Efficacy of oral potassium chloride administration in treating lactating dairy cows with experimentally induced hypokalemia, hypochloremia, and alkalemia.

Hypokalemia occurs commonly in lactating dairy cows. The objectives of this study were to determine (1) whether a 24-h oral KCl dose of 0.4 g/kg of body weight (BW) was effective and safe in hypokalemic cattle; (2) whether potassium was best administered as 2 large doses or multiple smaller doses over a 24-h period; and (3) the effect of oral KCl administration on plasma Mg concentration and urine Mg excretion in fasted lactating dairy cattle. Plasma K and Cl concentrations were decreased, and blood pH increased, in 15 lactating Holstein-Friesian cows by administering 2 intramuscular (i.m.) 10-mg injections of isoflupredone acetate 24h apart followed by 2 i.m. injections of furosemide (1mg/kg of BW) 8h apart and by decreasing feed intake. Cows were randomly assigned to 1 of 3 treatment groups with 5 cows/group: untreated control (group C); oral administration of KCl at 0.05 g/kg of BW 8 times at 3-h intervals (group K3); and oral administration of KCl at 0.2g/kg of BW twice at 12-h intervals (group K12). A 24-h KCl dose rate of 0.4 g/kg of BW increased plasma and milk K concentration and plasma Cl concentration, and corrected the metabolic alkalosis and alkalemia, with no clinically significant difference between 2 large doses (group K12) or multiple small doses (group K3) of KCl over 24 h. Oral KCl administration decreased peripheral fat mobilization in cattle with experimentally induced hypokalemia, as measured by changes in plasma nonesterified fatty acid concentration, and slightly augmented the fasting-induced decrease in plasma Mg concentration. Our findings support recommendations for a 24-h oral KCl dose of 0.4 g/kg of BW for treating moderately hypokalemic cattle. Additional Mg may need to be administered to inappetant lactating dairy cattle being treated with oral KCl to minimize K-induced decreases in magnesium absorption.

Enteral electrolytic solutions administered in continuous flow via naso-ruminal route in adult goats.

This study aimed to investigate the effects of maintenance enteral electrolytic solutions administered naso-ruminally in continuous flow in adult goats subjected to water and food restriction. Six adult non-pregnant and non-lactating female goats, aged between two and five years old, were used in a crossover (6 × 2) study. Solution 1 (SEE1) comprised: 4.5 g sodium chloride (NaCl); 1 g potassium chloride (KCl); 0.5 g magnesium chloride (MgCl); 1 g calcium chloride in 1,000 ml of water (measured osmolarity: 202 mOsm/l). Solution 2 (SEE2) comprised: 4.5 g of NaCl; 1 g of KCl; 0.5 g of MgCl; 2 g of calcium acetate in 1,000 ml of water (measured osmolarity: 212 mOsm/l). The solutions were administered naso-ruminally at a dose rate of 15 ml/kg/hr, for 12 hr. The animals were evaluated at times T-24, T0, T4, T8, T12, and T24. Both enteral electrolytic solutions were effective in expanding blood volume. SEE1 showed a low-intensity acidifying potential, while SEE2 showed behavior of a neutral enteral electrolytic solution.

KCl cotransport activity in light versus dense transferrin receptor-positive sickle reticulocytes.

A subset of sickle cells becomes K(+)-depleted and dehydrated before or soon after leaving the bone marrow. These young cells may be identified in blood as transferrin receptor-positive (TfR+) dense reticulocytes. KCl cotransport, which is normally active in young erythroid cells with a maximum at pH 6.8, is a candidate pathway for K+ depletion of sickle reticulocytes. In this investigation, KCl cotransport activity was evaluated in young, TfR+ cells which had become dense in vivo and in age-matched cells which had retained normal hydration. Sickle erythrocytes were first separated into three primary density fractions, with care taken to preserve the in vivo hydration state. After normalization of intracellular hemoglobin concentration with nystatin, the cells were incubated at 37 degrees C for 20 min at pH 6.8 and 7.4. Before and after incubation, each primary fraction was separated into four secondary density fractions. The percentage of TfR+ cells in each secondary fraction was measured and a density distribution for TfR+ cells was determined for each primary fraction before and after incubation. The density shift during incubation was a measure of KCl cotransport. TfR+ cells from the denser primary fractions II and III had significantly more density shift than TfR+ cells from the light fraction I. Although the shifts were larger at low pH, differences between primary fractions were also observed at pH 7.4. These data indicate that the cells which become dense quickly in vivo have more KCl cotransport activity than those which remain light in vivo, and support this pathway as a primary mechanism for dehydration of young sickle cells.

