of the intervention was determined by comparing the rate of rise (slope) of blood pressure among the groups using a random-coefficient growth curve model. The boys groups and the girls placebo group had similar positive blood pressure slopes that were significantly different from zero. The girls low sodium group had a slightly negative slope (significantly lower than the slope of the girls placebo group), and the girls potassium group had a slightly positive slope. Both of these slopes were not significantly different from zero and were significantly lower than the slopes of the respective boys groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Potassium Chloride Supplementation on Growth of Heat-Distressed Broilers

Broiler chicks were reared under cyclic temperature conditions (26.8° to 36.7°C) and given supplemental potassium chloride (KCl) in the drinking water during a 21 day trial. Four treatments were evaluated: No KCl (control), KCl supplementation continuously; KCl during only the hot 12 hours of the ambient temperature cycle; and KCl during only the cool 12 hours of the ambient temperature cycle. No treatment differences for feed consumption were observed. Birds supplied continuously with KCl gained 7% more weight (P<. 05) than unsupplemented birds. There was a trend for increased gain in birds supplied with potassium during the hot 12 hour period, but not during the cool 12 hour period.

Effect of dietary potassium chloride in borderline hypertensive rats.

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.

False diagnosis of intestinal obstruction in a fetus with congenital chloride diarrhea

Intestinal obstruction is often diagnosed prenatally by ultrasound, providing an opportunity for prenatal counseling, genetic investigation, and planned delivery at a perinatal center. We describe a patient with typical features of fetal bowel obstruction, who was found at birth to have congenital chloride diarrhea. A 25-year-old white woman had marked polyhydramnios; multiple dilated, fluid-filled loops of intestine were seen in the fetal abdomen on prenatal ultrasound. However, postnatally, there was no evidence of bowel obstruction. The infant girl passed large amounts of watery stools, but tolerated feeds well. A rectal biopsy showed normal ganglion cells. On the fourth day of life her serum sodium and chloride were markedly decreased, and stool chloride levels were diagnostic of congenital chloride diarrhea. She was placed on sodium chloride and potassium chloride supplements, and her serum electrolytes normalized. Congenital chloride diarrhea is a rare, inherited condition caused by an abnormality of intestinal electrolyte transport. This case illustrates that it may present prenatally with a picture similar to that seen with intestinal obstruction.

Potassium Affects Actigraph-Identified Sleep

The present study examines the effects of potassium supplementation on sleep quality and phase, as indirectly inferred from wrist actigraphy and sleep logs, in normal young males on a low-potassium diet. A randomized, double-blind, placebo-controlled, counterbalanced crossover design compared 1 wk of oral potassium chloride supplements (96 meq/day) to 1 wk of identical placebo capsules. Outcome measures were taken from sleep logs and wrist actigraphy. Sleep was indirectly inferred from wrist-actigraph data using a computer algorithm. Potassium supplementation significantly delayed sleep-log-identified Bedtime (p less than 0.001). Potassium reduced Sleeping Interval for both sleep-log (p less than 0.01) and wrist-actigraph (p less than 0.1) data. Potassium significantly increased actigraphic Sleep Efficiency (p less than 0.05) due to a reduction in actigraphic Wake after Sleep Onset (WASO) (p less than 0.05). No effect of potassium on actigraphic sleep phase was observed. Side effects were minimal and not significantly different between treatment conditions. The results may indicate an improvement in sleep consolidation with potassium supplementation. Further studies using standard polysomnography are required to define potassium's effects on human sleep.

Blood and Urinary Aggregator and Inhibitor Composition in Controls and Renal-Stone Patients from Northeastern Thailand

Renal-stone disease (RSD) is common in the rural communities of northeastern Thailand. We report the biochemical composition of blood and urine in 25 healthy city dwellers (G1), 12 healthy village dwellers (G2) and 25 village dwellers who had RSD (G3). They were male with a range of ages between 20 and 50 years and were free of renal failure, urinary infection, urinary obstruction and systemic illness. The results showed that hypocitraturia, hypokalemia and hypokaliuria were more common in the latter 2 groups. The 24-h urinary citrate excretion correlated significantly with urinary potassium in G3 cases (r = 0.704, p = 0.0002). After potassium chloride supplementation, serum and urinary potassium increased remarkably (p less than 0.003 and p = 0.002, respectively), whereas urinary citrate remained unchanged. Our results suggest that the predominant abnormality in our RSD patients were hypocitraturia and potassium deficiency and that these may be related.

