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PubMed1985

Contribution of the Bohr effect to the fall in fetal PO2 caused by maternal alkalosis.

A decrease in the PO2 of fetal arterial blood is observed in maternal alkalosis caused by hyperventilation in labour or exercise. The contribution of altered blood oxygen affinity to this effect was studied experimentally and by computer simulation of placental gas exchange. Thirteen guinea pigs near term of pregnancy were anesthetized and the right atrium of the fetus was catheterized to enable continuous and simultaneous measurement of PO2 and PCO2 by mass spectrometry. An infusion of base was given through a catheter in the descending aorta of the dam and the effect on fetal respiratory gas tensions observed. The mean change in maternal arterial pH measured in blood taken from a femoral artery was 0.07 +/- 0.04 (mean +/- S. D.). There was an immediate decrease in PO2 in the right atrium of the fetus, but no consistent alteration in PCO2. Two minutes after the start of the infusion, PO2 had fallen by 3.2 +/- 1.6 Torr (p less than 0.001) and PCO2 had risen by 1.7 +/- 1.8 Torr (not significant). The experiments were simulated using a mathematical model of placental gas exchange in the guinea pig. The model was able to predict the change in fetal arterial PO2, given numerical values for the pH, PO2 and PCO2 of fetal and maternal arterial blood prior to infusion of base and for maternal blood during the infusion of base. These values were obtained from the experimental data. Other input variables of the model were maternal and fetal hematocrit and DPG concentration, and the rates of blood flow on the two sides of the placenta.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkalosis↗
PubMed1998

Hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis. A new syndrome. 1962.

A new syndrome, characterized by hypertrophy and hyperplasia of the juxtaglomerular apparatus of the kidneys, aldosteronism resulting from adrenal cortical hyperplasia, and persistently normal blood pressure is described in two patients. Overproduction of aldosterone could not be prevented by sodium loading or by administration of albumin intravenously; it was associated with hypokalemic alkalosis and Pitressin-resistant impairment of urinary concentrating ability. In both subjects, increased amounts of circulating angiotensin were demonstrated; infusion of angiotensin II produced rises of blood pressure in both subjects considerably less than the rises induced by comparable doses in normal subjects. The sequence of events, (1) primary resistance to the pressor action of angiotensin, (2) compensatory overproduction of renin and thus of angiotensin, and (3) stimulation of adrenal cortex by angiotensin is consistent with all the information available about the syndrome.

Alkalosis↗
PubMed1980

Effect of acidosis, alkalosis and monofluoroacetate administration on citrate and ATP content of rat renal medulla and papilla.

1. --Renal distribution of citrate showed that there is an increase in citrate content from cortex to medulla and a decrease from medulla to papilla. Alkalosis produced an increase in citrate content and acidosis a decrease in renal citrate content, in each of the studied renal area. Monofluoroacetate produced no significant change in citrate content of medulla or papilla; it did not interfere with the acido-basic related changes in cortex citrate content, but its effect was additive. 2. --Renal distribution of ATP significantly decreased from cortex to medulla and from medulla to papilla. Acid or basic diet had no influence on intratissular ATP content. Fluoroacetate decreased renal ATP content.

Acidosis↗
PubMedDate not supplied

The effects of hypocapnic alkalosis on the myocardial contractility of isovolumic perfused rabbit hearts.

