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At least 253 records · Page 14Linked to original sources
PubMed1981

Hypokalemic metabolic alkalosis in normotensive infants with elevated plasma renin activity and hyperaldosteronism: role of dietary chloride deficiency.

The role of chloride deficiency in the generation of hypokalemic metabolic alkalosis with elevated plasma renin activity and plasma aldosterone levels, normal blood pressure, and a renal concentrating defect was studied in six infants given a soy formula that was deficient in chloride. A deceleration in linear growth, weight gain, and head circumference with age and delayed neurologic development were noted in every infant during the first six months of life. Microscopic hematuria and persistent elevation of plasma creatinine were noted in four of the infants. A renal biopsy in two infants revealed no juxtaglomerular hyperplasia, but interstitial tubular calcification was observed in one, and interstitial fibrosis was found in both. The generation of the hypokalemic metabolic alkalosis in these infants was explained by the reduced intake of chloride, and the addition of chloride alone to the diet resulted in a correction of the electrolyte abnormalities and the alkalosis.

Alkalosis↗
PubMed1976

Urinary excretion of beta2-microglobulin in renal stone patients under normal conditions and during acidosis and alkalosis.

The urinary excretion of beta2-microglobulin was studied under normal conditions and during acidosis and alkalosis in 65 patients with renal stones. Eleven patients were studied under two of these conditions. Four out of 51 patients examined under normal conditions had an increased excretion of beta2-microglobulin in their urine. Four out of five patients with distal acidification defects were found to have an increased excretion of beta2-microglobulin during induced acidosis. During alkalosis, four out of eight patients with acidification defects increased their excretion of the protein. The tubular proteinuria that could be provoked during acute acidosis and alkalosis was considered to be secondary to changes in the acid-base status and may indicate a renal tubular defect.

Acidosis↗
PubMed1994

Metabolic alkalosis mimicking the acute sequestration of HCl in rats: bucking the alkaline tide.

Loss or sequestration of HCl induces an acute metabolic alkalosis. The purpose of these experiments was to examine the renal handling of bicarbonate (HCO3-) in awake, euvolemic rats to determine if a significant degree of bicarbonaturia would develop because, if present, it could lead to large negative balances for sodium (Na+) and/or potassium (K+). Metabolic alkalosis was induced acutely by creating the equivalent of an acute and large loss of HCl; the net effect was to lose Cl- and gain equimolar HCO3- in rats that were in Na+ and K+ balance. A loop diuretic induced the loss of 1,860 mumol Na+, 842 mumol K+ and 2,444 mumol Cl- over a 4-h period; the loss of Cl- was replaced as its Na+ or K+ salt by infusing equivalent amounts of NaHCO3 and KHCO3 (ultimately, a "simple exchange" of 2,444 mumol of HCO3- for Cl-). Metabolic alkalosis was sustained for 4 h (mean plasma [HCO3-] = 43 mmol/L); there was a parallel fall in the plasma [Cl-]. From a renal perspective, the fractional excretion of HCO3- was only 0.4%. This adaptation could be viewed as potentially life-saving, because excretion of NaHCO3 would result quickly in a severe reduction in ECF volume and metabolic acidosis and, in addition, in a severe degree of K(+)-depletion.

Alkalosis↗
PubMed1994

Normal acid-base equilibrium in acute hyponatremia and mixed alkalosis in chronic hyponatremia induced by arginine vasopressin or 1-deamino-8-D-arginine vasopressin in rats.

The effects of acute and chronic water intoxication induced by the administration of oral water and arginine vasopressin (AVP) or 1-deamino-8-D-arginine-vasopressin (DDAVP) on blood acid-base equilibrium and aldosterone, corticosterone, and thyroxine secretion were studied in rats. Acute hyponatremia (3 hours) was associated with normal bicarbonate and blood acid-base equilibrium and a decrease in aldosterone and thyroxine concentrations, while corticosterone was increased. When similar levels of hyponatremia (serum sodium 110 mEq/L) were maintained for 24 or 72 hours, a normal serum bicarbonate concentration was observed, but blood acid-base equilibrium showed a mixed respiratory and metabolic alkalosis. Blood pH was negatively correlated with serum sodium concentration (R = -0.65; p < 0.001), as was the metabolic alkalosis (base excess; R = -0.64; p < 0.001) and the aldosterone concentration (R = -0.52; p < 0.01), while the PCO2 was positively correlated (R = +0.49; p < 0.01). Hyperaldosteronism was similar whether hyponatremia was induced with AVP or DDAVP and was observed even for mild hyponatremia. When hyponatremia was induced by a high water and salt intake (2.5% D-glucose, 0.45% NaCl; 15% body weight), aldosterone concentration was as high (about three times control values) as in rats with similar levels of hyponatremia but with a salt-free diet. The high salt intake was associated with a more severe metabolic alkalosis (base excess +5,5 mEq/L). In chronic hyponatremia, corticosterone and thyroxine values were normal. In hyponatremia related to syndrome of inappropriate secretion of antidiuretic hormone, the normal serum bicarbonate level is an expected observation; as in acute water intoxication, it stays normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1977

