Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACIDOSIS”

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 1,567 records · Page 87Linked to original sources
PubMed1988

Acid-base regulation following acute acidosis in seawater-adapted rainbow trout, Salmo gairdneri: a possible role for catecholamines.

A fall in blood pH was induced by intra-arterial infusion of HCl in seawater-adapted rainbow trout (Salmo gairdneri). The acute acidosis resulting from HCl infusion caused a short-lived decrease in plasma bicarbonate concentration ([HCO3-]) and an increase in arterial CO2 tension (PaCO2). Erythrocyte pH and bicarbonate concentrations were not significantly altered by the infusion of acid. Injection of acid did, however, stimulate a branchial net H+ efflux which could be primarily accounted for by a net uptake of bicarbonate equivalent ions from the environmental water. Acid infusion of animals pre-treated with the beta-adrenergic blocking agent, propranolol, induced a similar pattern of change in plasma acid-base status. However, the recovery of plasma pH and restoration of plasma [HCO3-] were slower than in animals infused with acid alone. Red cell pH fell significantly in the face of plasma acidosis in the beta-blocked animals. Erythrocyte [HCO3-] showed a similar pattern of change to that of erythrocyte pH. Branchial net H+ efflux increased to a lesser extent following acid infusion in animals treated with propranolol. We conclude that catecholamines released into the bloodstream during periods of acute acidosis may play an important role in facilitating branchial H+ efflux in seawater-adapted rainbow trout.

Acclimatization↗
PubMed2004

Antimicrobial-associated renal tubular acidosis.

OBJECTIVE: To review the literature documenting the association of various antimicrobial medications with the development of renal tubular acidosis (RTA). DATA SOURCES: A search of the English literature via MEDLINE (1966-November 2003) and International Pharmaceutical Abstracts (1970-November 2003) was conducted to identify human reports of RTA associated with various drugs from all available classes of antimicrobial agents. Major search terms included renal tubular acidosis, acidosis, antibiotics, and antimicrobials. Bibliographies of selected articles were also searched to identify additional reports of RTA. STUDY SELECTION AND DATA EXTRACTION: Case reports, observational studies, and experimental studies documenting the association of any antimicrobial agent with the development of RTA were included. DATA SYNTHESIS: Antimicrobial-associated RTA is a relatively uncommon adverse effect, with most reports involving amphotericin B, trimethoprim/sulfamethoxazole, and outdated tetracycline. These agents may induce RTA either through direct tubular toxicity or as a function of their pharmacologic action. The time course for the development of RTA varies depending on the antimicrobial utilized. In most instances, RTA is reversible; however, some patients may experience prolonged recovery after the offending agent is removed. CONCLUSIONS: Given that antimicrobial-associated RTA is a relatively uncommon adverse effect, review of the patient's drug regimen may reveal these agents as otherwise unrecognized causes of RTA. Likewise, underlying causes of RTA other than medications must be ruled out. Diagnosing antimicrobial-induced RTA may be difficult, given many of these agents may be used in combination and some are intrinsically nephrotoxic.

Acidosis, Renal Tubular↗
PubMed2003

Regulatory mechanisms and physiological relevance of a voltage-gated H+ channel in murine osteoclasts: phorbol myristate acetate induces cell acidosis and the channel activation.

UNLABELLED: The voltage-gated H+ channel is a powerful H+ extruding mechanism of osteoclasts, but its functional roles and regulatory mechanisms remain unclear. Electrophysiological recordings revealed that the H+ channel operated on activation of protein kinase C together with cell acidosis. INTRODUCTION: H+ is a key signaling ion in bone resorption. In addition to H+ pumps and exchangers, osteoclasts are equipped with H+ conductive pathways to compensate rapidly for pH imbalance. The H+ channel is distinct in its strong H+ extrusion ability and voltage-dependent gatings. METHODS: To investigate how and when the H+ channel is available in functional osteoclasts, the effects of phorbol 12-myristate 13-acetate (PMA), an activator for protein kinase C, on the H+ channel were examined in murine osteoclasts generated in the presence of soluble RANKL (sRANKL) and macrophage-colony stimulating factor (M-CSF). RESULTS AND CONCLUSIONS: Whole cell recordings clearly showed that the H+ current was enhanced by increasing the pH gradient across the plasma membrane (delta(pH)), indicating that the H+ channel changed its activity by sensing delta(pH). The reversal potential (V(rev)) was a valuable tool for the real-time monitoring of delta(pH) in clamped cells. In the permeabilized patch, PMA (10 nM-1.6 microM) increased the current density and the activation rate, slowed decay of tail currents, and shifted the threshold toward more negative voltages. In addition, PMA caused a negative shift of V(rev), suggesting that intracellular acidification occurred. The PMA-induced cell acidosis was confirmed using a fluorescent pH indicator (BCECF), which recovered quickly in a K(+)-rich alkaline solution, probably through the activated H+ channel. Both cell acidosis and activation of the H+ channel by PMA were inhibited by staurosporine. In approximately 80% of cells, the PMA-induced augmentation in the current activity remained after compensating for the delta(pH) changes, implying that both delta(pH)-dependent and -independent mechanisms mediated the channel activation. Activation of the H+ channel shifted the membrane potential toward V(rev). These data suggest that the H+ channel may contribute to regulation of the pH environments and the membrane potential in osteoclasts activated by protein kinase C.