Potassium chloride supplementation alone may not improve hypokalemia in thyrotoxic hypokalemic periodic paralysis.

This article reports a 29-year-old man who came to the Emergency Department because of sudden onset of bilateral lower extremity weakness and inability to walk after intake of a high carbohydrate meal and alcohol. He was found to have severe hypokalemia, with K(+) level at 1.7 mmol/L. However, after administration of potassium chloride (KCl), 10 mEq/h intravenous (i.v.) drip for 4 h, follow-up serum potassium was even lower at 1.5 mmol/L and the patient complained of persistent weakness. Twenty mg of propranolol, a non-selective beta-blocker, was given orally and a dramatic improvement of muscle power to grade 5 was noted after 30 min of administration. On the fifth day after discharge, he had another episode of bilateral lower extremity weakness after ingesting a mouthful of alcohol. Muscle power recovered completely after i.v. drip of KCl, 20 mEq. Laboratory data revealed an underlying primary hyperthyroidism for which he was given anti-thyroid agents and beta-blockers.

Evidence for the presence of volume-sensitive KCl transport in 'young' human red cells.

'Young' human red cells are shown to possess a specific K+ pathway which is dependent on Cl- and sensitive to cell volume. This system was latent in 'mature' cells but was revealed by high hydrostatic pressure. This suggests the pathway is functionally active in 'young' cells but becomes masked with cell maturation.

Effects of potassium adaptation on blood pressure and pressor responses in normotensive and renal hypertensive Wistar rats.

Potassium adaptation reduces blood pressure (BP) in hypertensive humans and animals but its effects on normotensive BP and the nature of pressor responses to vasoactive drugs are not known. We measured directly, the mean arterial pressure (MAP) of normotensive control, normotensive potassium-adapted (given 0.75% potassium chloride solution for 5 weeks), renal hypertensive (RHP), and renal hypertensive Wistar rats later adapted to potassium. The maximum percentage change, the ED25, and recovery times after bolus injections of noradrenaline (NA), angiotensin II (Ang. II), sodium nitroprusside (SNP), and acetylcholine (ACh) were compared. The MAP of normotensive potassium-adapted rats was significantly lower than that of the normotensive controls (95.6+/-5.0 vs. 110.8+/-2.8 mmHg, p<0.05). The potassium-adapted hypertensive rats (RHP-A) also had significantly lower MAP values than the non-adapted hypertensive ones (116.0+/-4.4 vs. 138.2+/-4.1 mmHg, p<0.01). Potassium adaptation significantly blunted responses to NA and augmented responses to SNP but while the duration of action of Ang. II was significantly shortened, that of SNP was significantly increased. We conclude that potassium adaptation reduces BP in the normotensive and hypertensive rats and may influence both the degree and duration of action of vasoactive drugs given as bolus injections.

[Salt wasting syndrome caused by congenital, insufficient synthesis or aldosterone function--etiology, diagnosis and management]. / Zespól utraty soli spowodowany wrodzona, niedostateczna synteza lub funkcja aldosteronu -- etiologia, diagnostyka i postepowanie.

Salt wasting syndrome is caused by a congenital or acquired synthesis disorder or by the aldosterone function disorder. It manifests itself by ionic disorders where the sodium and chlorine level decrease with the simultaneous potassium retention. Synthesised aldosterone is in the glomerular zone of the adrenal cortex. Symptoms of dyselectrolitemia are not distinctive, they develop within a few first days of life. The suction aversion, apathy, lack of growth or progressing, body mass loss is being noticed. The most often cause of salt wasting syndrome is the congenital cortical adrenal hyperplasia (CAH) caused by 21-hydroxylase enzyme deficit. The classic form with and without salt wasting (SW), as well as non-classic form is distinguished. The therapy of SW form depends on Hydrocortisone and Cortineff administering. The other forms of salt wasting syndrome occur not so often and these are: aldosterone synthesis deficit, dehydrogenase 3beta-hydroxysteroid deficit, lipoid cortical hyperplasia, adrenal hypoplasia congenital (AHC), adrenoleukodystrophy and pseudohypoaldosteronism. The knowledge of the symptoms and causes of salt wasting syndrome allows for the proper therapeutic management and contributes to the regular psychophysical infantile development of the children.