Acidosis, alkalosis, and aqueous humor dynamics in rabbits.

Systemic acidosis induced by intravenous administration of hydrochloric acid lowered intraocular pressure in unanesthetized rabbits. Aqueous humor flow was reduced by approximately 50%, as measured by the iodide method and as calculated from tonographic data. Outflow facility, episcleral venous pressure, plasma osmolality, blood pressure, pulse, and body temperature were not altered by systemic acidosis. Systemic alkalosis induced by intravenously administered sodium bicarbonate was associated with an increased intraocular pressure. Aqueous humor flow following systemic alkalosis was increased by approximately 100%, as measured by the iodide method and as calculated from tonographic data. Alkalosis was not associated with alterations in outflow facility, episcleral venous pressure, plasma osmality, blood pressure, pulse, or rectal temperature.

Acidosis↗
PubMed1997

[Efficacy of acetazolamide treatment of patients with hypercapnia and superimposed metabolic alkalosis].

BACKGROUND: Metabolic alkalosis usually complicates the evolution of patients with hypercapnia under diuretic or steroid therapy. The objective of this study was to analyze the efficiency of therapy with acetazolamide, a reversible carbonic anhydrase inhibitor, in this condition. PATIENTS AND METHODS: Prospective study conducted at our hospital from June 1994 to March 1996, with 45 patients who had chronic respiratory acidosis and metabolic alkalosis. After a previous stabilization of the patient and eventually the discontinuation of diuretic or corticosteroid drugs fro 24-48 hours, 500 or 750 mg of acetazolamide were administered daily for 48 hours. Later, variations both in arterial gasometry and venous electrolytes were analyzed by comparing two means of paired data. RESULTS: After therapy with acetazolamide a clinical improvement was observed in patients, a decrease in PaCO2, pH and CO3H (p < 0.001) and an increase in PaO2 (p < 0.001). Hypochloremia (82.2%) and hypopotassemia (33.3%) were the most common electrolytic abnormalities before therapy. Both abnormalities improved significantly after the administration of acetazolamide. In five patients (11.1%) acetazolamide was discontinued when metabolic acidosis appeared, which only in three cases was associated with acidemia. No secondary effects were observed. CONCLUSIONS: Acetazolamide is an efficient alternative for treatment of patients with respiratory acidosis and metabolic alkalosis, particularly when other more common measures in this condition (discontinuation of diuretics and/or volemic replacement) have failed or are contraindicated. On the other hand, the emergence of relevant secondary effects is unlikely.

Acetazolamide↗
PubMed1992

Metabolic alkalosis and the response of the trout, Salmo fario, to acute severe hypoxia.

