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Results for “Alkalosis”

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At least 19 recordsLinked to original sources

PubMed1979

Hypoelectrolytemia and metabolic alkalosis in infants with cystic fibrosis.

The records of all children in the Tucson area diagnosed as having cystic fibrosis (CF) before the age of 12 months were reviewed to ascertain the prevalence of metabolic alkalosis as a major presenting manifestation of CF. Five of eleven infants (46%) in whom CF had been diagnosed between 1 and 12 months of age initially were seen with hypokalemia, hypochloremia, and metabolic alkalosis unassociated with marked dehydration, hyperpyrexia, or major pulmonary and/or gastrointestinal symptoms. Two infants had repeated episodes of metabolic alkalosis; for one of these infants, both episodes of metabolic alkalosis occurred before the diagnosis of CF. It is postulated that chronic loss of sweat electrolytes together with mild gastrointestinal or respiratory illness may predispose the infant with cystic fibrosis to a severe electrolyte and acid-base disturbance. The lack of shock and hyperpyrexia together with the apparent chronicity of electrolyte losses differentiates metabolic alkalosis from the heat prostration syndrome, a more acute complication of cystic fibrosis. Quantitative sweat testing should be part of the evaluation of any infant with unexplained metabolic alkalosis. Serum electrolytes should be assessed regularly in infants with cystic fibrosis during hot weather months.

Alkalosis↗

PubMedDate not supplied

The effects of acidosis and alkalosis on coronary flow and cardiac nucleotide metabolism.

The changes of the coronary flows and of the cardiac nucleotide metabolism during acidosis and during alkalosis were studied in 50 perfused guinea pig hearts with and without hypoxia. At pH 7.0 the coronary flows increased, and at pH 7.8 a significant reduction of the flows took place. At 20% O2, acidosis elicited a further flow increase, whereas alkalosis inhibited the flow increase produced by hyoxia. The increases after adenosine injections and after coronary occlusions were greater during acidosis and smaller during alkalosis than at pH 7.4. The cardiac nucleotide contents did not clearly differ from the controls whereas adenosine exhibits higher levels in acidotic hearts. Alkalosis always induced a decreased production of adenine nucleoside irrespective of the presence or the absence of hypoxia. At 20% O2 a decreased ATP level and increased ADP- and CrP-contents could be observed during alkalosis.

Acidosis↗

PubMed1975

Tetany: quantitative interrelationships between calcium and alkalosis.

Tetany occurs with hypocalcemia and alkalosis or both. The interrelationship of calcium and acid-base balance necessary for inducing tetany, the role of the central nervous system, and the rate of development of hypocalcemia have been investigated. Tetany occurred in less than 50 percent of one group of dogs made alkalotic by hyperventilation or made hypocalcemic by infusion of ethylene glycol-bis(beta-amino ethyl ether) N, N'-tetraacetate. In contrast, hypocalcemia combined with hypocapnic alkalosis always produced tetany. Slowly evolving hypocalcemia was achieved inanother group of dogs by thyroparathyroidectomy, and tetany was induced postoperatively by hypocapnic alkalosis. An identical relationship between serum calcium ion concentration and arterial pH or CO2 tension was found in both groups. Tetany could not be related to the cerebrospinal fluid (CSF) calcium ion content in either group. Hypocalcemia and alkalosis are therefore coparticipants in the development of tetany and are independent of the rate of development of hypocalcemia and of CSF calcium ion concentration. The importance of alkalosis in tetany with hypoparathyroidism is emphasized.

Alkalosis, Respiratory↗

PubMed1975

Uteroplacental blood flow during alkalosis in the sheep.

Uteroplacental blood flow was measured by the radioactive-microsphere technique in eight near-term pregnant ewes during a normal control period and during maternal metabolic alkalosis. All measurements were made on awake, unanesthetized animals. Alkalosis, defined for this study as an arterial pH of 7.60 or greater, was produced by the oral administration of sodium bicarbonate, 3 g/kg body wt. The rise in pH thus produced was unaccompanied by significant changes in systemic arterial blood pressure and cardiac output, while maternal arterial Pco2 rose slightly from control levels. Cotyledonary blood flow declined from a control value of 1,177 ml/min to 1,025 ml/min during alkalosis. This decline of 13 percent in cotyledonary blood flow is significant (P smaller than 0.002). Blood flow to the remaining uterine tissue, or noncotyledonary uterus, did not change with alkalosis, being maintained at approximately 195 ml/min. It is concluded that maternal alkalosis, unaccompained by major changes in Pco2 and systemic arterial pressure, causes a small increase in the resistance of the uteroplacental circulation.

Alkalosis↗

PubMed1976

Importance of changes in plasma HCO-3 on regulation of CSF HCO-3 in respiratory alkalosis.

