Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ALKALOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1992

[Diagnosis, therapy and classification of alkalosis].

The pathogenesis, classification, diagnosis and treatment of alkalosis are described. Alkalemia is defined as an elevation in the blood pH and alkalosis refers to processes that tend to raise the pH, and divided into two types; metabolic alkalosis (a primary increase in plasma HCO3- concentration) and respiratory alkalosis (a primary decrease in PCO2). These disorders are most frequently observed in the hospitalized patients. As the critically ill-patients with severe alkalemia are often associated with high mortality, treatment should be directed to the underlying diseases and severe alkalemia should be corrected promptly.

Alkalosis↗
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↗
PubMed1982

Parathyroid-hormone-induced metabolic alkalosis in dogs.

We examined the effect of parathyroid hormone (PTH), administrated for 24-48 h, on acid-base homeostasis in dogs. Parathyroid extract (PTH), 15 IU/kg/day, given subcutaneously, caused metabolic alkalosis (control vs. experimental; mean +/- SEM): plasma HCO3, 21.3 +/- 0.3 vs. 24.2 +/- 0.5 mEq/l (p less than 0.001); plasma H+, 37.7 +/- 1.1 vs. 35.7 +/- 1.4 nEq/l (p less than 0.05), and net acid excretion, 48.6 +/- 2.0 vs. 65.1 +/- 4.0 mmol/day (p less than 0.01). PTH administered by continuous intravenous infusion had similar effects (control vs. experimental): plasma HCO3, 21.4 +/- 0.4 vs. 23.6 +/- 0.7 mEq/l (p less than 0.001) and net acid excretion, 54.0 +/- 3.5 vs. 68.3 +/- 5.7 mmol/day (p less than 0.05). PTH, 8 IU/kg/day, had qualitatively similar but quantitatively less profound consequences. Bicarbonaturia was not observed in any group. The effects of PTH were similar in adrenalectomized dogs maintained on hormone replacement. Indomethacin (150 mg/day) prevented the renal effects of PTH so that no increase in net acid secretion occurred. However, metabolic alkalosis still developed: control vs. experimental plasma HCO3, 21.8 +/- 0.5 vs. 23.9 +/- 0.5 mEq/l (p less than 0.001). Dichloromethanediphosphonate blunted both the renal and nonrenal effects of PTH, such that hypercalcemia, metabolic alkalosis and increased net acid excretion were quantitatively less and delayed in onset. In summary, PTH administration for 24-48 h causes metabolic alkalosis in dogs, the result of renal and nonrenal mechanisms.

Acid-Base Equilibrium↗
PubMed1983

Corticotropin-induced alkalosis in the weanling rat and its relation to the balance of non-metabolizable base.

Studies of whole body balances of non-metabolizable base (NB) and several electrolytes and of the acid-base status of blood and urine during development of corticotropin-induced alkalosis in the weanling rat were carried out in order to identify the primary source of base and factors instrumental in maintenance of the alkalotic state. The data were compared to baseline and running control values and to the results of whole carcass analysers. Primary accumulation of NB was accounted for by ongoing gastrointestinal NB absorption in the weight-losing animal, distributed to extracellular and non-extracellular compartments of the body. An increase in the rate of renal excretion of non-metabolizable acid (NA), from negative values to zero, corresponded to an increased load of endogenous sulphuric acid and a reduced rate of gastrointestinal NB absorption. Accordingly, the renal response did not per se contribute to the induction of extracellular alkalosis. Maintenance of alkalosis occurred in spite of ample chloride in the renal tubular lumen and a moderate increase in relative extracellular volume. In the absence of evidence of overloading (with base) or malfunction of the kidney, corticotropin-induced alkalosis is classifiable as a 'set-point disturbance' of acid-base metabolism in which fluctuations in the (non-renal) load of NA lead to commensurate changes in renal NA excretion at an elevated extracellular pH. Withdrawal of corticotropin injections was followed by prompt restoration of a normal extracellular acid-base status and a return to reference values for renal NA excretion despite a marked fall in the balance of NB. This observation supports a concept of the extracellular compartment as the immediate reference system of the kidney.

