alkalosis/kalium

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Correction of metabolic alkalosis by potassium chloride in ectopic adrenocorticotropic hormone syndrome.

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A 57-year-old white man presented with metabolic alkalosis, hypokalemia (pH 7.58, HCO3 >50 mEq/L, serum K 1.8 mEq/L) and hypertension. The initial evaluation was significant for markedly elevated serum cortisol and adrenocorticotropic hormone (ACTH) level; neither hormone showed circadian rhythm or

Ventilatory adaptation to metabolic alkalosis in adult awake potassium restricted rats.

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The resting ventilation of awake rats, developing metabolic alkalosis as a result of sustained dietary potassium (K) restriction, was compared to that of age-matched controls. Extending the measurements over 17 weeks and using adult rats indicated, as soon as the third week, a significant

Dietary NaCl determines severity of potassium depletion-induced metabolic alkalosis.

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It is uncertain whether, in humans, potassium depletion can cause or sustain metabolic alkalosis of clinically important degree in the absence of coexisting known alkalosis-producing conditions. Previously we found, in normal humans ingesting abundant NaCl, that dietary K+ depletion alone can induce

Long-term combined treatment with thiazide and potassium citrate in nephrolithiasis does not lead to hypokalemia or hypochloremic metabolic alkalosis.

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BACKGROUND Potassium citrate is commonly used in combination with a thiazide diuretic in the medical management of recurrent hypercalciuric nephrolithiasis. However, concerns have been raised that administration of this nonchloride potassium alkali with a kaliuretic and natriuretic agent such as

Blockade of ATP-sensitive potassium channels in cerebral arterioles inhibits vasoconstriction from hypocapnic alkalosis in cats.

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OBJECTIVE Recent studies have shown that the cerebral arteriolar dilation from hypercapnic acidosis is blocked by agents which inhibit KATP channels. These findings suggested that this response is due to opening of KATP channels. Because the repose to CO2 is a continuum, with hypercapnic acidosis

The distribution of potassium, sodium and chloride across the apical membrane of renal tubular cells: effect of acute metabolic alkalosis.

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Studies were undertaken to define the effect of acute metabolic alkalosis (hypertonic sodium bicarbonate i.v.) on the chemical gradients for potassium, sodium and chloride across the apical membrane of individual renal tubule cells. Electron microprobe analysis was used on freeze-dried cryosections

Potassium-depletion alkalosis in the rat.

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Studies were performed to investigate the role of concomitant chloride depletion in potassium-depletion alkalosis in the rat and the relationship between potassium depletion, plasma bicarbonate (PHCO3), and net acid excretion. 1) Selective potassium depletion (K-DEPL), potassium plus chloride

Plasma potassium response to acute respiratory alkalosis.

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Acute respiratory alkalosis (hyperventilation) occurs in clinical settings associated with electrolyte-induced complications such as cardiac arrhythmias (such as myocardial infarction, sepsis, hypoxemia, cocaine abuse). To evaluate the direction, magnitude and mechanisms of plasma potassium changes,

Development of the respiratory compensation to progressive metabolic alkalosis resulting from potassium depletion in conscious rats.

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1. 288 arterial blood samples were obtained at successive times, through indwelling catheters, from conscious rats subjected to selective dietary potassium restriction for up to 5 weeks. 2. In control rats with unrestricted access to potassium [HCO-3]a = 25.4 mmol/l, pHa = 7.47, PaCO2 = 34 mmHg,

Metabolic alkalosis reduces exercise-induced acidosis and potassium accumulation in human skeletal muscle interstitium.

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Skeletal muscle releases potassium during activity. Interstitial potassium accumulation is important for muscle function and the development of fatigue resulting from exercise. In the present study we used sodium citrate ingestion as a tool to investigate the relationship between interstitial H+

Intracellular alkalosis induced by increasing extracellular potassium. Ionic dependence and effects of amiloride and DIDS.

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The intracellular alkalinization produced when extracellular potassium concentration is increased above its normal levels was studied in the rat diaphragm muscle by determination of the steady-state distribution of [14C]-5,5-dimethyl-2,4-oxazolidinedione (DMO). Replacement of external Na+ with

Elevation of arterial potassium during acute systemic hypoxia is abolished by alkalosis.

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BACKGROUND Small elevations in plasma potassium evoke vasodilation in the peripheral circulation. Systemic hypoxia elevates arterial potassium and also modifies arterial pH. OBJECTIVE We examined the interaction between pH and potassium in blood during systemic hypoxia and the effect of pH on the

Dynamics of serum potassium change during acute respiratory alkalosis.

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In summary, one should be aware that hyperventilation and hypokalaemia occur frequently in the operating room under ordinary clinical conditions. An awareness of the rapidity with which these changes occur, and their extent as well as their potential hazards, should cause consideration of more

Hypokaliemic, hypochloremic alkalosis in cushing's syndrome. Observations on the effects of treatment with potassium chloride and testosterone.

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Effect of potassium salts administration on the renal excretion of bicarbonate during acute respiratory acidosis and hypochloremic alkalosis in the dog.

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