In respiratory alkalosis the fall in CSF bicarbonate is in part due to increased CSF lactate. The rest of CSF HCO3 fall may be actively regulated or as more recent evidence suggests is dependent on plasma HCO3 fall. Therefore, the relationship between plasma and CSF HCO3 changes was studied during 4 hours of respiratory alkalosis (PaCO2=20 mm Hg) in anesthetized dogs when plasma HCO3: (1) fell normally, (2) kept 'normal' by NaHCO3 infusion, (3) increased by infusing more NaHCO3, and (4) reduced by infusing HCl. In respiratory alkalosis plasma and CSF HCO3 fell 4.6 and 3.8 mEQ/L, respectively. In hypocapnia and 'normal' plasma HCO3 CSF HCO3 fell 2 mEq/L and lactate increased 1.33 mEq/L. In hypocapnia and metabolic alkalosis plasma HCO3 increased 6.5 mEq/L and CSF HCO3 remained unchanged and lactate increased 2.12 mEq/L. In combined hypocapnia and metabolic acidosis plasma HCO3 fall 10.5 mEq/L but CSF HCO3 fell 3.1 mEq/L and CSF pH returned to normal at 4 hours. Therefore CSF HCO3 fall in hypocapnia is primarily and critically dependent on the simultaneous fall in plasma HCO3 content, with a minimal contribution from CNS lactate increase. When CSF PH has returned to normal, however, CSF HCO3 fall is stopped despite further falls in plasma HCO3.

Acid-Base Equilibrium↗

PubMed1979

Cimetidine in the management of metabolic alkalosis induced by nasogastric drainage.

Metabolic alkalosis resulting from nasogastric drainage is a well recognized and potentially serious clinical problem. In the postoperative patient with acute renal failure, the management of the metabolic alkalosis is particularly difficult, and established modalities of therapy are sometimes ineffective and can be hazardous to the patient. In this article, we report on the successful use of cimetidine (an H2-receptor antagonist) as an adjunct in the treatment of severe metabolic alkalosis in a postsurgical renal failure patient. To our knowledge, this is the first reported successful use of cimetidine in the treatment of metabolic alkalosis due to gastric acid loss.

Acute Kidney Injury↗

PubMed1975

Lactic acid permeation rate in working gastrocnemii of dogs during metabolic alkalosis and acidosis.

In isolated, blood perfused, supramaximally stimulated, isotonically working gastrocnemii of dogs lactic acid (LA) output and O2-consumption (V O2) were measured according to the Fick principle. Simultaneously concentration of muscle tissue was determined at rest and at different times during exercise. In one series of experiments metabolic alkalosis was induced by infusions of THAM of Na bicarbonate. As a result arterial pH increased to about 7.5 and standard [HCO3-1] to 31-35 mmol per 1. In another group of experiments metabolic acidosis was induced by HCl infusions. In these experiments pH decreased to 7.0-7.1 and standard [HO301] to 8-11 mmol per 1. During the first 3-4 min after the onset of exercise LA concentration of muscle tissue rose to 18-19 mumol per g wet weight in both series of experiments. During acidosis the highest average values for LA release from the muscle were about 1.1 mumoles per g per minute. During alkalosis LA permeation rate was nearly three times as high. As a consequence of increased rate of permeation, LA concentration of muscle tissue decreased more rapidly in alkalosis than in acidosis. In both series of experiments work per time and VO2 were practically equal during the first 5-6 min of exercise. Thereafter work per time and VO2 decreased more rapidly in acidosis than in alkalosis, a result which probably is due to higher LA concentration in muscle at this time in acidosis. It is concluded that LA permeation rate across muscle cell membrane is increased by high extracellular HCO3- concentration in combination with low H+ activity and vice versa.

Acidosis↗

PubMed1978

Effect of metabolic alkalosis on the B-cell sensitivity to alloxan in vivo.

Metabolic alkalosis was induced in starved mice by treatment with NaHCO3, which did not significantly alter the blood glucose concentration, but protected against the diabetogenic effect of subsequently given alloxan. This protection and the alkalosis had disappeared 4 hr after NaHCO3 treatment. Protection against alloxan, and metabolic alkalosis, were found also in starved mice pretreated with sodium lactate. The findings indicate that metabolic alkalosis, directly or indirectly, protects against alloxan toxicity in vivo.

Alkalosis↗

PubMed1977

Effects of saline infusion and acute metabolic acidosis and alkalosis on water and electrolyte transport in the human colon.