Sodium reduction during cardiopulmonary bypass: Plasma-Lyte 148 versus trial fluid as pump primes.

OBJECTIVES: We compared effects on plasma sodium concentrations plus calculated plasma tonicity of two "balanced" crystalloid solutions used as 2 L pump primes during cardiopulmonary bypass (CPB): Plasma-Lyte 148 (sodium concentration, 140 mmol/L; potassium concentration, 5 mmol/L) versus a bicarbonate-balanced fluid (sodium concentration, 140 mmol/L; potassium concentration, 0 mmol/L). DESIGN, SETTING AND PARTICIPANTS: We analysed pooled data from two prospective interventional studies performed in university-affiliated hospitals, from 50 patients undergoing elective cardiac surgery. INTERVENTIONS: Participants were allocated equally to Plasma-Lyte 148 or bicarbonate-balanced fluid, with plasma electrolytes measured by direct ion selective electrodes immediately before bypass (pre-CPB), within 3 minutes of commencement (T2), and before bypass cessation (end-CPB). RESULTS: Plasma sodium fell at T2 in 46 patients (92%) (P<0.0005). With Plasma-Lyte 148, the mean sodium decreased by 3.0 mmol/L (SD, 1.7 mmol/L), and with bicarbonate-balanced fluid it decreased by 2.2 mmol/L (SD, 1.1 mmol/L) (P=0.002). The mean tonicity fell by >5 mOsm/kg for both groups (P<0.0005). At end-CPB, the mean sodium for both groups remained reduced by >2 mmol/L (P<0.0005). In the group receiving Plasma-Lyte 148, 52% of patients were hyponatraemic (sodium<135 mmol/L) at T2 and end-CPB. CONCLUSIONS: Sodium reductions were common with both priming solutions, but more severe with Plasma-Lyte 148. Crystalloid priming solutions require sodium concentrations>140mmol/L to ensure normonatraemia throughout CPB.

Band-3 protein-mediated anion conductance of the red cell membrane. Slippage vs ionic diffusion.

The band 3 protein-mediated, valinomycin-induced KCl efflux continues to increase with increasing [KCl] when the Cl-/Cl- equilibrium exchange becomes saturated. This suggests the existence of a band 3-mediated component of Cl- flux that contributes to the electrical conductance without being related to slippage; i.e., equilibration of the unloaded transport protein between the two membrane surfaces.

The study of some possible measurement errors in clinical blood electrolyte potentiometric (ISE) analysers.

The understanding of the most important sources of error in potentiometric blood analyser which might contribute to better instruments measurement repeatability is very often marginalized in fabrications and daily operation of some commercial blood analysers. In this paper ISEs-potentiometric measurements were performed and validated in Clinical Institute of Laboratory Diagnosis of the Zagreb University School of Medicine and Clinical Hospital Centre, using a carefully designed and constructed fully automated (computerised) homemade ISE-based blood electrolyte analyser constructed with an in-line five-channel flow-through measuring cell. The influence of electrolyte concentration of the salt bridge is reported. Special attention has been paid to the reference electrode design, and constructions which can operate in open liquid junction and membrane restricted liquid junction modes are described.

KCl cotransport in HbAA and HbSS red cells: activation by intracellular acidity and disappearance during maturation.

Low intracellular pH was shown to be a potent activator of the KCl cotransport system in HbSS red cells, and in reticulocyte-rich fractions of HbAA red cells. Rheological experiments indicated that cell dehydration via the KCl cotransporter in response to low pH decreased the filterability of HbSS red cells. In vitro maturation experiments showed that the KCl cotransport system was rendered cryptic rapidly, in contrast to choline transport, and serine transport via system ASC, which disappeared much more slowly.

The relationship between KCl infusion and changes of ECG, electrolytes of plasma and K content of donkey's red blood cells.