Trout (Salmo fario) were acutely transferred from seawater to freshwater in order to induce blood metabolic alkalosis (cf. Maxime et al., J. Comp. Physiol. 160: 31-39, 1990). After 2 weeks, the fish were exposed to severe environmental hypoxia (final water oxygen partial pressure, PWO2 = 25-45 Torr, reached within 20 min), to assess the impact of the experimentally induced alkalosis, and hence increased haemoglobin-oxygen (Hb-O2) affinity, on various aspects of the hypoxic response. This was accomplished by monitoring oxygen partial pressure and total oxygen content of arterial blood (PaO2 and CaO2), extracellular pH (pHe), red blood cell (RBC) intracellular pH (pHi), and the concentrations of plasma adrenaline, noradrenaline, lactate and haemoglobin (Hb) at 5 min intervals. Blood from normoxic fish exhibited high pHe and RBC pHi values (8.32 +/- 0.02 and 7.53 +/- 0.03, respectively). During hypoxia PaO2 declined to 10 Torr within 25 min; the first 5 min provoked increases of pHe and pHi to 8.43 +/- 0.03 and 7.71 +/- 0.03, respectively; thereafter, pHe decreased whilst pHi remained elevated. The blood lactate concentration increased from 2.30 +/- 0.76 mmol.L-1 in normoxia to 14.94 +/- 5.7 mmol.L-1 at the conclusion (60 min) of the hypoxic exposure and catecholamine levels also increased progressively (from 2.94 +/- 0.51 and 1.90 +/- 0.50 nmol.L-1, in normoxia, to 191.91 +/- 64.25 and 72.00 +/- 25.02 nmol.L-1, at their highest levels, for adrenaline and noradrenaline, respectively). Determination of the PaO2 thresholds for lactate and catecholamine release demonstrated that these substances appeared in the bloodstream when the degree of O2 saturation of the haemoglobin fell below 60%. The results demonstrate that initial blood alkalosis does not prevent the typical physiological responses of trout to hypoxia but simply shifts to lower PaO2 values the threshold at which these responses begin.

Acid-Base Equilibrium↗
PubMed1986

Experimental studies on therapy of metabolic alkalosis during the beginning of uremia. Influences of ammonium chloride on the intra- and extracellular acid-base status of the rat.

Metabolic alkalosis during renal failure or uremia presents a difficult problem for the clinician. In this study the effects of ammonium chloride, an agent clinically used for the correction of severe metabolic alkalosis, were studied on the extra- and intracellular acid-base balance of nephrectomized rats. While the extracellular acid-base status was determined from blood gas measurements, intracellular pH was calculated from the distribution of 5,5-dimethyl-2,4-oxazolidinedione. It was found that the administration of NH4Cl leads to a significant increase of intracellular pH though extracellular plasma pH decreases, and that ammonium chloride causes only an insignificant reduction of the intracellular bicarbonate concentration. The observed intracellular pH increase may have adverse consequences for patients and raises objections to the further use of ammonium chloride in the treatment of metabolic alkalosis, especially during renal failure or uremia.

Acid-Base Equilibrium↗
PubMed1972

Metabolism of glutamine by the intact functioning kidney of the dog. Studies in metabolic acidosis and alkalosis.

The renal conversion of glutamine to glucose and its oxidation to CO(2) were compared in dogs in chronic metabolic acidosis and alkalosis. These studies were performed at normal endogenous levels of glutamine utilizing glutamine-(34)C (uniformly labeled) as a tracer. It was observed in five experiments in acidosis that mean renal extraction of glutamine by one kidney amounted to 27.7 mumoles/min. Of this quantity, 5.34 mumoles/min was converted to glucose, and 17.5 mumoles/min was oxidized to CO(2). Acidotic animals excreted an average of 41 mumoles/min of ammonia in the urine formed by one kidney. In contrast, in five experiments in alkalosis, mean renal extraction of glutamine amounted to 8.04 mumoles/min. Of this quantity, 0.92 mumole/min was converted to glucose, and 4.99 mumoles/min was oxidized to CO(2). Alkalotic animals excreted an average of 3.23 mumoles/min of ammonia in the urine. We conclude that renal gluconeogenesis is not rate limiting for the production and excretion of ammonia in either acidosis or alkalosis. Since 40% of total CO(2) production is derived from oxidation of glutamine by the acidotic kidney and 14% by the alkalotic kidney, it is apparent that renal energy sources change with acid-base state and that glutamine constitutes a major metabolic fuel in acidosis.

Acid-Base Equilibrium↗
PubMed1981

[Clinical application of the alkalosis induction test for coronary artery spasm].