Acidosis↗
PubMed1993

Carbicarb, sodium bicarbonate, and sodium chloride in hypoxic lactic acidosis. Effect on arterial blood gases, lactate concentrations, hemodynamic variables, and myocardial intracellular pH.

The effects of Carbicarb, sodium bicarbonate, and sodium chloride on arterial blood gases, lactate concentrations, hemodynamics, and myocardial intracellular pH were compared in hypoxic lactic acidosis with controlled carbon dioxide elimination. Twenty-one young mongrel dogs were anesthetized, mechanically ventilated, and randomly allocated into one of three treatment groups. After hypoxic lactic acidosis was induced and maintained, 2.5 mEq/kg of one of the agents was infused over 30 min. Arterial blood gases, pH, lactate concentrations, and hemodynamic variables were measured immediately prior to the infusion of the agent and 30 min after the infusion was completed. With sodium bicarbonate administration, there was a significant increase in arterial PCO2 as compared to both Carbicarb or sodium chloride administration. With Carbicarb administration, there was a significant increase in arterial pH, base excess, and cardiac index, without a significant increase in arterial lactate concentration as compared to sodium bicarbonate or sodium chloride administration. Stroke volume index was also increased significantly with decreased heart rate. The data suggest that Carbicarb administration in hypoxic lactic acidosis improved hemodynamics compared with sodium bicarbonate or sodium chloride administration. The increased stroke volume and cardiac contractility appear to be due to improved myocardial intracellular pH.

Acidosis, Lactic↗
PubMed2001

Severe pectus excavatum associated with cor pulmonale and chronic respiratory acidosis in a young woman.

Pectus excavatum has never been reported to cause hypercapnic respiratory failure. In this report, we describe the first such case in a young woman with severe pectus excavatum who presented with chronic respiratory acidosis, pulmonary hypertension, and chronic cor pulmonale. An extensive diagnostic workup failed to uncover any other cause of respiratory acidosis, which led us to conclude that the severe chest wall deformity and the resulting severe restrictive defect were responsible for the development of chronic respiratory acidosis and cor pulmonale.

Acidosis, Respiratory↗
PubMed1990

Helium-oxygen mixtures in intubated patients with status asthmaticus and respiratory acidosis.

Seven patients with status asthmaticus intubated for respiratory failure who had elevated airway pressures and persistent respiratory acidosis were successfully ventilated using a mixture of 60 percent helium and 40 percent oxygen. All patients experienced a rapid reduction in airway pressures, CO2 retention, and resolution of acidosis while breathing a helium-oxygen mixture. There were no untoward effects. Helium-oxygen mixtures improve ventilation by reducing the Reynolds number and reducing density dependent resistance. Helium's beneficial effects are due to its high kinematic viscosity, high binary diffusion coefficient for CO2, and high diffusivity. Helium-oxygen mixtures should be considered for use in mechanically ventilated asthmatics with respiratory acidosis who fail conventional therapy.

Acidosis, Respiratory↗
PubMed1990

Dialysis-induced respiratory acidosis.

The inability to increase alveolar ventilation can lead to CO2 retention and acute respiratory acidosis in patients with ventilatory limitation. In this case, a young woman receiving maximum ventilatory support was unable to excrete excess CO2, associated with increasing dianeal concentrations of peritoneal dialysis. Since the patient's lung disease had necessitated a large amount of ventilatory support, the patient was unable to increase VE appropriately to handle excess CO2. Peritoneal dialysate was an additional source of carbohydrates. Peritoneal dialysate is an additional carbohydrate source that may result in hypercapnia and respiratory acidosis in patients with respiratory compromise. To our knowledge, this is the first case report in an adult which demonstrates that peritoneal dialysis with high glucose loads produced an acute respiratory acidosis that was reversed by decreasing the glucose concentrations in the dialysate. Excess CO2 production should be considered with respiratory disorders associated with dialysis.