During acute respiratory alkalosis myocardial contractility first increases but then decreases towards control levels. The mechanism of this response was investigated in isovolumic perfused rabbit hearts. Developed pressure (DP) and its first derivative (dP/dt) were measured before, during and after hypocapnia induced by equilibrating the perfusate with 2% CO2 rather than the 5% used in control. pH of the perfusate (pHo) changed from 7.36 +/- .02 to 7.71 +/- .01. After about 20 s, an increase in DP of about 20% was detected. This increase in contractility is followed by a partial recovery towards control levels. After the partial recovery a new mechanical steady state is reached in about 2 min. Neither 5-[N-ethyl-N-isopropyl]amiloride (EIPA) 10(-6) M, a blocker of the Na+/H+ exchanger, nor 4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid (SITS) 10(-4) M, or 5-[aminosulfonyl]-4-chloro-2-[(2-furanylmethyl)-amino] benzoic acid (furosemide) 10(-4) M, blockers of Cl-/HCO3- exchanger, abolished the recovery in contractility towards control levels. The recovery was not abolished by replacing 50% of extracellular Cl- concentration by either sulfate or gluconate. The lack of blockade of this mechanical recovery in spite of the intervention performed suggests a mechanism other than the exchangers as the cause of the biphasic changes.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1986

Effects of thermal-induced respiratory alkalosis on blood ionized calcium levels in the domestic hen.

An experiment was conducted to determine the change with time in the blood ionized calcium concentration of hens exposed to an acute heat stress. Five hens were surgically fitted with carotid artery cannulae and placed in cages inside a temperature-controlled chamber. Blood samples were drawn before (23 C), during (35 C), and after (23 C), a 3-hr heat-stress exposure. Whole blood ionized calcium, blood gas, plasma pyruvate, and lactate were determined. Respiratory alkalosis developed 1 hr after the start of heat exposure (35 C). Approximately 1 hr later, there was a concomitant decline in blood pH as plasma lactate and pyruvate concentration increased (P less than .05). In addition, the blood ionized calcium level was reduced (P less than .05) by 19% and was negatively correlated (P less than .05) with plasma pyruvate (-.77) and lactate (-.81). These results suggest that changes in acid-base balance during heat stress reduce the blood ionized calcium level, which may in turn limit the availability of calcium for egg shell formation.

Alkalosis, Respiratory↗
PubMed2006

Metabolic alkalosis in a hemodialysis patient--successful treatment with a proton pump inhibitor.

Hemodialysis patients develop metabolic acidosis due to their impaired excretion of daily produced protons (H+). The following report will show a rare case of severe metabolic alkalosis (predialysis pH 7.52, base excess (BE) +17) in a hemodialysis woman caused by self-provoked upper gastrointestinal H+ losses based on an eating disorder. Treatment with a proton pump inhibitor resulted in the normalization of acid/base homeostasis (predialysis pH 7.40, BE +1.6).

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1975

Postoperative metabolic alkalosis and acute renal failure: rationale for the use of hydrochloric acid.

Metabolic alkalosis secondary to chloride depletion, especially following gastrointestinal surgery and associated with acute renal failure, is a frequent clinical occurrence. Management of the resultant acid-base disturbance mandates chloride replacement. The presence of oliguria limits the choice of accompanying cation. The use of intravenous hydrochloric acid to correct and maintain proper chloride balance, secondary to external gastric fluid losses, is recommended as a straightforward approach. Two brief case synopses are presented. Both patients, florid examples of profound chloride depletion, required large amounts of intravenous hydrochloric acid. The options regarding the choice of chloride solution, hazards involved, and a simplified schema of replacement therapy are presented. Combined gastrointestinal and renal dysfunction create unusual biochemical and clinical alterations and may result in a complex management problem.

Acute Kidney Injury↗
PubMed1976

Evidence of a pure "contraction alkalosis= in awaken rat.

A pure contraction alkalosis with no urinary loss of bicarbonate was evidenced in awaken rat, after a Furosemide IV injection. We observed: 1) an early and important respiratory compensation possibly owing to a simultaneous contraction of CSF volume, thus increasing bicarbonate concentration. 2) a net shift of HCO3- towards intracellular compartment, in proportion to the magnitude of the contraction rather than to bicarbonate gradient across the membrane.

Acid-Base Equilibrium↗
PubMed1975

[Metabolic alkalosis in patients following resuscitation].