The Influence of Oral Potassium Chloride on Blood Pressure in Hypertensive Men on a Low-Sodium Diet

Clinical and epidemiologic studies suggest that the intake of potassium chloride lowers blood pressure. To investigate whether supplemental potassium chloride (96 mmol of microcrystalline potassium chloride a day) reduced the need for antihypertensive medication in hypertensive men on a restricted-sodium diet, we conducted a randomized, placebo-controlled, double-blind clinical trial. A total of 287 men 45 to 68 years of age, 142 given potassium chloride and 145 given placebo, were followed for an average of 2.2 years after the withdrawal of their antihypertensive medication. Men in both groups received instructions on following a low-sodium diet. Overnight urinary sodium excretion fell from 63 mmol per eight hours at base line to an average of 45 mmol per eight hours during follow-up. Participants given supplemental potassium chloride had significantly higher (P less than 0.001) serum potassium levels and urinary potassium excretion (averaging 4.5 mmol per liter and 42.5 mmol per eight hours, respectively) during follow-up than participants given placebo (4.2 mmol per liter and 20.0 mmol per eight hours). Seventy-nine participants in each group required reinstitution of antihypertensive medication according to strict indications defined by the protocol. No significant differences in systolic or diastolic blood pressure were observed between the two groups. During follow-up, systolic and diastolic blood pressure averaged 130.6 and 82.5 mm Hg, respectively, for participants given supplemental potassium, and 132.5 and 83.1 mm Hg for participants given placebo. We conclude that supplemental potassium chloride does not reduce the need for antihypertensive medication in hypertensive men on a restricted-sodium diet.

Lymphocytic sodium and potassium pump function in Bartter's syndrome.

Bartter's syndrome is characterized by chronic hypokalaemia, activation of the renin-angiotensin system and normal blood pressure. To investigate whether a generalized disturbance of sodium-potassium pump function might be of pathogenetic importance, lymphocytic sodium-potassium homeostasis was examined in 5 patients suffering from Bartter's syndrome. Two of the patients were treated with potassium chloride supplementation, the others were without medical treatment when studied. All were severely hypokalemic (serum potassium 2.8 +/- 0.24 mmol/l, mean +/- SEM). Lymphocyte sodium and potassium concentration (14.4 +/- 0.37 and 94.4 +/- 7.7 mmol/l, respectively), ouabain sensitive 22Na-efflux rate constant (2.68 +/- 0.25 h), and absolute ouabain sensitive efflux rate (38.16 +/- 4.2 mmol l-1 h) did not differ from matched controls. Ouabain binding capacity was 126 900 +/- 23 500 sites/cell in patients vs 50 400 +/- 17 900 in controls (p less than 0.05). In conclusion, patients with Bartter's syndrome may have an intrinsic abnormal pump function, characterized by an increased pump density and a low cation turn-over rate per pump unit.

Electrolyte disarray and cardiovascular disease

Thiazide diuretics have frequently been recommended as initial therapy in patients with mild to moderate hypertension. However, their undesirable metabolic consequences have been suspected of contributing to increases in cardiovascular morbidity and mortality. Even at low doses, there is a definite decrease in both potassium and magnesium levels. The degree of decrease in potassium and magnesium levels has been shown to be directly related to the hydrochlorothiazide dosage. Many investigators have now reported an increase in ventricular ectopy associated with diuretic-induced hypokalemia. Whereas there is no single study that conclusively proves that thiazide therapy results in malignant arrhythmias and an increased risk of sudden death, the circumstantial evidence is strong. Although sodium restriction is critical to potassium restoration, it rarely works alone. Potassium chloride supplementation can be effective in restoring potassium but not magnesium. Potassium-sparing diuretic combinations can both prevent and treat hypokalemia and hypomagnesemia, possibly reducing the risk of potentially lethal arrhythmias and sudden death.