Acid-Base Imbalance↗
PubMed1983

Proximal tubular acidification in metabolic alkalosis.

Metabolic alkalosis was induced in rats by acute bicarbonate loading in the presence and absence of extracellular volume (ECV) expansion. Proximal tubular acidification was studied by stopped-flow microperfusion and the determination of luminal pH by antimony microelectrodes. Stationary pH and bicarbonate were markedly increased in proximal tubules of alkalotic rats, and acidification half-times were increased, leading to a fall in net bicarbonate reabsorption (JHCO-3) to 36% of control values. Net H+ ion secretion (JH+) into phosphate buffer fell to 56% of controls, whereas alkalinization t/2 and H+ fluxes, measured during perfusion with acid phosphate, were unaltered. ECV expansion reduced proximal JHCO-3 36% in control rats, without affecting JH+, and caused a fall in alkalinization t/2, compatible with increased bicarbonate back-flux into the lumen. However, it did not affect JHCO3 and JH+ in alkalotic rats. Carbonic anhydrase inhibition did not significantly reduce acidification in alkalotic rats. An analysis of the components of bicarbonate reabsorption showed that alkalosis reduced catalyzed H+ -ion secretion to 7% of the control values. It is concluded that proximal H+ ion secretion is significantly reduced in metabolic alkalosis leading to lower JHCO-3. No evidence for modification of H+/HCO-3 apparent permeabilities was obtained. The effects of alkalosis were not significantly altered by ECV expansion or by carbonic anhydrase inhibition.

Acid-Base Equilibrium↗
PubMed1983

Magnesium oxide induced metabolic alkalosis in cattle.

A study was designed to compare the metabolic alkalosis produced in cattle from the use of an antacid (magnesium oxide) and a saline cathartic (magnesium sulphate). Six, mature, normal cattle were treated orally with a magnesium oxide (MgO) product and one week later given a comparable cathartic dose of magnesium sulphate (MgSO(4)). The mean percent dry matter content of the cattle feces changed significantly (P<0.001) following administration of both MgO (15.6-8.1) and MgSO(4) (17.0-8.7) but there was no significant difference between treatments. The mean rumen pH values changed significantly (P<0.001) following administration of both MgO (7.-8.7) and MgSO(4) (7.3-8.3) but there was no significant difference between treatments. However, use of the MgO product caused a more severe (P<0.001) metabolic alkalosis as determined by base excess values. The base excess values remained elevated for 24 hours in the MgO treated group compared to only 12 hours after MgSO(4) administration. Following MgO administration, mean hydrogen ion concentration (pH), bicarbonate ion concentration ([HCO(3)-]) and base excess were 7.44, 33.3 mmol/L and +8.0 respectively compared to 7.38, 27 mmol/L and +3.0 after MgSO(4). Since the oral use of MgO in normal cattle causes a greater and more prolonged metabolic alkalosis compared to MgSO(4), MgO is contraindicated as a cathartic in normal cattle or in cattle with abomasal abnormalities characterized by pyloric obstruction and metabolic alkalosis.

Alkalosis↗
PubMed1980

Neo-Mull-Soy metabolic alkalosis: a model of Bartter's syndrome?

A case of Neo-Mull-Soy-induced metabolic alkalosis occurred in an 8-month-old child. This child had hypochloremic hypokalemic alkalosis as well as hyperreninemia. Initially, a diagnosis of Bartter's syndrome was made and treatment consisted of KCl replacement, indomethacin, and aspirin. In retrospect, the diagnosis of Neo-Mull-Soy induced metabolic alkalosis could have been suspected on the basis of the low chloride concentration in his urine. Proposed mechanisms for the etiology of Bartter's syndrome are reviewed. Neo-Mull-Soy induced metabolic alkalosis simulates Bartter's syndrome and supports the concept that the primary abnormality in Bartter's syndrome is chloride deficiency. The chloride deficiency in Bartter's syndrome results from a defect in active chloride transport in the thick ascending limb of the loop of Henle.

Alkalosis↗
PubMed1987

Activation of amino acid uptake at fertilization in the sea urchin egg. Requirement for proton compartmentalization during cytosolic alkalosis.