Both the kidney and colon secrete bicarbonate and transport water and electrolytes. The respective contributions of these two organs to acid-base and electrolyte balance in normal man has thus been studied in eight healthy male volunteers who underwent simultaneous renal clearance studies, and colonic perfusion with a 0.9% saline or 7.2% mannitol solution, during metabolic alkalosis and acidosis, extracellular volume expansion, and control conditions. There was no influence of these acid-base conditions on electrolyte transport in the colon. In the urine, preferential loss of chloride over sodium averaged 81, 143 (P less than 0.001), and 141 (P less than 0.05) muequiv./min, during control, metabolic acidosis, and extracellular volume expansion conditions, respectively. During alkalosis more sodium than chloride was lost (146 muequiv./min) (P less than 0.001). Colonic pH averaged 7.41 during saline and 6.75 (P less than 0.005) during mannitol perfusion. Titratable acid was not produced in the colon during saline perfusion, and averaged 18 muequiv./min during mannitol perfusion. Urinary titratable acid increased from 19 to 25 muequiv./min (P less than 0.01) during volume expansion. With saline perfusion, bicarbonate secretion rate in the colon rose from 249 muequiv./min during control conditions to 289 muequiv./min during metabolic alkalosis (P less than 0.05). More bicarbonate was excreted in the urine during alkalosis when mannitol was introduced in the colon (243 muequiv./min) than when saline was perfused (152 muequiv./min) (P less than 0.05). This study indicates that the response of the human colon is trivial compared with that of the kidney during acute changes in acid-base balance.

Acid-Base Equilibrium↗

PubMed1979

A short communication. Congenital renal alkalosis.

Patients with idiopathic hypokalemic metabolic alkalosis and hyperrenienmia have been lumped under the heading of Bartter's syndrome. However, the clinical picture is not totally uniform. Recently, Gullner et al. described a familial disorder with hypokalemic metabolic alkalosis, hyperreninemia, and aldosteronism, but without juxtaglomerular hyperplasia. They suggested that this family had a condition other than Bartter's syndrome. The present report details the followup from infancy to adulthood of a patient with hypokalemic metabolic alkalosis, salt wasting, and hyperreninemia, but with normal aldosterone level and without juxtaglomerular hyperplasia. The authors suggest that this new condition be termed renal alkalosis. The studies suggest that the distal tubular reabsorptive capacity was defective in this patient.

Adolescent↗

PubMedDate not supplied

Acid-base balance and blood gases changes and "lactate excess" in acute respiratory alkalosis during general anaesthesia.

In 40 young males aged 18-20 years operated on for inguinal hernioplasty acute respiratory alkalosis was obtained in the 45th minute of general anaesthesia. The values of basic acid-base balance parameters, blood gases, pyruvate and lactate levels and "lactate excess" were determined before and after hyperventilation. Shifts in the concentrations of hydrogen and bicarbonate ions were found which are both typical of acute respiratory alkalosis. No changes were observed in the oxygenation of capillary blood and the values of "lactate excess" were normal which rules out tissue hypoxia during acute respiratory alkalosis. Passive hyperventilation being a less dangerous alternative of hypoventilation is a frequent occurrence during general anaesthesia and it causes transient respiratory alkalosis.

Acid-Base Equilibrium↗

PubMed1977

Effect of metabolic alkalosis on respiratory function in patients with chronic obstructive lung disease.

Eleven instances of a mixed acid-base disorder consisting of chronic respiratory acidosis and metabolic alkalosis were recognized in eight patients with chronic obstructive lung disease and carbon dioxide retention. Correction of the metabolic alkalosis led to substantial improvement in blood gas values and clinical symptoms. Patients with mixed chronic respiratory acidosis and metabolic alkalosis constitute a common subgroup of patients with chronic obstructive lung disease and carbon dioxide retention; these patients benefit from correction of the metabolic alkalosis.

Acetazolamide↗

PubMed1979

Determination of liver intracellular pH in vivo and its homeostasis in acute acidosis and alkalosis.

An in vivo method is presented for the determination of liver intracellular pH (pHi) using [14C]dimethadione (DMO) in dogs. This method differs from those previously published in that hepatic venous and portal venous blood pH were selected as the extracellular reference pH, and liver blood space corrections are applied to whole liver tissue [14C]DMO activity. Using these corrections, a normal liver pHi of 6.99 +/- 0.03 (SE) was obtained. During acute metabolic acidosis and alkalosis, as well as during acute respiratory acidosis and alkalosis, the liver pHi remained normal; metabolic acidosis was 7.04 +/- 0.04; metabolic alkalosis was 6.92 +/- 0.08; respiratory acidosis was 6.98 +/- 0.04; and respiratory alkalosis was 7.00 +/- 0.10. None of these values was significantly different from normal (P greater than 0.05). Changes in intracellular bicarbonate and lactate appeared to account in part for the observed stability of the liver pHi despite acute manipulations resulting in a range of pH values between 7.09 and 7.63 in arterial blood.

Acid-Base Imbalance↗

PubMed1975

Hydrochloric acid in the correction of metabolic alkalosis.

