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PubMed1983

A sibship with hypokalemic alkalosis and renal proximal tubulopathy.

A new syndrome, characterized by hypokalemic alkalosis, hyperreninemia, aldosterone, high urinary prostaglandin E2 excretion, normal BP, and resistance of BP to angiotensin II is described in three of four siblings. Histologic examination of tissue obtained by biopsy from the kidneys showed an intense staining of the proximal tubular cells, as well as an extreme hypertrophy of the proximal tubular basement membranes, features that previously have not been observed. On electron microscopic examination, the characteristic changes of the tubular cells consisted of very dense cytoplasm, compact mitochondria, and pyknotic nuclei. In contrast to Bartter's syndrome, the juxtaglomerular apparatus were of normal appearance. Glomerular filtration rate and renal plasma flow were within normal limits. Fractional distal delivery of proximal tubular solute and fractional chloride reabsorption in the thick ascending limb of the loop of Henle were normal. The findings of a genetic linkage between the syndrome and the major histocompatibility system suggests that this familial tubulopathy is an inherited disorder.

Aldosterone↗
PubMed1986

Intravenous hydrochloric acid in patients with metabolic alkalosis and hypercapnia.

During a seven-year period, 15 patients admitted to an intensive care unit with a metabolic alkalosis resistant to saline and potassium chloride infusions and with an arterial pH of greater than 7.44 and arterial carbon dioxide pressure (PaCO2) of greater than 50 mm Hg, while breathing spontaneously, were given hydrochloric acid at 200 mmol/24 h through a central venous line until the arterial pH had decreased to less than 7.36 or PaCO2 had decreased to less than 40 mm Hg. Five patients without respiratory failure had a significant decrease in PaCO2, pH, bicarbonate Ion (HCO3-), and base excess (BE). Four patients with acute respiratory failure had a significant decrease in PaCO2, HCO3-, and BE and an increase in arterial oxygen pressure, indicating that in both of these patient groups alveolar ventilation had improved. Six patients with chronic respiratory failure had a significant decrease in pH, HCO3-, and BE, although there was no significant change in PaCO2, indicating that in this patient group alveolar ventilation could not be consistently increased in response to a reduction in arterial pH.

Acute Disease↗
PubMed1991

Rebound alkalosis and persistent lactate: multinuclear (1H, 13C, 31P) NMR spectroscopic studies in rats.

Intracellular pH levels of infarcted brain determined by phosphorus-31 nuclear magnetic resonance (NMR) spectroscopy disclosed a notable phenomenon. The acidotic brain pH seen in the acute stage of infarction was observed to rebound into the alkalotic range in the subacute phase before returning to the normal range in the chronic phase. This "rebound alkalosis" which was usually observed between the 24th and the 48th hour after experimental induction of infarction in rats was accompanied by significant lactate levels as detected by proton NMR spectroscopy. Analysis of the satellite methyl resonance of 13C-lactate using high-resolution proton NMR spectroscopy after 13C-glucose infusion indicated that no lactate was produced in the subacute phase of infarction and that the lactate detected during this phase must have been generated prior to this phase of infarction.

Alkalosis↗
PubMed1979

Ultrastructural responses of pancreatic beta cells to metabolic alkalosis.

The ultrastructural changes in pancreatic beta cells were studied following glucose-induced insulin secretion in vitro, at two different extracellular pH (7.4 and 7.8). The pancreata perfused at pH 7.4 exhibited a biphasic insulin response to glucose challenge together with signs of increased emiocytotic activity and numerous microtubules in the beta cells. Conversely, the pancreata perfused at pH 7.8 showed a significant decrease in insulin secretion, and their beta cells revealed scarce emiocytotic images and a marked increase of intracellular granulolysis. These results represent the ultrastructural correlate of the reduced insulin secretion produced by metabolic alkalosis in the perfused rat pancreas.

Alkalosis↗
PubMed1991

Combined effects of nicardipine and hypocapnic alkalosis on cerebral vasomotor activity and intracranial pressure in man.