Acidosis, Respiratory↗
PubMed2003

Helium pneumoperitoneum ameliorates hypercarbia and acidosis associated with carbon dioxide insufflation during laparoscopic gastric bypass in pigs.

BACKGROUND: In the morbidly obese patient undergoing laparoscopic gastric bypass (LGBP), insufflation with carbon dioxide to 20 mmHg for prolonged periods may induce significant hypercarbia and acidosis with attendant sequelae. We hypothesize that the use of helium as an insufflating agent results in less hypercarbia and acidosis. METHODS: The study was performed between May and November 2002. A Paratrend 7 fiberoptic probe was placed via a carotid artery catheter in 5 adult Yorkshire swine as continuous pH and pCO2 levels were measured. Animals were ventilated to a constant pCO2, after which LGBP was performed. Blood gas values were measured during the procedure and for 1 hour after release of pneumoperitoneum. Helium was used for insufflation in 3 of the pigs and CO2 in 2. Comparison of arterial pH and pCO2 were made between groups. RESULTS: Mean maximum pCO2 for the control group (CO2 insufflation) was 99.75 +/- 22.98 mmHg, while for the experimental group (helium insufflation) was 52.86 +/- 6.27 mmHg (P=.036). Mean low pH for the groups were 7.10 +/-.056 and 7.36 +/-.015 (P =.004) respectively. Normalization of pCO2 in the helium group occurred at a mean of 14.58 min (SD 13.3 min) after release of pneumoperitoneum, while in the control group levels did not normalize (mean final pCO2= 71.5 mmHg). CONCLUSIONS: Helium pneumoperitoneum in LGBP is associated with less intraoperative hypercarbia and acidosis than is the use of CO2. In addition, pCO2 returns to normal more rapidly postoperatively with the use of helium insufflation. Study of helium insufflation in humans undergoing LGBP is needed to prove its benefits in the clinical setting.

Acidosis↗
PubMed2004

Severe metabolic acidosis resulting from a dislocated gastric band.

A 32-year-old morbidly obese woman with an obstructing dislocated gastric band is presented. Because of prolonged vomiting, a metabolic alkalosis would be expected, but instead an impressive high anion gap acidosis was observed. Because of a highly positive urine ketone test and a high serum concentration of beta-hydroxybutyrate, a ketoacidosis caused by starvation appears to be the primary cause of this metabolic acidosis. This type of acidosis was treated successfully with intravenous administration of glucose and insulin as well as sodium bicarbonate, with urgent removal of the band.

Acidosis↗
PubMed2004

Maternal and fetal insulin-like growth factors 1 and 2 (IGF-1, IGF-2) and IGF BP-3, and their relationship to fetal acidosis at delivery.

OBJECTIVE: To investigate the relationship between levels of insulin-like growth factors 1 and 2 (IGF-1, IGF-2), and insulin-like growth factor binding protein 3 (IGFBP-3) in antenatal maternal serum and in fetal cord blood at delivery. METHODS: Prospective cohort study of 1650 low-risk Caucasian women in a University teaching hospital in London. Statistical analysis was performed using commercial software (SPSS for Windows, version 6.1, SPSS, Chicago, Illinois, USA), with p<0.05 as significant. Maternal IGF 1, IGF 2 and IGF BP-3 were assessed on maternal blood at booking and in fetal blood by cord blood analysis at delivery. Cord pH was also recorded. RESULTS: There was no significant correlation between maternal IGF-1, IGF-2, or IGFBP-3 levels and fetal acidosis. However, a significant correlation does exist between cord IGF-1 levels and fetal acidosis. CONCLUSION: Fetal cord IGF-1 has a significant correlation with fetal acidosis at delivery.

Acidosis↗
PubMed1976

The effect of modern intensive monitoring in obstetrics on infant mortality and the incidence of hypoxia and acidosis.

