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 991 records · Page 55Linked to original sources
PubMed1988

Acidosis, hypoxia and stress hormone release in response to one-minute inhalation of 80% CO2 in swine.

The study pertains to a series of investigations on the effects of CO2 inhalation as used for pre-slaughter anaesthesia in swine. Acid/base parameters, blood oxygen tension, plasma Na, K, Ca and stress hormone concentrations were monitored in Yorkshire swine before, during, and for 10 min after the animals were descended for 1 min into 80% CO2 in air. Severe respiratory acidosis (PaCO2 approximately 50 kPa, arterial pH approximately 6.6) and hypoxia (PaO2 approximately 4kPa) had developed after 45 s of the CO2 inhalation. The corresponding changes in venous blood were less drastic (PvCO2 approximately 17 kPa, pH 7.1, PvO2 approximately 4 kPa). Readjustment to PaCO2 approximately II kPa, arterial pH 7.2, and PaO2 approximately 13 kPa had occurred at 1 min post CO2. Four minutes later the respiratory acidosis had become converted into metabolic acidosis subjected to partial respiratory compensation (arterial pH 7.3 in the presence of moderate hypocapnia and hyperoxaemia). The cause of this metabolic acidosis (present also at 10 min post CO2) was apparently hypoxia-induced anaerobic metabolism (= lactic acid production). Apparently due to hydrogen ion transport into the cells in exchange for other cations, hyperkalaemia (K approximately 6.6 mmol l-1), and a 7 mmol l-1 increase in plasma Na had developed at 1.5 min later. The CO2 inhalation did not change the total plasma Ca significantly. The transport of the swine from the stable to the immediate pre-experimental situation induced a 3-fold increase in plasma cortisol concentration (PC, to approximately 130 mmol l-1). No further increase in PC occurred in response to the CO2 inhalation. It indicates that no additional emotional strain was imposed upon the animals during the CO2 exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗
PubMed2005

Clinical acidosis in a Gippsland dairy herd.

OBJECTIVE: To report on spontaneous clinical and subclinical acidosis in a large dairy herd, to evaluate the diets and feeding strategies involved, and to report on measures of rumen function in the cows affected. DESIGN: A Gippsland dairy herd was sampled as part of a wider randomised cross-sectional study that examined the prevalence, risk factors for, and effects of, acidosis on rumen function of dairy cattle. Three herds on the farm were involved in the study: the transition herd (cows 3 weeks prior to calving), the very fresh lactating herd (1 < days in milk < 10, herd 1) and the fresh lactating herd (10 < days in milk < 120, herd 2) including a small lame herd fed separately. The transition cows were fed 2 kg dry matter triticale per cow per day and hay with an estimated total dry matter intake of 4.8 kg per cow per day. The lactating cow diet included 6.75 kg dry matter triticale per cow per day with total concentrate fed being 8.1 kg dry matter per cow per day in the milking parlour. Silage, lucerne cubes, hay and pasture (herd 2 only) was also fed to the lactating cows with the estimated total dry matter intake for cows in herds 1 and 2 being 13.7 kg and 20.8 kg per cow per day respectively. Three primiparous and five multiparous cows in early lactation (< 100 days in milk) were randomly selected from each of two lactating herds: herds 1 and 2. Rumen fluid was sampled from each cow by both rumenocentesis and stomach tube. The rumenocentesis samples were tested for pH at the time of sampling. Stomach tube samples were frozen and subsequently tested for volatile fatty acid, ammonia, and D- and L-lactate concentration. RESULTS: In the very fresh herd, there was a high prevalence of severe lameness and scouring, coupled with a mean rumen pH 5.67, low mean total volatile fatty acid concentration 71.0 mM and high mean concentrations of L- and D-lactate, (7.71 mM and 7.31 mM), respectively. Cows in the fresh herd had moderate signs of scouring and lameness. A lame herd comprising approximately 50 cows separated from the fresh herd was also present on the farm. The mean rumen pH of the fresh herd was 5.74 and mean rumen concentrations of volatile fatty acids, ammonia, L- and D-lactate were within ranges considered normal. CONCLUSIONS: The transition diet failed to supply sufficient energy and protein for maintenance of cows of this live weight in late gestation. The diet fed to the very fresh herd was low in effective fibre and contained an excessive content of non-structural carbohydrate in the form of processed, rapidly fermentable grain. The sudden change from the transition diet to the diet fed to the very fresh herd probably also precipitated the outbreak of acidosis. This case report provides unique detail, including information on diets and rumen parameters, of an outbreak of acidosis in a pasture-fed herd.