The effect of hypocapnic alkalosis (HA) on nicardipine-induced cerebral vasodilatation was studied in 2 groups of patients undergoing stereotaxic brain biopsy under general anaesthesia. Arterial diameter (AD) was measured in 16 different locations on a carotid arteriogram (lateral view), and intracranial pressure (ICP) was recorded with an intraventricular catheter. At time T0, in normocapnia an arteriogram was performed in both groups. The first group (GI) was then studied in hypocapnia (T1) and following an injection of nicardipine (T2), while the second group (GII) was studied first after injection of nicardipine (T1) and then in hypocapnia (T2). Groups GI (n = 6; 44 y) and GII (n = 6; 46 y) were similar with regard to age, blood pressure, heart rate and PaO2 at all three phases of the study. HA caused a 9.5% decrease in AD (GI.T1) compared to baseline values, and a 15.2% decrease when preceded by injection of nicardipine (GII.T2). In the latter case the decrease was 3% in comparison with baseline. Nicardipine increased AD by 14.7% (GII.T1) and by 18.5% when preceded by HA (GI.T2), but the rise (7.3%) was not significant in comparison with the baselines value. The changes variations were similar whether the entire arterial trunk or only the supraclinoid region were studied. HA decreased ICP by 44% (GI.T1) and by 50% after nicardipine (GII.T2). Nicardipine did not cause an increase in ICP. Nicardipine and HA antagonise each others vasomotor effects, as previously shown in the baboon using nimodipine.

Adult↗
PubMed1988

Assessment of collecting tubule hydrogen ion secretion in acute respiratory alkalosis using the urinary pCO2.

The use of the urine-blood (U-B) pCO2 difference as a marker of collecting tubule H+ secretion (CTH+S) faces serious interpretative pitfalls when applied to animals with respiratory acidosis. The present study was aimed to examine the use of this parameter in rats with acute respiratory alkalosis. During infusion of sodium bicarbonate, the U-B pCO2 was only slightly lower in hypocapnic than in eucapnic rats (30 +/- 2.2 and 39 +/- 3.3 mmHg, p less than 0.05) and this difference was no longer significant when this parameter was examined as a function of urine bicarbonate concentration. In contrast, the increment in urine pCO2 elicited by bicarbonate loading (i.e. the delta pCO2) was markedly reduced in hypocapnic as compared to eucapnic rats (22 +/- 3.0 and 38 +/- 4.5 mmHg, respectively, p less than 0.01). The infusion of carbonic anhydrase while the urine was highly alkaline and the blood pCO2 kept constant resulted in a decrement in urine pCO2 which was less in hypocapnic than in eucapnic rats (-23.9 +/- 1.9 vs -33 +/- 2.8 mmHg, p less than 0.02). These findings indicate that pCO2 generation from CTH+S and titration of bicarbonate is reduced in hypocapnic rats. The data are in accord with our proposal that the delta pCO2 is a better index of CTH+S than the U-B pCO2 is the assessment of respiratory acid-base disorders.

Alkalosis, Respiratory↗
PubMed1988

Induced metabolic alkalosis and its effects on 400-m racing time.

Six trained male athletes who competed regularly in 400 metre races, were studied under control, alkalotic (NaHCO3) and placebo (CaCO3) conditions to study the effect of induced metabolic alkalosis on 400 m racing time. Pre and post exercise blood samples in the three conditions were analysed for pH, bicarbonate and base excess. Following ingestion of NaHCO3, pre-exercise pH, bicarbonate and base excess levels were significantly higher than either control or placebo conditions. In the alkalotic condition the subjects ran significantly (p less than 0.005) faster (1.52 s) than either the control of placebo conditions. The post-exercise pH, bicarbonate and base excess levels were all lower in the alkalotic condition than in the others. The results suggest that NaH-CO3 can be used as an effective ergogenic aid and support the speculation that the increased extracellular buffering afforded by NaHCO3 ingestion facilitated efflux of H+ from the working tissues, thus decreasing intracellular pH and hence offsetting fatigue.

Adult↗
PubMed1990

Chronic renal magnesium loss, hypocalciuria and mild hypokalaemic metabolic alkalosis after cisplatin.