UNLABELLED: We consider intensive monitoring to be fetal monitoring during labor and in the newborn period of all births using the most efficient methods. During the last ten years we have sequentially used the following techniques: Amnioscopy, blood analysis, estrogen determinations in urine, external and internal cardiotokography and internal pressure determinations, gas analyses of umbilical blood. amniotic fluid analyses (phospholipids), ultrasound (B-apparatus) and HCS determinations. All clinics dealing with risk pregnancies should have these techniques available. Total perinatal mortality decreased to below 2% after introduction of cardiotokography. During the last year it decreased to 0.89%. Premature mortality shows the same decrease and is 50% of total mortality. The frequency of premature deliveries remained unchanged at 6.2%. Both improved intensive monitoring and neonatal reanimation and intensive care contributed to the reduction of perinatal mortality. Continuous heart rate recordings make it possible to uncover hypoxic and acidotic states in time and this is of particular value for the premature infant. The incidence of acidosis (pH less than 7.10) was 2.03% before monitoring was introduced and fell to 0.45% this year when intensive monitoring became the rule. No pH lower than 7.0 was found this year. It is thus not sufficient to monitor only cases at risk, since in about 50% of infants born with acidosis no alarming symptoms were found that would have indicated the need for intensive monitoring. CONCLUSION: Infant mortality should be reduced to less than 1% if the diagnostic tools available are applied. Below this nonviable infants limit further improvement. Perinatal hypoxia and acidosis (below pH 7.10) should also be lower than 0.5% but at least lower than 1%.

Acidosis↗
PubMed1983

Systematic pH-measurements in the umbilical artery: causes and predictive value of neonatal acidosis.

Subpartal and neonatal blood gas analyses have attracted increasing interest during the past 20 years. Different studies have been carried out to investigate the causes and immediate consequences of perinatal acidosis. It was the aim of this study to examine the long term outcome of acidotic-born babies. During 16 consecutive months all deliveries in the Obstetric Department of the Centre Hospitalier Universitaire Vaudois (CHUV) were investigated with regard to incidence and causes of a perinatal acidosis (pHa.umb. less than 7.15). The psycho-motor development of all acidotic newborns was followed up for an average of 15 months. Out of 1922 deliveries a blood sample was available in all but 11 cases (0.57%). Seven newborns were excluded from the study on the assumption that their acidosis and outcome might be related to the underlying condition (congenital malformation and infection, extreme prematurity) rather than perinatal events. From the remaining 1904 deliveries 6.4% (N = 121) had a pHa.umb. less than 7.15 (Tab. I). The incidence of certain perinatal factors was compared in the acidotic and the non acidotic groups (Tab. II). The percentage of acidotic newborns is significantly higher in primipareae, in deliveries done on peridural analgesia in cord complications and premature rupture of the membranes, and in forceps deliveries. No difference could be found with regard to multiple pregnancies, meconiumstained amniotic fluid, cesarean sections, prematurity of 28-37 weeks, and sex. The relationship between CTG score and pHa.umb. is summarized in Tab. III.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1991

How to assess fetal metabolic acidosis from cord samples.

The degree of metabolic acidosis at birth has been calculated in cord artery and vein samples from 21 term fetuses with cord artery pH less than 7.20. The aim of the study was to compare base deficit values calculated from either Siggaard-Andersen alignment nomogram (BD blood) or the Acid-Base chart (BD extra cellular fluid, BDecf). BDblood was found to be consistently higher in the cord artery as compared with BDecf, 13.2 +/- 3.5 and 9.9 +/- 2.9 mmol/l (Mean +/- SD), respectively. A significant correlation was found between cord artery PCO2 and BDblood whereas BDecf appeared unaffected by PCO2. In cases with cord entanglement BDecf a-v differences were increased to 3.4 +/- 2.3 mmol/l as compared with the small a-v difference noted in acidotic cases without cord entanglement, 1.1 +/- 1.25 mmol/l. It is speculated that with acutely emerging, intermittent asphyxia due to cord compression, a cord artery and vein difference in metabolic acidosis may exist and where the vein captures the basal level and the artery the acute changes. It is concluded that BDecf in both cord artery and vein add valuable information on the mechanisms behind metabolic acidosis.

Acidosis, Lactic↗
PubMed1994

Histometric investigations of placental villi in cases of unexpected fetal acidosis.

It is not unusual that, after an apparently uneventful pregnancy and birth, postpartal analysis of fetal blood unexpectedly reveals the presence of peripartal acidosis, a finding that is inexplicable on the basis of routine observation of the placenta. Using computer-assisted histometric procedures, it is possible to make a quantitative assessment with respect to the maturity and differentiation of villi, thus casting light on the functional anatomy of these structures. 89 single-birth pregnancies were grouped in accordance to the pH of blood in the umbilical artery (pre-acidosis, acidosis, non acidotic). In acidotic newborns, there is an absolute reduction in the surface area of the placenta available for fetomaternal metabolic exchange as well as a reduced surface/weight ratio largely attributable to the significantly reduced villous density. These changes lead to a compensatory increase of epithelial plates on the surface of villi and also causes a decrease in the fetomaternal diffusion distance. The application of a modern computer-assisted structural analysis helps toward clarifying the diagnosis.