Among 3425 patients treated in the general reanimation department metabolic alkalosis was observed in 445 patients (13%). More than a half of these patients (241) showed marked hemodynamic disturbances on admission (massive blood loss, multiple grave traumas or major operations). The phenomena of hypovolemia and disturbances in peripheral circulation with recommendations on their correction are described.

Alkalosis↗
PubMed1976

[Metabolic alkalosis and secondary hyperaldosteronism in cystic fibrosis (author's transl)].

The prolonged use of a salt restricted infant formula (1.9 mEq Na/kg/day and 1,4 mEq C1/kg/day) in a child with undiagnosed cystic fibrosis led to a life threatening metabolic disturbance. The main features were hypochloraemic alkalosis due to massive loss of electrolytes in the sweat. Urinary electrolyte excretion, however, had been lowered to a minimum due to aldosteron induced reabsorption. Plasma aldosterone levels were initially high, but returned to normal after addition of salt to the feeds. Prior to admission a sweat test had been negative. The patient clearly demonstrates the unique metabolic feature of cystic fibrosis of the ability to retain electrolytes in the tubulus and at the same time the inability of the sweat glands to reabsorb sodium and chloride. Contrary to present experience severe prolonged salt restriction is believed to be able to diminish sweat electrolytes to subpathological values.

Aldosterone↗
PubMed1992

[Hypomagnesemia associated with hypokalemia, hyponatremia and metabolic alkalosis. Possible complication of gentamycin therapy].

Hypomagnesemia is a serious abnormality with different causes and usually associated to other disorders of electrolyte metabolism. We report a female patient developing hypomagnesemia after administration of gentamycin. This was associated to severe hypokalemia, hyponatremia and metabolic alkalosis. Possible pathogenetic mechanisms and therapeutic measures are discussed.

Aged↗
PubMed1992

Hemoperfusion with a new anion exchange resin corrects the metabolic alkalosis in pyloric stenosis: an experimental demonstration.

An experimental model of hypertrophic pyloric stenosis was made by suture of the pyloric wall and gastrostomy in 10 rabbits under general anesthesia. Blood sampling indicated severe alkalosis and hypochloremia 3h 30 min after surgery. To correct the derangement, we tested an ion exchange resin (Dowex SAR), coated with a methacrylic hydrogel. A cartridge containing 18 g of this resin was inserted in an extracorporeal circuit. This chloride charged resin achieved uptake of HCO3- ions, and elution of Cl- ions. The electrolytic balance was fully restored after 10 min of treatment.

Alkalosis↗
PubMed2004

[Hypokalemic metabolic alkalosis: apropos of a case of Gitelman's syndrome].

We present a case of Gitelman's Syndrome in a 20 year-old woman who came to our service with weakness, asthenia, leg cramps and tetany. Laboratory studies revealed metabolic alkalosis with hypokalemia, hypomagnesemia and low calcium in a 24-hour urine test. The diagnosis of this syndrome is made in some cases during adult life because this syndrome is asymptomatic over several years. Gitelman's Syndrome is autosomal recessive as is Bartter's Syndrome. The gene is located in chromosome 16q, which encodes the cotransporter Na/Cl sensitive to thiazide in the distal convoluted tubule. The defect of cotransporter produces an alteration of sodium reabsorption that causes electrolytic disorders typical of this Syndrome and different from Bartter's Syndrome. The typical electrolytic alterations are hypocalciuria and hypomagnesemia secondary to high urinary magnesium excretion. The prognosis of this syndrome is excellent and treatment consists in correction of serum electrolytes with oral administration of magnesium and potassium. In spite of this treatment, in some cases it is very difficult to reach normal serum levels of magnesium because of the high doses of oral magnesium, which produce common crises of diarrhea that increase magnesium gastrointestinal losses.

Alkalosis↗
PubMed2004

Use of bicarbonate/lactate-buffered dialysate with a nighttime cycler, associated with a daytime dwell with icodextrin, may result in alkalosis in children.