The comparative importance of the release of intracellular ionic calcium, Na+/H+ exchange and cytosolic alkalosis as activator signals was studied on the development of amino acid uptake at fertilization in sea urchin eggs. We show that, once stimulated, the rate of valine uptake is greatly dependent upon intracellular pH. Suppression of the Na+/H+ exchange at the time of activation, by applying ionophore (A23187) in sodium-free artificial sea water (ONaASW), inhibits the development of valine influx. This cannot be restored by a further (30 min later) alkalosis by transferring eggs into sea water. Suppressing the alkalosis in the presence of Na+/H+ exchange at fertilization by simultaneous addition of acid into sea water results in activation of the amino acid carrier which exhibits an increased rate of transport as soon as the eggs are replaced in sea water at pH 8.0. The absence of alkalosis in eggs activated in ONaASW can be counterbalanced either by adding NH4Cl 10 mM or by transfer into ASW at pH 9.0 at activation. Ammonia-treated eggs absorbed amino acid as controls, whereas eggs in sea water at pH 9.0 failed to develop a valine uptake system, suggesting that ammonia can completely replace the effect of Na+/H+ exchange. Furthermore, addition of NH4Cl immediately before fertilization conceals the Na+/H+ exchange but stimulates valine uptake as in controls. These data suggest that: the occurrence of the intracellular calcium increase alone is not sufficient for the develpment of the amino acid transport system; cell alkalinization at fertilization derives from the cytoplasmic membrane-located Na+/H+ exchange and an inward movement of protons into a cortical acidic compartment, which is discussed.

Amino Acids↗
PubMed2003

Extracellular alkalosis activates ERK mitogen-activated protein kinase of vascular smooth muscle cells through NADPH-mediated formation of reactive oxygen species.

Extracellular alkalosis induced phosphorylation of extracellular signal-regulated kinase (ERK) and enhanced serum-induced ERK phosphorylation in cultured rat aortic smooth muscle cells. While extracellular alkalinization increased verapamil-sensitive (45)Ca(2+) uptake into the cells, ERK phosphorylation induced by extracellular alkalosis was not affected by verapamil. On the other hand, probes for oxidant signaling, such as superoxide dismutase, 4,5-dihydroxy-1,3-benzene-disulfonic acid, a cell-permeable antioxidant, and diphenyliodonium, a NADPH oxidase inhibitor, inhibited extracellular alkalosis-induced phosphorylation of ERK. These results suggest that activation of ERK induced by extracellular alkalosis is not dependent on transplasmalemmal Ca(2+) entry but is caused by reactive oxygen species derived from an activation of NADPH oxidase.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗
PubMed1994

Continuous Infusion Ranitidine in Postoperative Pediatric Liver Transplant Patients: Effects on Intragastric pH, Gastrointestinal Bleeding and Metabolic Alkalosis.

The effects of ranitidine, an H(2)-receptor antagonist, on gastric pH, incidence of upper gastrointestinal hemorrhage and postoperative metabolic alkalosis were evaluated in 23 pediatric liver transplant recipients. Intragastric pH probes were inserted postoperatively and pH was monitored for 48 h. Ranitidine was infused for 48 h at 0.2 mg kg(minus sign1) h(minus sign1) (0.15 with renal impairment) and increased once by 0.05 mg kg(minus sign1) if the pH was less than 4.0 for 4 h. The pretreatment gastric pH was 2.1 plus minus 0.7; ranitidine infusion raised the pH to 6.8 plus minus 0.6 (p greater-than-or-equal 0.05). An intragastric pH > 4 was achieved in 64 plus minus 36 min, with a median ED(50) (50% of maximum response) of 0.24 mg kg(minus sign1). The pH was < 4 for 5.3 plus minus 4.8% of the time after the initial response. Loss of pH control occurred in three patients, two of whom had bacterial sepsis. The incidence of upper gastrointestinal bleeding and metabolic alkalosis was evaluated by comparing the study patients to age- and weight-matched historic controls from our center. Bleeding occurred in 1 of 23 (4%) study patients compared to 7 of 23 (30%) controls (p greater-than-or-equal 0.05). Metabolic alkalosis did not develop in the study patients at 24 or 48 h postoperatively (p greater-than-or-equal 0.05 versus controls). Whole blood cyclosporine levels and hepatocellular enzymes were similar in the two groups. We conclude that continuous intravenous infusion of ranitidine in the postoperative pediatric liver transplant recipient raises intragastric pH, decreases the incidence of upper gastrointestinal hemorrhage and prevents the development of metabolic alkalosis.

