Rise In Potassium Concentration Research Articles

A Biochemical and Histological Assessment of Postmortem Changes to the Eyes of Domestic Pigs: A Preliminary Study.

The Postmortem Interval (PMI) is the time from the death of an animal to its discovery. From a veterinary forensic standpoint, an accurate estimation of the PMI is of particular importance, especially with the observed increase in deaths of domestic and wild animals. A preliminary study was conducted using the eyes of domestic pigs. A biochemical analysis was conducted on the vitreous humor of the eye, whilst a histological analysis was conducted on the retina. The eyes were stored at +4 °C and changes were assessed at time intervals of 0, 12, 24, 48, and 120 h. The biochemical analysis during the PMI established a decrease in sodium, chlorine, and glucose concentrations, and a rise in potassium concentration. Accordingly, a simple linear regression showed a significant correlation between changes in concentrations of sodium (Na+), potassium (K+), chloride (Cl-), and glucose, in relation to the PMI. The histological analysis showed evident morphological changes in the retina, which included homogenization of the rod and cone cells, pyknosis of the outer nuclear layer, homogenization of the outer plexiform layer, pyknosis of the inner nuclear layer, homogenization of the inner plexiform layer, and pyknosis of the nuclei of the ganglion layer of the retina.

Thanatochemistry: Study of vitreous humor potassium

This study has been carried out to determine the death interval from the biochemical parameter of vitreous potassium. In 308 medicolegal cases vitreous humor was taken and analyzed for potassium with known time of death. There was a linear rise in potassium concentration with increasing death interval. Regression equation was calculated for the same. The study indicates that potassium levels in vitreous for determining death interval are useful and can afford a good method of determining the death interval along with other traditional methods. Also the previously established formulae for estimating death interval from vitreous potassium were also studied.

Amiodarone attenuates fluoride-induced hyperkalemia in vitro.

Poisoning by hydrofluoric acid or fluoride salts results in hypocalcemia, hypomagnesemia, and hyperkalemia with subsequent cardiac dysrhythmias. In previous studies, quinidine attenuated fluoride-induced hyperkalemia in vitro, and enhanced survival in animals. Like quinidine, amiodarone is a potassium channel blocker, although amiodarone is more familiar to clinicians due to its recent inclusion in advanced cardiac life support (ACLS) protocols. This in-vitro study of human erythrocytes was designed to determine whether amiodarone could attenuate fluoride-induced hyperkalemia. Six healthy volunteers each donated 60 mL of blood on three occasions. Each specimen was divided into 12 tubes, incubated at 37 degrees C, and oxygenated with room air. An aqueous sodium fluoride (F(-)) solution was added to tubes 1-9. Incremental amounts of quinidine were added to tubes 1-4 (Q(1)-Q(4)) to attain calculated concentrations of 0.73 microg/mL, 1.45 microg/mL, 2.9 microg/mL, and 5.8 microg/mL, respectively. Incremental amounts of amiodarone were added to tubes 5-8 (A(1)-A(4)) to attain calculated concentrations of 0.38 microg/mL, 0.75 microg/mL, 1.5 microg/mL, and 3.0 microg/mL, respectively. Tubes 9-12 were controls for each of F(-), amiodarone, quinidine alone, and no additive, respectively. Extracellular potassium concentration ([K(+)]) was followed, and an objective endpoint was defined as the rise in potassium concentration at 6 hours. Fluoride produced a significant change in [K(+)] by 6 hours in all samples. Quinidine produced a J-shaped curve in its ability to attenuate the rise in [K(+)], with only one concentration, Q(3), demonstrating significance versus tube 9 (control). Amiodarone also demonstrated a J-shaped dose-response effect, with statistical significance at A(1), A(2), and A(3) versus tube 9 (control). There was no significant difference among the effective concentrations (Q(3), A(1), A(2), and A(3)) of both drugs. In this in-vitro model using human blood, amiodarone and quinidine both attenuated F(-)-induced hyperkalemia. Further study is indicated to determine whether amiodarone enhances survival in F(-)-poisoned animals.