The aim of peritoneal dialysis (PD) remains to deliver "appropriate" renal replacement therapy, including sufficient ultrafiltration, correction of acid-base balance, and adequate dialysis dose. We switched our pediatric patients on automated PD from standard lactate-buffered glucose solution (Dianeal: Baxter Healthcare SA, Castlebar, Ireland) to bicarbonate/lactate-buffered solution (Physioneal: Baxter Healthcare SA) as soon as it became available in our country. We also decided to deliver "optimal" dialysis in children by prescribing a long daytime dwell with icodextrin solution (Extraneal: Baxter Healthcare SA). But, adding those three benefits together--APD, Physioneal, and a long dwell with icodextrin--the result, at least in children, was a possible overcorrection of acidosis and an evolution to alkalosis. Thought must be given to developing solutions with varying bicarbonate concentrations for various treatment modalities.

Alkalosis↗
PubMed1991

[Severe metabolic alkalosis during hemodialysis].

Severe metabolic alkalosis in a patient while being hemodialysed with dialysate of bicarbonate is presented. The evolution was satisfactory after a session of hemodialysis with a bath of acetate. Disorders in the acid-base balance which appear following dialytic technics more complex each time are discussed.

Acute Disease↗
PubMed1991

Hypochloremic metabolic alkalosis from ingestion of a chloride-deficient infant formula: outcome 9 and 10 years later.

In 1978 and 1979 two infant formulas, Neo-Mull-Soy and Cho-Free, were found to be deficient in chloride. The Centers for Disease Control received reports that hypochloremic metabolic alkalosis (HMA) had developed in 141 children as a result of exposure to these formulas. Thirty-five of these children were examined at 9 and 10 years of age and compared with a group of 32 children who were exposed to the chloride-deficient formulas but were not reported to experience HMA and a group of 61 children who received chloride-sufficient soy formulas in infancy. The control children were matched to the HMA children on sex, race, age, and maternal education. Growth characteristics, performance on the Wechsler Intelligence Scale for Children-Revised (WISC-R), the Boston Naming Test, the Rey-Osterrieth Test, the Clinical Evaluation of Language Fundamentals-Revised (CELF-R), and subtests from several other speech and language tests were compared across the groups. After adjustment for family income and the level of the father's education, significantly lower scores were observed in the HMA children on the WISC-R Arithmetic subtest (mean = 10.5) compared with the soy control children (mean = 12.0, P less than .05) and on the WISC-R Coding subtest (mean = 9.0) compared with the soy control children (mean = 10.8, P less than .01). All the WISC-R subtest scores were, however, within the normal range. Although no significant differences occurred on the CELF-R between groups, the risk of an HMA child falling below the range expected for a standard population was increased on the CELF-R Composite Total, Receptive, and Expressive Language scores: risk ratios = 2.14, 2.14, and 3.03 respectively. Significant differences were observed between the children exposed, both HMA and non-HMA children, and the soy control children for behavioral problems as determined by the Achenbach Childhood Behavioral Checklist. It is concluded that as a group, children with documented HMA appear to have recovered from their growth failure and have normal cognitive development. They may, however, be at risk for deficits in language skills that require expressive language abilities.

Alkalosis↗
PubMed1990

[Gas acidosis and alkalosis].

Arterial concentration of CO2 (PaCO2) is dependent of pulmonary excretion. When this excretion is lower than cellular production respiratory acid-basis occurs: rise in PaCO2 which lowers pH and produces secondary increases in bicarbonate (HCO3-) plasma concentration. Respiratory alkalosis, generated by a CO2 pulmonary excretion greater than metabolic production is characterized by a fall in PaCO2 which raises pH and induces secondary reduction of plasmatic HCO3- concentration. Attention to the possibility of serious hypoxemia, cause or consequence, should always be regarded and treated in respiratory acid-base disorders.

Acidosis, Respiratory↗