Renotubular handling of sodium, potassium (K) calcium (Ca), phosphate, hydrogen ions and glucose, and urinary concentrating ability were studied in three children (aged 8, 8.5, 11 years) with renal magnesium (Mg) loss, persisting for more than 2 years after discontinuation of cisplatin treatment for neuroblastoma. A group of healthy children served as controls. Besides renal Mg wasting, a clear-cut tendency towards reduced calciuria associated with normal or slightly elevated plasma Ca was observed. Plasma K tended to be low (3.4-3.7 mmol/l), and plasma chloride was normal. Plasma bicarbonate (HCO3) ranged from 24.9 to 27.8 mmol/l, and urinary pH was always less than 6.0, indicating a renal HCO3 threshold exceeding 24 mmol/l. Plasma creatinine levels, glucosuria and phosphaturia, and urinary concentrating capacity were adequate. Comparable features were found in three children (aged 4.5, 9, 13 years) with primary renotubular hypomagnesaemia-hypokalaemia and hypocalciuria. This study complements the picture of chronic cisplatin tubulopathy in childhood demonstrating that, apart from Mg wasting, a reduced Ca excretion, and a tendency to hypokalaemia and metabolic alkalosis exist. Thus cisplatin may induce renal functional damage identical to that found in primary renotubular hypomagnesaemia--hypokalaemia with hypocalciuria.

Alkalosis↗
PubMed1988

Alkalosis and renal excretion of ammonia by rat kidney.

Upon sulfate administration, UpH falls more in alkalotic rats than in controls. Alkalosis can lead to a reduction in UNH3 V at highly acidic urine. The significance of this process is doubtful at UpH ranging from about 6 to 7. At lower UpH less NH3 would be excreted, thereby less H+ would be trapped in urine and some acid would be conserved.

Alkalosis↗
PubMed1991

Chronic metabolic alkalosis in an infant with cystic fibrosis.

A 6-month-old infant suffering from cystic fibrosis is reported. In spite of an apparently appropriate treatment and in absence of respiratory infection, the patient showed progressive anorexia, intermittent vomiting and weight loss. These non-specific signs and symptoms could all be explained by metabolic alkalosis and disappeared immediately after oral supplementation with sodium and potassium chloride. This unusual metabolic complication should be searched for in every cystic fibrosis infant with unexplained anorexia and failure to thrive.

Alkalosis↗
PubMed1984

Respiratory alkalosis and reduced plasmatic concentration of ionized calcium in rats treated with 1,25 dihydroxycholecalciferol.

The daily administration of supraphysiological doses of 1,25 dihydroxycholecalciferol (0.1-2.5 micrograms/d/100 g body weight) to rats, produced respiratory alkalosis. With the doses of 0.1-0.2 micrograms/d/100 g and feeding a diet with 0.7% of calcium, calcemias did not exceed 2.75 mM, and significantly reduced plasma ionized calcium levels were measured. The latter phenomenon was found associated with increased urinary excretion of cAMP, soft tissue calcium content, and polyuria with hypostenuria, all known effects of parathyroid hormone. These effects were absent in thyroparathyroidectomized rats treated in the same fashion. Present results suggest that the stimulus of low levels of plasma ionized calcium overcomes the probably inhibitory effect of the steroid on parathyroid hormone secretion.

Alkalosis, Respiratory↗
PubMed1977

Reduction of hypoxic pulmonary vasoconstriction by diethyl ether in the isolated perfused cat lung: the effect of acidosis and alkalosis.

Hypoxic pulmonary vasoconstriction is a protective mechanism diverting pulmonary blood flow away from hypoxic areas toward more optimally oxygenated lung units. Venous admixture is reduced and arterial oxygenation improved. Hypoxic pulmonary vasoconstriction was demonstrated during acidosis, alkalosis and normal pH in the isolated perfused cat lung under conditions of constant flow and constant left atrial and airway pressures. Two per cent diethyl ether markedly reduced hypoxic vasoconstriction under all acid-base conditions, the hypoxic pressor response returning after wash-out of diethyl ether. Modification of hypoxic pulmonary vasoconstriction during acid-base disturbances and possible implications of concurrent anaesthetic administration are discussed.

Acidosis↗
PubMed2006

Severe normotensive metabolic alkalosis in a 2-month-old boy with hyperekplexia.

A 2-month-old infant with hereditary hyperekplexia, umbilical and bilateral inguinal hernias and history of poor feeding was noted to have severe normotensive metabolic alkalosis: sodium 132 mmol/L, potassium 3.4 mmol/L, chloride 77 mmol/L, pH 7.55, carbon dioxide tension 56.3 mmHg and bicarbonate 48.0 mmol/L. After parenteral rehydration and treatment with clonazepam, laboratory parameters normalized.

Alkalosis↗
PubMed1988

Systemic alkalosis as a provocative test for coronary artery spasm in patients with infrequent resting chest pain.