Metabolic Effects of Hydrochlorothiazide and Enalapril During Treatment of the Hypertensive Diabetic Patient

To determine the effect of enalapril maleate and low-dose hydrochlorothiazide therapy on blood pressure and glucose and lipid homeostasis in hypertensive type II diabetic patients, we treated nine of these patients sequentially with placebo, hydrochlorothiazide (25 mg/d with supplemental potassium chloride), and enalapril (10 to 20 mg/d). Sitting blood pressure fell significantly and to comparable levels with both hydrochlorothiazide and enalapril monotherapy. Enalapril monotherapy was associated with a slight, but not significant, fall in fasting blood glucose levels and with a significant fall in hemoglobin A1c levels. This improved glucose homeostasis could not be explained satisfactorily by changes in peripheral insulin sensitivity or hepatic glucose output, determined with the euglycemic clamp technique, or by changes in fasting serum insulin levels or monocyte insulin binding. In these low doses, hydrochlorothiazide did not worsen glucose homeostasis. Serum total cholesterol levels were significantly lower with enalapril therapy than with hydrochlorothiazide therapy or with placebo, and serum high-density lipoprotein cholesterol and triglyceride levels did not change significantly with either treatment. Thus, by providing effective blood pressure control and beneficial metabolic effects, enalapril therapy appears ideal for treatment of hypertension in diabetic patients. Similarly, low-dose hydrochlorothiazide therapy appears to have fewer metabolic complications in these patients and is, therefore, a logical alternative to substitute for, or add to, enalapril therapy.

Ventricular Ectopic Activity With Diuretic Therapy

The arrhythmogenic potential of diuretic-induced hypokalemia in patients with uncomplicated hypertension has been controversial. Thirty-two hypertensive patients with previous diuretic-induced hypokalemia, normal 24-hour ambulatory ECG monitoring, and normal exercise testing were treated with 100 mg hydrochlorothiazide (HCTZ) daily (Group 1) to induce hypokalemia or with a combination of HCTZ with amiloride (Group 2) to attempt to maintain plasma potassium levels in the normal range during diuretic therapy. Those Group 1 patients (Group 1A) with increased ventricular ectopic activity (VEA) during HCTZ therapy were subsequently potassium-repleted with amiloride and with supplemental potassium chloride to evaluate the effect of these treatments on VEA. One Group 1 patient died suddenly after 12 days of HCTZ therapy. Autopsy findings suggested an arrhythmic death. Six Group 1 patients who had increased VEA with HCTZ treatment had reductions in VEA with amiloride or supplemental potassium chloride. Group 2 patients did not have a significant increase in VEA. Thus, diuretic therapy appears to cause VEA primarily by electrolyte changes that are induced.

Intracellular sodium and potassium concentrations in erythrocytes of patients with primary aldosteronism.

Intracellular concentration of sodium ([Na]i) and potassium ([K]i), and the ouabain sensitive sodium efflux rate constant (ERCos) in erythrocytes were determined in patients with primary aldosteronism, before and after the surgical removal of the adrenocortical adenoma and in comparison to those in healthy controls. Without treatment, [Na]i was higher and ERCos was lower in patients with primary aldosteronism than in controls (10.60 +/- 0.96 vs. 8.25 +/- 0.89 mmol/l cells, p less than 0.01; 0.156 +/- 0.040 vs. 0.255 +/- 0.047/hour, p less than 0.01, respectively). After the surgery, [Na]i was decreased to 7.70 +/- 0.64 mmol/l cells and ERCos was increased to 0.273 +/- 0.031/hour and these values were similar to those in controls. [K]i in primary aldosteronism was not affected by the surgery (from 96.79 +/- 2.03 to 98.8 +/- 3.84 mmol/l cells) and was not different from that in controls (99.11 +/- 3.42 mmol/l cells). In 2 patients, normalization of the serum potassium following an oral potassium chloride supplement caused only partial improvement in [Na]i and ERCos. These results suggest that an inhibition of sodium pump activity resulting in elevated [Na]i may play an important role in the pathogenesis of high blood pressure in patients with primary aldosteronism.