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PubMedDate not supplied

[Comparative evaluation of the toxicity of potassium hydrocarbonate and potassium chloride].

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.

Animals↗
PubMed1989

A comparison of the effects of central v peripheral bolus injections of potassium chloride on aortic root potassium concentrations in swine.

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.

Animals↗
PubMed1977

Lidocaine treatment of experimental cutaneous lesions from potassium chloride injection.

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.

Animals↗
PubMed1987

The natriuretic effect of an acute peroral load of potassium chloride after inhibition of potassium secretion with amiloride or lithium.

The ability of the kidneys to excrete potassium after an acute peroral potassium load was studied in rats in which the kidney function was influenced by administration of amiloride or lithium for one month. Water, potassium chloride, or sodium chloride solutions were given by gastric tube immediately before a 2-hour clearance period. The results showed that a load of potassium given by gastric tube leads to an increase of potassium excretion in rats given either no treatment, amiloride, or lithium but the increase was about 50% lower in the lithium group. KCl administration provoked a considerable increase of sodium clearance (CNa) compared with the increase of CNa in the control group. The exaggerated natriuresis was apparently specific for potassium, since a peroral load of sodium chloride led to a more modest increase of CNa, an increase which was significant in control rats only. The increase of CNa in rats given a peroral load of potassium could not be explained by an increase of the proximal tubular fluid output, since the latter as measured by lithium clearance (CLi) remained unaltered. Since CNa/CLi rose considerably, the effect could be ascribed to an inhibition of the fractional distal sodium reabsorption.

Administration, Oral↗
PubMed1992

NuLYTELY (PEG 3350, sodium chloride, sodium bicarbonate and potassium chloride for oral solution).

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.

Colonoscopy↗
PubMedDate not supplied

A single blind normal volunteer bioavailability study of a new microencapsulated potassium chloride tablet compared with two reference potassium formulations.

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.

Administration, Oral↗
PubMed1982

Diffusion of lysozyme chloride in water and aqueous potassium chloride solutions.

The diffusion of lysozyme chloride in aqueous solution has been studied at 25 degrees C using the Goüy interferometric technique. The concentration dependence of the diffusion coefficient in water has been measured over the concentration range 1.1599-9.1556 gcm-3 and the results suggest a value of D 25, w at infinite dilution of 5.838 x 10(-6) cm2s-1. The variation in diffusion coefficient with ionic strength has also been considered by following the diffusion of 0.45% lysozyme chloride in a series of potassium chloride solutions. The value of D in 0.15 M KCl has been found to be approximately one quarter of that in water alone an the diffusion coefficient has been shown to increase markedly as the KCl concentration is reduced below 0.05 M. Interpretation of these observations involves consideration of solution electrostatic effects.

Chemical Phenomena↗
PubMed1978

Availability of Chloride Affects the Balance between Potassium Chloride and Potassium Malate in Guard Cells of Vicia faba L.

Electron probe microanalysis for K and Cl and enzymic determination of malate were performed on epidermal strips of Vicia faba L. which had been incubated with 0.1 equivalent of K(+) per liter in the absence or presence of Cl(-). In the absence of Cl(-), iminodiacetate, a presumed impermeant zwitterion, served as anion. With no Cl(-) in the medium, 91% of the K(+) imported into the guard cells during stomatal opening was neutralized by malate production; import of Cl(-) (presumably from the rest of the epidermal tissue) contributed 6%. In the presence of Cl(-), 50% of the necessary negative charges were provided by malate synthesis, 45% by Cl(-) import. Stomatal opening was not obviously affected by the chloride concentration in the incubation medium, but malate production declined roughly linearly with the logarithm of [Cl(-)] between 10(-5) and 10(-1) equivalent per liter.

Journal Article↗
PubMed1991

Formulation, bioavailability, and pharmacokinetics of sustained-release potassium chloride tablets.

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.

Adult↗
PubMed1989

Urinary kallikrein excretion during potassium chloride infusion in potassium-adapted rats: effect of amiloride.

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.

Amiloride↗
PubMed2003

Protective effects of dietary potassium chloride on hemodynamics of Dahl salt-sensitive rats in response to chronic administration of sodium chloride.

BACKGROUND: Dietary potassium supplementation decreases blood pressure and prevents strokes in humans, and prevents strokes and renal damage in Dahl salt-sensitive (DSS) rats. OBJECTIVE: To study the effects of various concentrations of dietary potassium chloride (KCl) on the hemodynamics of Dahl salt-resistant (DSR) and DSS rats receiving a 1% sodium chloride (NaCl) diet for 8 months, to determine whether there is an optimal dietary concentration of KCl that minimizes increases in blood pressure and causes least impairment of blood flow in the brain and kidneys. METHODS AND RESULTS: We found a biphasic effect on hemodynamic parameters as a function of dietary KCl in DSS rats of the Rapp strain fed 1% NaCl with increasing dietary KCl (0.7, 2.6, 4 and 8%). After 8 months receiving a diet containing 1% NaCl and 0.7% KCl, DSS rats had mean arterial pressures (MAP), plasma volumes, cardiac outputs and renal and cerebral vascular resistances that were significantly increased compared with those of DSR rats receiving the same diet. With a 2.6% KCl diet, all these parameters were significantly reduced compared with those in DSS rats fed the 0.7% KCl diet and were similar to those in DSR rats fed 2.6% KCl. Total peripheral resistance in DSR and DSS rats was similar on all diets. When KCl was increased to 4 and 8%, MAP, plasma volume, cardiac output and renal vascular resistance progressively increased in DSR and DSS rats, without changing total peripheral resistance. These changes paralleled increases in plasma aldosterone, which resulted from adrenocortical stimulation by the increasing dietary KCl; however, cerebral vascular resistance of DSR and DSS rats decreased significantly with a 4% KCl diet, despite increased aldosterone and sodium retention. Only DSS rats fed a 2.6% KCl diet had hemodynamics similar to those of DSR control rats fed the same diet, and hyperaldosteronism, sodium retention and increased plasma volume did not occur. CONCLUSION: 'Optimal' dietary KCl (2.6%) prevents hypertension and preserves cerebral and renal hemodynamics in DSS rats fed a diet containing 1% NaCl for 8 months, which causes hypertension when dietary KCl is limited or excessive.

Aldosterone↗
PubMed1992

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.

Animals↗
PubMed1987

Microencapsulation of potassium chloride with mastic.

The present investigation deals with the microencapsulation of potassium chloride with mastic. Spherical potassium chloride crystals with a mean particle diameter of approximately 450 microns were used. It could be shown that with a layer of mastic wall material thicker than 21 microns the release of potassium chloride in the in vitro test can be controlled for more than 6 h. The thickness of the wall material over the tested range of 21 to 33 microns has only a limited effect on the kinetics of release of potassium chloride. Increasing the thickness of the layer from 21 to 33 microns merely leads to a reduction of about another 10% in the amount of drug released in 6 h.

Capsules↗