Systemic alkalosis was used to detect coronary spasm in 237 patients with infrequent, resting, angina-compatible chest pain. The provocative test was performed without previous coronary arteriography but only in patients with negative submaximal exercise test results. Rapid infusion of alkaline solution followed by maximal hyperventilation raised arterial pH above the 7.65 value necessary for diagnostic significance in 196 (83%) patients. In 24 (12%) of these patients the provocative test induced significant ischemic ST segment changes. In all patients with a positive response, coronary artery disease, which was predominantly vasospastic (19 patients) or atheromatous with a vasospastic contribution (five patients), was demonstrated by coronary arteriography followed, if necessary, by ergot derivative injection. Chest pain and ECG changes were always reversed within 5 minutes by intravenous nitroglycerin. Coronary arteriography was not performed in all patients with a negative response; therefore, the sensitivity of the procedure could not be assessed. However, 36 patients with a negative response to hyperventilation underwent coronary arteriography; 33 (92%) had normal arteriograms and a negative response to ergot derivatives. Hyperventilation appears to be a safe and specific diagnostic procedure in a subset of patients in whom the probability of coronary artery disease may not be judged sufficient to warrant coronary arteriography as a primary diagnostic approach.

Adult↗
PubMed1981

Correction of hypokalemia by magnesium repletion in familial hypokalemic alkalosis with tubulopathy.

The effect of magnesium treatment on serum potassium and potassium balance was examined in three siblings with a recently described syndrome of hypokalemic alkalosis with renal tubulopathy. Oral magnesium supplementation for 11 days in the three siblings increased mean serum potassium from 2.7 +/- 0.1 meq/liter to 3.3 +/- 0.2 meq/liter (p less than 0.05). In addition, urinary and fecal potassium excretion decreased by about 11 meq/day. Magnesium chloride did not affect plasma renin activity while the patients were supine or upright. In contrast, mean supine plasma aldosterone concentration increased from 5.3 +/- 1.5 ng/dl to 13.2 +/- 4.1 ng/dl (p greater than 0.1) and mean upright plasma aldosterone concentration increased from 17.4 +/- 3.8 ng/dl to 66.1 +/- 7.3 ng/dl (p less than 0.01). These findings suggest that hypokalemia and potassium loss in this disorder may be caused by abnormal magnesium metabolism. The increase in plasma aldosterone concentration may have been caused by the positive potassium balance or a direct effect of magnesium on aldosterone secretion from the adrenal gland.

Adolescent↗
PubMed1983

Metabolic alkalosis due to absorption of "nonabsorbable" antacids.

In a patient with end-stage renal disease undergoing long-term maintenance hemodialysis, moderately severe metabolic alkalosis developed in the absence of vomiting or gastric drainage. The cause of the acid-base disorder was exogenous alkali administration, in the form of combined ingestion of "nonabsorbable" antacids (aluminum hydroxide and magnesium hydroxide), neutral phosphate, and a cation-exchange resin (sodium polystyrene sulfonate). In this report, the relevant data of this patient are detailed, and the literature on this well-documented, albeit poorly recognized, acid-base derangement is summarized.

Absorption↗
PubMed1988

On the mechanism by which chloride corrects metabolic alkalosis in man.

To determine whether administration of chloride corrects chloride-depletion metabolic alkalosis (CDA) by correction of plasma volume contraction and restoration of glomerular filtration rate or by an independent effect of chloride repletion, CDA was produced in normal men by the administration of furosemide and maintained by restriction of dietary sodium chloride intake. Negative sodium balance (-112 +/- 16 meq) and reduced plasma volume (2.53 versus 2.93 liters, p less than 0.05) developed. The cumulative chloride deficit of 271 +/- 16 meq was then repleted by oral potassium chloride (267 +/- 19 meq) over 36 hours with continued serial measurements of glomerular filtration rate, effective renal plasma flow, plasma volume, body weight, and plasma renin and aldosterone levels. CDA was corrected, even though body weight, plasma volume, glomerular filtration rate, and renal plasma flow all remained reduced and plasma aldosterone was elevated; urinary bicarbonate excretion increased during correction. Administration of an identical potassium chloride load to similarly sodium-depleted but not chloride-depleted normal subjects produced no change in acid-base status. It is concluded that chloride repletion can correct CDA by a renal mechanism without restoring plasma volume or glomerular filtration rate or by altering sodium avidity.

Adult↗