Acidosis↗
PubMed2004

Blastoid variant of mantle cell lymphoma with lactic acidosis: a case report.

Approximately 20% of mantle cell lymphomas (MCL) present with the blastoid variant associated with poor prognosis. Lactic acidosis complicated with hematologic malignancies is seen infrequently and is associated with a poor outcome. Here we report the case of a patient with the blastoid variant of MCL complicated by lactic acidosis and who achieved complete remission through chemotherapy combined with rituximab therapy. A 77-year-old man presented with peripheral blood lymphoma cells, huge splenomegaly, abdominal and mediastinal lymphadenopathy, and pleural effusion. A bone marrow smear showed an increase in large, abnormal lymphoid cells with oval or round nuclei, distinct nucleoli, and abundant basophilic cytoplasm with vacuolization. Splenic sections also showed massive and diffuse infiltration by these cells. Flow cytometry analysis showed these cells to be positive for CD5, CD19, CD20, and kappa chain and negative for CD10 and CD23. A blastoid variant of MCL was diagnosed from the results of histologic, immunohistochemical (cyclin D1), and cytogenetic (chimeric bcl-1/IgH fusion gene) analyses. The patient recovered from the 2 episodes of severe lactic acidosis for which he had been given chemotherapy, and he achieved complete remission after subsequent chemotherapy combined with rituximab treatment.

Acidosis, Lactic↗
PubMed2005

Topiramate and severe metabolic acidosis: case report.

Topiramate infrequently induces anion gap metabolic acidosis through carbonic anhydrase inhibition on the distal tubule of the nephron--a type 2 renal tubular acidosis. We report on a 40 years old woman previously healthy that developed significant asymptomatic metabolic acidosis during topiramate therapy at a dosage of 100 mg/day for three months. Stopping medication was followed by normalization of the acid-base status within five weeks. This infrequent side effect appears unpredictable and should be given careful attention.

Acidosis, Renal Tubular↗
PubMed1998

Effect of metabolic acidosis on renal tubular sodium handling in rats as determined by lithium clearance.

Systemic metabolic acidosis is known to cause a decrease in salt and water reabsorption by the kidney. We have used renal lithium clearance to investigate the effect of chronic, NH4Cl-induced metabolic acidosis on the renal handling of Na+ in male Wistar-Hannover rats (200-250 g). Chronic acidosis (pH 7.16 +/- 0.13) caused a sustained increase in renal fractional Na+ excretion (267.9 +/- 36.4%), accompanied by an increase in fractional proximal (113.3 +/- 3.6%) and post-proximal (179.7 +/- 20.2%) Na+ and urinary K+ (163.4 +/- 5.6%) excretion when compared to control and pair-fed rats. These differences occurred in spite of an unchanged creatinine clearance and Na+ filtered load. A lower final body weight was observed in the acidotic (232 +/- 4.6 g) and pair-fed (225 +/- 3.6 g) rats compared to the controls (258 +/- 3.7 g). In contrast, there was a significant increase in the kidney weights of acidotic rats (1.73 +/- 0.05 g) compared to the other experimental groups (control, 1.46 +/- 0.05 g; pair-fed, 1.4 +/- 0.05 g). We suggest that altered renal Na+ and K+ handling in acidotic rats may result from a reciprocal relationship between the level of metabolism in renal tubules and ion transport.

Acidosis, Renal Tubular↗
PubMed2004

The impact of extracellular acidosis on dendritic cell function.

Dendritic cells (DCs) are the most efficient antigen-presenting cells. They are activated in the periphery by conserved pathogen molecules and by inflammatory mediators produced by a variety of cell types in response to danger signals. It is widely appreciated that inflammatory responses in peripheral tissues are usually associated with the development of acidic microenvironments. Surprisingly, there are relatively few studies directed to analyze the effect of extracellular acidosis on the immune response. We focus on the influence of extracellular acidosis on the function of immature DCs. The results presented here show that acidosis activates DCs. It increases the acquisition of extracellular antigens for MHC class I-restricted presentation and the ability of antigen-pulsed DCs to induce both specific CD8+ CTL and B-cell responses. These findings may have important implications to our understanding of the mechanisms through which DCs sense the presence of infection or inflammation in nonlymphoid tissues.

Acidosis↗