Alkalosis was used for stress testing for coronary artery spasm in 70 patients (average age: 56 years) with resting angina. A rapid intravenous infusion of an alkaline buffer (THAM) immediately followed by 5 minutes' maximal ventilation increased the arterial pH to 7.67 +/- 0.5. Anginal pain and ECG changes were observed in 24 Patients, with ST elevation in 10 cases and ST depression in 14 cases. The ischaemic changes occurred during hyperventilation in 16 cases and in the 3 minutes following the test in 8 cases. The heart rate increased from 66 +/- II to 71 +/- 14 bpm (p less than 0,01) but systolic blood pressure fell from 139 +/- 12 to 130 +/- 12 mm Hg during hyperventilation; there was no significant change in the rate-pressure product (1130 +/- 1750 to 8990 +/- 2690). In all cases, the angina and ischaemic changes regressed after intravenous Trinitrin. Coronary angiography was performed in 56 patients: in the 24 patients with positive responses (Group I) and in 30 of the 46 patients with negative responses (Group II). Significant coronary artery narrowing (greater than 70%) was observed in 21 patients of Group I: in the 3 patients without coronary lesions an intravenous injection of 0.4 mg methylergometrine provoked coronary spasm. In Group II, significant narrowing was demonstrated in 18 patients: in the 12 other patients, coronary spasm could not be induced by methylergometrine. Therefore, in the absence of organic coronary lesions, an excellent correlation has been shown between the alkalosis and methylergometrine tests. This stress test was repeated in 16 of the 24 patients in Group I one hour after administration of 20 mg of Nifedepine: the test was negative in all cases. We conclude that the alkalosis test could be useful in the coronary care unit as a stress test for coronary spasm to determine the antianginal treatment of choice and to evaluate its efficacity.

Coronary Angiography↗
PubMed1981

Influence on cerebral blood flow of infusion of sodium bicarbonate during respiratory acidosis and alkalosis in the dog.

In anaesthetized dogs, a mixed acid-base disturbance was induced by adding a pronounced metabolic alkaline to an established respiratory acidosis or alkalosis. Cerebral blood flow (CBF) was measured by the radioisotope washout method. In the hypocapnic dogs, the addition of metabolic alkalosis did not significantly change cerebral blood flow. In the hypercapnic dogs, the intravenous infusion of alkali led to a substantial reduction of cerebral blood flow, parallelled by a reduction of cerebrovenous oxygen tension. Acid-base analysis of cerebrospinal fluid (CSF) indicated an increased bicarbonate concentration. Hypercapnia is suggested to facilitate the passage of bicarbonate over the blood-brain barrier, leading to cerebral vasoconstriction by means of increased extravascular pH.

Acidosis, Respiratory↗
PubMed1975

Intracellular pH and K+ of cardiac and skeletal muscle in acidosis and alkalosis.

The effects of a metabolic and respiratory acidosis and alkalosis on intracellular pH (pHi) and K+ have been compared in cardiac and skeletal muscle from the anesthetized rabbit. The extracellular space and pHi were calculated from the distribution volumes of [51Cr] EDTA and [14C]DMO, respectively. When pHe was varied by altering PCO2, the slope of the line relating pHi to the extracellular pH (pHe) was greater (P less than 0.05--0.001) than that obtained during metabolic changes of pHe in right and left ventricles, atria, diaphragm, and quadriceps. During metabolic acidosis and alkalosis, the slope of pHi/pHe line did not vary between tissues. During respiratory acidosis, there was no difference in slope between cardiac tissues, but it was less in left ventricle than quadriceps (P less than 0.001). In left ventricle intracellular K+ increased in a metabolic (P less than 0.05) or respiratory acidosis (P less than 0.02), whereas in diaphragm it decreased (P less than 0.02). Intracellular K+ correlated with pHe and pHE-PHi. Changes in pHi but not intracellular K+ could explain known differences in myocardial function in respiratory and metabolic acidosis.

Acidosis↗
PubMed1985

[Acid-base equilibrium in anesthesiology and operative intensive care medicine. Physiology, pathophysiology and clinical aspects of alkalosis and mixed disorders].

This review details basic and clinical aspects of metabolic and respiratory alkalosis and mixed acid-base disturbances. New experimental results show that NH4Cl and arginine-HCl should no longer be used in antialkalotic therapy because they increase intracellular pH and have no effect on intracellular bicarbonate concentration. Appropriate HCl solutions should be employed in severe metabolic alkalosis because they reduce pH and the bicarbonate concentrations in both body compartments.

Acid-Base Equilibrium↗
PubMed1980

Pancreatic tissue pH in experimental acidosis and alkalosis.

The pH was studied in pancreatic tissue and arterial blood in 22 dogs. Respiratory acidosis was induced by CO2 inhalations in 5 dogs, respiratory alkalosis by hyperventilation in 5 dogs, metabolic acidosis by intravenous(i.v.) infusion of 0.1 N HCl in 5 dogs, metabolic alkalosis by i.v. infusion of 4.2% Na bicarbonate in 5 dogs. The differences between the shifts of blood pH and tissue pH were not significant statistically. Infusion of Ringer's solution failed to affect the pH in blood and pancreatic tissue in two control animals. It is concluded, that with an adequate tissue blood flow the pancreatic tissue pH is uninformative unless the blood pH is known.