Sudden marked increases in the serum potassium concentration, up to 8 to 9 meq L(-1), are the result of transcellular movement of potassium and are associated with profound electrocardiographic abnormalities and fluid shifts. Electrocardiographic changes associated with hyperkalemia have been described in the cat, the dog, the horse and are well documented in man. Since there is no research about the effects of hyperkalemia on electrocardiogram of donkey, the purpose of this study was to induce the experimentally hyperkalemia in donkey and studying the relationship between KCl infusion and changes of ECG, electrolytes of plasma and K content of donkey's red blood cells. This research was carried out in seven clinically healthy female donkeys, injected with 0.35 molar potassium chloride solutions to jugular vein. Results indicated that potassium content of RBC at 30, 45, 60, 75 and 90 min, blood potassium level at 30, 45, 60, 75 and 90 min, blood calcium at 60, 75, 90 and 105, increased significantly and blood magnesium decreased significantly at 135 min. Electrocardiographic changes were first degree A-V block, wandering pacemaker, inversion of negative to positive T-wave, flattening of the P-wave, ventricular premature beat, sinus arrest, bradycardia and sinus tachycardia.

Plasma chloride and alkalaemia in pyloric stenosis.

Fifty infants with infantile hypertrophic pyloric stenosis were studied prospectively to evaluate the reliability of plasma chloride estimation in the assessment of the acid-base status on admission and during correction of alkalaemia. Four cases were subsequently excluded because of a breach of the study protocol, leaving 46 cases in the study. Seventeen (37 per cent) were normoacidaemic on admission; 13 had plasma chloride concentrations of greater than or equal to 106 mmol/l and four had chloride concentrations of 100-105 mmol/l on admission. Twenty-nine (63 per cent) were alkalaemic on admission; six cases had chloride concentrations of 100-105 mmol/l and 23 cases had concentrations of less than 100 mmol/l. Of those 29 cases requiring correction of alkalaemia, normoacidaemia was achieved at a plasma chloride concentration of greater than or equal to 106 mmol/l in 21 cases (72 per cent) and at a concentration of 100-105 mmol/l in eight cases (28 per cent). Plasma chloride is a reliable parameter in the assessment and correction of alkalaemia in infantile hypertrophic pyloric stenosis provided that a concentration of at least 106 mmol/l is the goal.

Potassium loss and cellular dehydration of stored erythrocytes following incubation in autologous plasma: role of the KCl cotransport system.

We studied the regulation of cell volume and cation content in erythrocytes stored at 4 degrees C under blood bank conditions for various lengths of time and subsequently incubated in autologous plasma at 37 degrees C for 4 or 24 h. Cell swelled during storage at 4 degrees C whereas marked K+ loss and cell shrinkage were observed when erythrocytes were incubated at 37 degrees C in autologous plasma. The cell shrinkage was inhibited only by the K+ Cl- cotransport-specific inhibitor, [(dihydroindenyl)oxy] alkanoic acid, and not by other specific inhibitors of cation transport systems such as ouabain (Na(+)-K+ ATPase pump), bumetanide (Na(+)-K(+)-Cl- cotransport) or carbocyanine (Ca+(+)-activated K+ channel). Acidification and swelling of the erythrocytes are well known to be able to activate the K+ Cl cotransport; such conditions, which were demonstrated to occur during the storage, could lead to activation of the K+ Cl- cotransport in reinfused cells. These data strongly support the evidence that K+ Cl- cotransport plays a role in K+ loss and dehydration of stored erythrocytes, when incubated in autologous plasma.

Establishing the direct-potentiometric "normal" range for Na/K: residual liquid junction potential and activity coefficient effects.

The observed reference ranges for sodium and potassium as determined by direct potentiometry vary from instrument to instrument, depending on the composition of the calibration standards. To resolve the existing confusion as to which reference intervals are most appropriately considered "normal," we propose a straightforward convention (based on plasma-water concentration units) in which the difference between direct (undiluted sample) and indirect (diluted sample) methodologies is accounted for by the volume displacement effect of proteins, lipids, and other dissolved substances in a typical plasma sample. Thus, the proposed reference intervals for sodium and potassium are approximately 7% greater by direct potentiometry than by procedures involving dilution. Data consistent with this convention can be obtained with a variety of aqueous-based calibrants, provided care is taken to minimize the errors resulting from activity coefficient and liquid junction potential effects. Additional experimental results are presented to show that these effects also account for the apparent suppression of the sodium ion concentration observed in the presence of bicarbonate ion.