Journal Article↗
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↗
PubMed1984

Effects of SITS, an anion transport blocker, on CSF ionic composition in metabolic alkalosis.

Disulfonic stilbenes combine with the carrier protein involved in anion transport and inhibit the exchange of Cl- for HCO3- in a variety of biomembranes. Our aim was to determine whether such a mechanism is operative in the regulation of cerebrospinal fluid (CSF) [HCO3-] in metabolic alkalosis. In anesthetized, curarized, and artificially ventilated dogs either mock CSF (group I, 9 dogs) or mock CSF containing SITS, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (group II, 7 dogs) was periodically injected into both lateral cerebral ventricles. During 6 h of isocapnic metabolic alkalosis, produced by intravenous infusion of Na2CO3 solution, plasma [HCO3-] was increased by approximately 14 meq/l in both groups. In SITS-treated animals the mean cisternal CSF [HCO3-] increased by 7.7 meq/l after 6 h, and this was significantly higher than the respective increment, 3.5 meq/l, noted in the control group. Increments in CSF [HCO3-] in both groups were reciprocated by decrements in CSF [Cl-] with CSF [Na+] remaining unchanged. Cisternal CSF PCO2 and lactate concentrations showed similar increments in both groups. It is hypothesized that in metabolic alkalosis a carrier transports HCO3- out of cerebral fluid in exchange for Cl- and that SITS inhibits this mechanism. The efflux of HCO3- out of CSF in metabolic alkalosis would minimize the rise in CSF [HCO3-] brought about by HCO3-] influx from blood into CSF and therefore contributes to the CSF [H+] homeostasis.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1997

Cystic fibrosis presenting with hypokalemia and metabolic alkalosis in a previously healthy adolescent.

Cystic fibrosis (CF) is an exocrine disease affecting multiple organ systems. Patients with CF usually present with respiratory or gastrointestinal abnormalities. This study presents a case of a previously healthy 17-yr-old man who was diagnosed with CF after presenting with metabolic alkalosis and hypokalemia. The defect associated with CF is in the cystic fibrosis transmembrane regulator (CFTR), which acts primarily as a chloride channel. Partially functional CFTR may be associated with less severe pulmonary and gastrointestinal manifestations, as in the case presented. Dysfunctional CFTR in the sweat ducts of CF patients are responsible for excessive chloride and sodium losses, especially in warm weather. Hypokalemia seen with heat stress is secondary to sweat as well as renal potassium wasting. Metabolic alkalosis is maintained by the excessive sweat sodium chloride losses which leads to extracellular fluid (ECF) volume contraction and chloride depletion. Generation of alkalosis may be related to dysfunctional CFTR in the kidney, but is most likely secondary to hypokalemia with ECF volume contraction. Finally, one must consider CF when confronted with hypokalemia and alkalosis in a previously healthy patient.

Acidosis↗
PubMed1988

Effects of respiratory and metabolic alkalosis and acidosis on pipecuronium neuromuscular block.

Acute respiratory and metabolic acidosis as well as metabolic alkalosis increased (by 11, 11, 21%) whereas respiratory alkalosis antagonized (by 10%) the partial steady state block produced by pipecuronium infusion on the anterior tibialis muscle of the cat. The duration of neuromuscular block following six successive doses of pipecuronium was prolonged 1.4-fold during long-lasting metabolic alkalosis while this parameter was shortened to half of that in control cats during acidosis. Pipecuronium block could be fully antagonized by neostigmine.

Acidosis↗
PubMed1990

Effects of alkalosis on muscle ions at rest and with intense exercise.