Intravenous infusion of hydrochloric acid was used as a safe, effective, and quantitative method for correction of metabolic alkalosis in two patients. The first shows the risks of intravenously administered ammonium chloride, the currently available alternative to hydrochloric acid therapy. The second shows the efficacy of intravenously administered hydrochloric acid. While breathing spontaneously throughout the period of severe alkalosis, this patient showed compensatory hypoventilation with conspicuous increase in arterial carbon dioxide pressure. Normal spontaneous ventilation returned with correction of the metabolic alkalosis.

Aged↗

PubMed1978

Severe hypercapnia associated with a non-respiratory alkalosis.

A case of hypoventilation in response to a non-respiratory alkalosis is presented. It is postulated that the degree of hypoventilation encountered was a normal response and that a fall in intracellular hydrogen ion concentration was responsible for the hypoventilation. This explains why the alkalosis associated with potassium deficiency is not associated with hypoventilation since the intracellular hydrogen ion concentration then remains constant. The renal response in this condition is responsible for maintaining the alkalosis and seems to be aimed at sodium conservation and hence plasma volume control rather than defence of acid-base balance.

Alkalosis↗

PubMed1977

Hypoglycemia induced by alpha-adrenergic stimulation during alkalosis.

Hypoglycemia developed during respiratory alkalosis in fasted rats. This hypoglycemia was markedly potentiated by the simultaneous injection of inhibitors of hepatic gluconeogenesis or a beta-adrenergic blocking agent; was not influenced by anti-insulin serum; was attenuated by hexamethonium; and was abolished by an alpha-adrenergic blocking agent. The rate of removal of injected glucose by peripheral tissues increased during alkalosis in insulin-deficient rats. The uptake of [14C]-glucose by the adipose tissue in vivo, which is stimulated by a very minute amount of insulin, was also stimulated during alkalosis whether or not the circulating insulin was neutralized with anti-insulin serum. It was concluded that, in alkalotic rats, blood glucose is rapidly utilized by peripheral tissues dependent on alpha-adrenergic stimulation, but without mediation of insulin and that this leads to development of hypoglycemia.

Alkalosis, Respiratory↗

PubMed1979

Effects of metabolic acidosis and alkalosis on sodium and calcium transport in the dog kidney.

Clearance and micropuncture studies have been performed in dogs to examine the effects of acute and chronic metabolic acidosis and acute alkalosis on tubular sodium and calcium transport. Acute metabolic acidosis, induced by the infusion of hydrochloric acid, decreased proximal fluid reabsorption and increased the fractional delivery of sodium and calcium to the distal tubule, but not to the final urine. In comparison with normal dogs, dogs with chronic metabolic acidosis (induced by feeding ammonium chloride) showed an increase in proximal fluid reabsorption and a dissociation of calcium from sodium reabsorption more distally, leading to an increased delivery of calcium relative to sodium at the distal tubule and in the final urine. The infusion of sodium bicarbonate to correct chronic metabolic acidosis, both in intact and thyroparathyroidectomized (TPTX) dogs, reduced proximal fluid reabsorption and caused a selective enhancement of calcium reabsorption relative to sodium in the more distal nephron, resulting in a reversal of the dissociation observed in acidosis, both at the distal tubule and in the final urine. By contrastin fusion of sodium chloride in parathyroid-intact acidotic dogs did not reduce proximal fluid reabsorption or enhance tubular calcium reabsorption. In nonacidotic dogs, both intact and TPTX, infusion of sodium bicarconate to induce acute alkalosis resulted in selhese data demonstrate the presence of a component of tubular calcium reabsorption situated beyond the proximal tubule, which is inhibited by chronic (but not acute) metabolic acidosis and enhanced by metabolic alkalosis (or bicarbonate infusion) independently of parathyroid hormone.

Acidosis↗

PubMed1977

Effects of metabolic alkalosis, metabolic acidosis and uraemia on whole-body intracellular pH in man.

1. Whole-body intracellular pH (pHi) was measured by the 14C-labelled DMO method in twenty-four control subjects, eighteen normal subjects with induced acute metabolic alkalosis, ten normal subjects with induced acute metabolic acidosis, twelve normal subjects with chronic acidosis and in fifteen patients with chronic renal insufficiency and acidosis. 2. The change in pHi per unit change in extracellular pH is significantly larger in acute metabolic alkalosis than in acute metabolic acidosis. In chronic metabolic acidosis, pHi decreased in proportion to the total amount of ammonium chloride administered; pHi was normal in patients with uraemic acidosis. 3. These observations confirm the role that tissue buffers play in the protection of the cellular environment in some forms of acidosis. When the acid load overwhelms tissue buffer capacity, pHi becomes a function of extracellular pH. 4. Cells seem more protected from acute acidosis than from acute alkalosis.

Acid-Base Equilibrium↗