Acidosis↗
PubMed1979

Treatment of alkalosis with ammonium chloride: a case report.

Coma due to ammonium chloride used in the treatment of severe metabolic alkalosis is reported in a patient with normal hepatic and renal function. All symptoms resolved following discontinuance. Ammonium chloride should be abandoned as a treatment for metabolic alkalosis.

Alkalosis↗
PubMed1994

Radiographic lung disease and response of persistent pulmonary hypertension to mean airway pressure and alkalosis.

Persistent pulmonary hypertension of the newborn (PPHN) is associated with multiple cardiopulmonary diseases. Therapy often includes hyperventilation/alkalosis despite little evidence as to its efficacy in diverse conditions. To determine (1) if part of the improvement of arterial oxygen tension (PaO2) attributed to alkalosis is actually related to increased mean airway pressure (P(aw)) and (2) if the presence of radiographic pulmonary disease predicts the response to alkalosis or mean airway pressure, we reviewed records of 19 newborns with well-documented PPHN. Arterial blood gases and corresponding ventilator settings were recorded during the first day of life. To adjust for lower FiO2, corrected PaO2 (cPaO2) was calculated when the FiO2 < 1.0, such that cPaO2 = calculated arterial/alveolar oxygen ratio x (713 - PaCO2/0.8). Regression equations were obtained and mean slopes of these were compared for P(aw) vs. cPaO2, and pH vs. cPaO2 by one group t-tests (with assumed population slope of zero). There was no correlation between P(aw) and cPaO2 (mean slope +/- SD = -8.4 +/- 30.8, P = 0.25), but there was a moderate correlation between pH and cPaO2 (mean slope = 333.1 +/- 480.5, P = 0.007). Patients were then classified by chest radiographs as having severe or minimal/no lung disease. Relationships of P(aw) and pH to cPaO2 were then re-examined. No correlation was present between P(aw) and cPaO2 in 11 patients with PPHN and severe radiographic disease (mean slope = -7.4 +/- 26.9, P = 0.38) or in eight patients with PPHN and minimal/no lung disease (mean slope = -9.8 +/- 37.5, P = 0.48).(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed1988

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

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 of the rat renal cortex to measure electrolyte concentrations in proximal tubule cells and in the various cell types of the superficial distal tubule. Analyses were also performed in fluid samples obtained by micropuncture from proximal and early and late distal collection sites. Compared with the appropriate controls (hypertonic sodium chloride i.v.), administration of sodium bicarbonate resulted only in small and mostly insignificant increases in cell potassium concentrations and induced only minor alterations in the cell/tubule fluid potassium concentration gradient for all cell types analysed. This observation suggests that under this condition factors other than an increase in cell potassium concentration are important in modulating potassium transfer across the apical membrane of potassium secreting cells. Nevertheless, since in alkalosis phosphorus and cell dry weight were decreased, and hence cell volume increased, in all but the intercalated cells, actually the potassium content of most tubular cells was higher under this condition. In comparison with animals infused with isotonic saline at low rates (hydropenic controls), infusion of either hypertonic sodium chloride or sodium bicarbonate led to a sharp increase in distal tubule fluid sodium concentrations and in the sodium concentrations of distal convoluted tubule, connecting tubule and principal cells, indicating that under both conditions the primary event causing enhanced transepithelial sodium absorption is stimulation of the sodium entry step.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkalosis↗
PubMed1990

Renovascular hypertension presenting with hypokalemic metabolic alkalosis.

This report describes two adolescents with severe hypertension secondary to renal artery stenosis who had evidence of a hypokalemic metabolic alkalosis in their initial laboratory evaluation. Hypokalemic metabolic alkalosis is known to occur in approximately 16% of adults with renal artery stenosis but has not been well described in the pediatric literature. It is the result of excess aldosterone secretion stimulated by renal artery stenosis-mediated activation of the renin-angiotension system and by an increase in natriuresis from the contralateral, non-stenotic kidney. Although primary hyperaldosteronism must be considered in children with hypertension and hypokalemia, it is a rare disease in children. This report supports current recommendations that the initial focus of medical investigation in the severely hypertensive child should remain on the kidney.

Adolescent↗