The effects of metabolic and respiratory alkalosis (MALK and RALK) on intracellular strong ion concentrations ([ion]i) and muscle to blood ion fluxes were examined at rest and during 5 min of intense, intermittent tetanic stimulation in the isolated, perfused rat hindlimb. Compared with the control (C), perfusion of resting skeletal muscle during MALK and RALK significantly increased [Cl-]i and [Na+]i, and RALK significantly lowered [K+]i; these changes, however, did not affect initial hindlimb force production. In both resting and stimulated muscle, the intracellular ion changes corresponded to appropriate perfusate to muscle ion fluxes. At rest, changes in slow-twitch soleus were greater than in fast-twitch white gastrocnemius (WG), but stimulation-induced changes in [Lac]i and [K+]i were greater in WG. At the end of stimulation [K+]i and [Mg2+]i had decreased less in MALK than in C and RALK, particularly in plantaris and WG muscles. Compared with C, the muscle to perfusate flux of Lac- increased by 37% in MALK and 27% in RALK. This was associated with significantly less Lac- accumulation in all muscles in MALK than in RALK, which, in turn, had significantly less lactate than C. Lactate efflux from contracting skeletal muscle was significantly correlated with an uptake of Cl- by muscle. It is concluded that extracellular alkalosis alters skeletal muscle intracellular ionic composition and increases Lac- efflux from skeletal muscle. In agreement with other studies, lactate release appears to occur by both ionic and molecular transport processes. Alkalosis had no apparent effect on muscle performance with this preparation.

Alkalosis↗
PubMed1984

Use of sodium bicarbonate to treat tricyclic antidepressant-induced arrhythmias in a patient with alkalosis.

Sodium bicarbonate has been recommended for the treatment of arrhythmias induced by tricyclic antidepressants. It is unclear, however, whether this therapy is effective only in the presence of acidosis. A case is presented in which there was an immediate response to sodium bicarbonate in three episodes of ventricular tachycardia despite the presence of alkalosis on two of the three occasions. Given the poor response to conventional therapy of arrhythmias induced by tricyclic antidepressants the use of sodium bicarbonate may be reasonable even in the presence of alkalosis. However, in the presence of pre-existing respiratory or metabolic alkalosis, such therapy is not without risk, and it is suggested that it be reserved for life-threatening situations when the arrhythmia has failed to respond to hyperventilation or antiarrhythmics or both.

Adult↗
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↗
PubMed2001

Patients with thrombotic thrombocytopenic purpura commonly develop metabolic alkalosis during therapeutic plasma exchange.

Thrombotic thrombocytopenic purpura (TTP) and myasthenia gravis (MG) are category I indications for therapeutic plasma exchange (TPE). This study was based on the hypothesis that the development of metabolic alkalosis during TPE is more common in TTP than in MG, based on our previous observations. In order to test it, we compared the levels of bicarbonate and potassium in both groups of patients undergoing plasmapheresis. Fifteen patients with TTP (190 procedures) and ten MG patients seen concurrently were studied. While baseline bicarbonate levels were similar among all patients, the post-procedure bicarbonate levels in TTP patients were mostly elevated with a mean +/- SD of 29.4 +/- 3.5 mEq/L, as opposed to decreased or unchanged in MG patients 26.3 +/- 3.1 mEq/L (mean +/- SD) (P = 1.4 x 10(-8)). Furthermore, alkalosis in the TTP group persisted throughout subsequent daily treatments. There was also a significant decrease between pre- and post-TPE potassium levels in TTP patients (P = 3 x 10(-21)) by paired Student's t test. Additionally, samples with levels <3.3 mEq/L were alkalotic 75% of the time. In the MG group, however, potassium was normal in 85% and 83% of the pre- and post-TPE samples, respectively. Consequently, the hypokalemia was significantly more marked in the TTP group (P = 0.0008). These data confirm that plasmapheresis commonly induces metabolic alkalosis in TTP patients, probably due to high citrate in fresh frozen plasma, the frequency of treatments, and perhaps decreased renal clearance due to disease involvement of the kidneys.

Adult↗