Amiodarone Attenuates Fluoride‐induced Hyperkalemia in Vitro

AbstractPoisoning by hydrofluoric acid or fluoride salts results in hypocalcemia, hypomagnesemia, and hyperkalemia with subsequent cardiac dysrhythmias. In previous studies, quinidine attenuated fluoride‐induced hyperkalemia in vitro, and enhanced survival in animals. Like quinidine, amiodarone is a potassium channel blocker, although amiodarone is more familiar to clinicians due to its recent inclusion in advanced cardiac life support (ACLS) protocols. Objectives: This in‐vitro study of human erythrocytes was designed to determine whether amiodarone could attenuate fluoride‐induced hyperkalemia. Methods: Six healthy volunteers each donated 60 mL of blood on three occasions. Each specimen was divided into 12 tubes, incubated at 37°C, and oxygenated with room air. An aqueous sodium fluoride (F−) solution was added to tubes 1–9. Incremental amounts of quinidine were added to tubes 1–4 (Q1–Q4) to attain calculated concentrations of 0.73 μg/mL, 1.45 μg/mL, 2.9 μg/mL, and 5.8 μg/mL, respectively. Incremental amounts of amiodarone were added to tubes 5–8 (A1–A4) to attain calculated concentrations of 0.38 μg/mL, 0.75 μg/mL, 1.5 μg/mL, and 3.0 μg/mL, respectively. Tubes 9–12 were controls for each of F−, amiodarone, quinidine alone, and no additive, respectively. Extracellular potassium concentration ([K+]) was followed, and an objective endpoint was defined as the rise in potassium concentration at 6 hours. Results: Fluoride produced a significant change in [K+] by 6 hours in all samples. Quinidine produced a J‐shaped curve in its ability to attenuate the rise in [K+], with only one concentration, Q3, demonstrating significance versus tube 9 (control). Amiodarone also demonstrated a J‐shaped dose–response effect, with statistical significance at A1, A2, and A3 versus tube 9 (control). There was no significant difference among the effective concentrations (Q3, A1, A2, and A3) of both drugs. Conclusions: In this in‐vitro model using human blood, amiodarone and quinidine both attenuated F−‐induced hyperkalemia. Further study is indicated to determine whether amiodarone enhances survival in F−‐poisoned animals.

Exercise-induced Rise in Arterial Potassium is Enhanced in Patients with Impaired Exercise Tolerance.

We assessed the changes in arterial potassium concentration during exercise and recovery in relation to exercise tolerance in patients with impaired exercise tolerance. Sixteen patients with cardiac disease were subjected to a cardiopulmonary exercise test on a cycle ergometer. Arterial potassium and lactate concentrations were measured every minute during and after exercise, and ventilatory threshold (VT) and lactate threshold (LT) were identified. Before exercise, arterial potassium concentration was 3.8 +/- 0.3 mEq/l. It increased to 4.1 +/- 0.3 mEq/l at LT (p < 0.002 versus at rest), to 4.2 +/- 0.3 mEq/l at VT, and to 4.8 +/- 0.5 mEq/l at peak exercise (p < 0.001 versus at LT, p < 0.001 versus at VT). At an exercise intensity equivalent to 30, 40, 50 or 60% of predicted maximum oxygen uptake, the increase in arterial potassium showed a negative and significant correlation with %LT (r = -0.62 approximately -0.72, p < 0.01 approximately 0.05) and %VT (r = -0.62 approximately -0.75, p < 0.001 approximately 0.05), where %LT and %VT represent the ratios of LT and VT to the predicted maximum oxygen uptake, respectively. There was a good correlation between the rate of fall in potassium concentration during recovery and its increase during exercise. It was concluded that in patients with impaired exercise tolerance, the greater the degree of exercise intolerance, the greater the increase in arterial potassium concentration during exercise, and the steeper the fall in potassium concentration during recovery. Because the rise in potassium concentration during exercise and its fall during recovery were greater when the exercise level exceeded the anaerobic threshold, exercise levels below the anaerobic threshold are recommended for patients with cardiac diseases.

Adrenergic modulation of potassium metabolism in uremia

The effect of chronic beta adrenergic blockade on potassium homeostasis during moderate intensity exercise (40% of VO2 max) was examined in seven end-stage renal patients who were being maintained on chronic dialysis treatment. Subjects participated in three study protocols: 1) exercise alone, 2) exercise plus propranolol (a nonselective beta-1, beta-2 antagonist), and 3) exercise plus metoprolol (a specific beta-1 antagonist). The basal potassium concentration was similar in all three studies and averaged 4.95 +/- 0.12 mEq/liter. During Study 1 (exercise alone), plasma potassium rose by 0.26 +/- 0.09 mEq/liter. During exercise with propranolol, plasma K concentration rose significantly higher (delta plasma K = 0.44 +/- 0.26 mEq/liter; P less than 0.05 vs. exercise alone). In contrast, the rise in plasma K during exercise with metoprolol (delta plasma K = 0.20 +/- 0.08 mEq/liter) was similar to that observed with exercise alone. Differences in potassium homeostasis between metoprolol and propranolol could not be explained by differences in hemodynamic parameters, levels of potassium regulatory hormones, or acid base status. Thus, the higher rise in potassium concentration during exercise with propranolol could only be explained by adrenergic blockade at the beta-2 receptor site. These results support the concept that adrenergic control of extrarenal potassium homeostasis in dialysis patients is mediated at the beta-2 receptor. Since a deterioration in potassium homeostasis during exercise is observed with beta-2, but not beta-1 blockade, selective beta-1 adrenergic blocking agents may be safer in dialysis patients.

Effects of Ethanol on Urine Sodium and Potassium Concentrations and Osmolality in Water‐Loaded Rats

AbstractThe effects of ethanol on urine sodium, potassium and osmolality were investigated in rats kept in a positive water balance produced by prior consecutive water loaclings. Ethanol loacling was followed by rapid rises in urine output, sodium concentration and osmolality and a somewhat slower rise in potassium concentration. Presumably water loacling led to an increased glomerular filtration rate, which, with the inhibition of ion reabsorption caused by ethanol, was responsible for this rise.

Changes in Ionic Composition of Allantoic Fluid during Adrenocorticotrophin Infusion into Fetal Sheep

Intravenous infusion of synthetic adrcnocorticotrophin (ACTH) at rates of 1.0 or 4.0 μg/h into 3 chronically catheterized fetal sheep coincided with a fall in sodium and a rise in potassium concentrations of allantoic fluid which continued until premature delivery of the lambs. This is consistent with an association between changes in activity of the fetal pituitary-ACTH-adrenal axis and variations in the ionic composition of allantoic fluid.

Plasma potassium changes during rebreathing in the dog.

SummaryPlasma potassium was determined on dogs before and during 90 minutes of rebreathing, and immediately following return to air breathing. Potassium concentration rose gradually with increasing CO2 tensions during the first 60 minutes of rebreathing and remained essentially constant for the last 30 minutes. On changing from the high CO2 concentration to air breathing, a further rapid rise in plasma potassium concentration appeared. No evidence of a transient early rise in potassium concentration was observed.

Studies of the isolated perfused human placenta: I. Methods and organ responses

Summary Methods of perfusing the isolated, surviving human placenta under nearly physiologic circumstances are presented. During periods up to 12 hours, the rate of glucose utilization is about 1 Gm. per kilogram per hour. The production of organic acids causes a steady rise in hydrogen ion concentration with a parallel rise in potassium concentration. No conjugation of bilirubin with glucuronic acid could be observed. Hypoxia results in vasodilatation with increased rates of flow through the fetal vascular bed, whereas high oxygen pressures cause the reverse. It is believed that similar responses occur in utero. The fetal circulation is not responsive to epinephrine or norepinephrine but responds with vigorous vasoconstriction to serotonin and histamine.

Potassium in Histamine-Stimulated Gastric Secretion in Man

Summary 1.Shortly after the stimulation by histamine of gastric acid secretion in man there is a consistent and significant rise in the potassium concentration of the gastric contents. 2.This rise in potassium concentration usually precedes that for acid and then falls to sub-baseline levels without regard to changes in acid concentration. 3.The changes in potassium concentration are not correlated, in time with the changes in concentration of acid, sodium, or total chloride. 4.Since the potassium concentration of gastric juice is not constant, potassium is not necessarily secreted by the cellular source of the primary acid secretion, as proposed by previous investigators. The absence of correlation between concentrations of potassium and acid suggests that the movement of potassium into the gastric lumen is not an integral part of the primary acid secretion of the stomach.

Small volume perfusion system of the isolated rat liver

A perfusion system utilizing 25 ml of heparinized whole blood as a perfusate has been developed to study the metabolism of the isolated rat liver. Changes in the composition of the plasma of the perfusate were studied by circulation of the whole blood for 3 hours in the presence and absence of the liver. The discharge of glucose by the liver is marked by a pronounced initial hyperglycemia, which is countered slightly by red cell glycolysis. Despite continuous carbohydrate metabolism, a fall in sodium and a rise in potassium concentration occurs, ascribable chiefly to alteration of red blood cells. The hepatic glycogen content decreased slightly during perfusion. Urea production and bile flow were well preserved. Note: (With the Technical Assistance of Donna Cary and Veronica Mena) Submitted on June 26, 1959

THE EFFECT OF MUSCULAR EXERCISE ON PLASMA SODIUM AND POTASSIUM IN THE RAT

After running a distance of 100 meters in 7 minutes, untrained rats showed a rise in plasma potassium and a fall in plasma sodium as measured in tail vein samples. These changes are in accord with in vitro observations of the effects of exercise on isolated muscle preparations and similarly are taken to indicate a gain of sodium and a loss of potassium by the exercised muscles in the whole animal. Within 10 minutes of completion of the exercise, plasma sodium concentration was restored to normal while potassium was restored within 20 minutes. Exercise was accompanied by a fall in haematocrit, which remained low for up to 40 minutes. A period of 2 months of preliminary training modified the response to exercise. In these trained animals, a fall in sodium concentration occurred as before but the rise in potassium concentration was less in degree and the haematocrit did not change. It is suggested that the rate of increase of plasma potassium is an index of muscle efficiency while the height of plasma potassium is correlated with the fatigue limit of exercise.

THE EFFECT OF MUSCULAR EXERCISE ON PLASMA SODIUM AND POTASSIUM IN THE RAT

After running a distance of 100 meters in 7 minutes, untrained rats showed a rise in plasma potassium and a fall in plasma sodium as measured in tail vein samples. These changes are in accord with in vitro observations of the effects of exercise on isolated muscle preparations and similarly are taken to indicate a gain of sodium and a loss of potassium by the exercised muscles in the whole animal. Within 10 minutes of completion of the exercise, plasma sodium concentration was restored to normal while potassium was restored within 20 minutes. Exercise was accompanied by a fall in haematocrit, which remained low for up to 40 minutes. A period of 2 months of preliminary training modified the response to exercise. In these trained animals, a fall in sodium concentration occurred as before but the rise in potassium concentration was less in degree and the haematocrit did not change. It is suggested that the rate of increase of plasma potassium is an index of muscle efficiency while the height of plasma potassium is correlated with the fatigue limit of exercise.