Acidosis↗
PubMed1993

The effect of acidosis on beta-adrenergic receptors in ferret cardiac muscle.

Acidosis decreases the force of contraction of cardiac muscle in response to noradrenaline. The role of beta-adrenergic receptors in this response to acidosis was investigated. Radioligand techniques were used to determine beta-adrenergic receptor number and the degree of G-protein coupling, and to see whether these were altered in tissues subject to acidosis. The effect of pH on agonist and antagonist binding to these receptors was also investigated. Tissue pre-exposure to acidic conditions had no effect on numbers of beta-adrenergic receptors and no effect on the affinity of [125I]iodocyanopindolol (ICYP) for the receptors. Agonist competition experiments indicated that there was no change in the affinity of isoprenaline for these receptors, and there was no change in the relative proportions of high and low affinity binding sites. When radioligand experiments were performed under acidic conditions, however, the total number of beta-adrenergic receptors increased, and the affinity of these receptors for isoprenaline increased. This increase in agonist affinity might, therefore, minimize the shift to the right seen in the dose-response curve to noradrenaline during acidosis.

Acidosis↗
PubMed2003

Acidosis inhibits oxidative phosphorylation in contracting human skeletal muscle in vivo.

This study tested the hypothesis that acidic pH inhibits oxidative ATP supply during exercise in hand (first dorsal interosseus, FDI) and lower limb (leg anterior compartment, LEG) muscles. We measured oxidative flux and estimated mitochondrial capacity using the changes in creatine phosphate concentration ([PCr]) and pH as detected by 31P magnetic resonance (MR) spectroscopy during isometric exercise and recovery. The highest oxidative ATP flux in sustained exercise was about half the estimated mitochondrial capacity in the LEG (0.38 +/- 0.06 vs. 0.90 +/- 0.14 mM ATP s(-1), respectively), but at the estimated capacity in the FDI (0.61 +/- 0.05 vs. 0.61 +/- 0.09 mM ATP s(-1), respectively). During sustained exercise at a higher contraction rate, intracellular acidosis (pH < 6.88) prevented a rise in oxidative flux in the LEG and FDI despite significantly increased [ADP]. We tested whether oxidative flux could increase above that achieved in sustained exercise by raising [ADP] (> 0.24 mM) and avoiding acidosis using burst exercise. This exercise raised oxidative flux (0.69 +/- 0.05 mM ATP s(-1)) to nearly twice that found with sustained exercise in the LEG and matched (0.65 +/- 0.11 mM ATP s(-1)) the near maximal flux seen during sustained exercise in the FDI. Thus both muscles reached their highest oxidative fluxes in the absence of acidosis. These results show that acidosis inhibits oxidative phosphorylation in vivo and can limit ATP supply in exercising muscle to below the mitochondrial capacity.

Acidosis↗
PubMed2003

Involvement of organic cation transporter 1 in the lactic acidosis caused by metformin.

Biguanides are a class of drugs widely used as oral antihyperglycemic agents for the treatment of type 2 diabetes mellitus, but they are associated with lactic acidosis, a lethal side effect. We reported previously that biguanides are good substrates of rat organic cation transporter 1 (Oct1; Slc22a1) and, using Oct1(-/-) mice, that mouse Oct1 is responsible for the hepatic uptake of a biguanide, metformin. In the present study, we investigated whether the liver is the key organ for the lactic acidosis. When mice were given metformin, the blood lactate concentration significantly increased in the wild-type mice, whereas only a slight increase was observed in Oct1(-/-) mice. The plasma concentration of metformin exhibited similar time profiles between the wild-type and Oct1(-/-) mice, suggesting that the liver is the key organ responsible for the lactic acidosis. Furthermore, the extent of the increase in blood lactate caused by three different biguanides (metformin, buformin, and phenformin) was compared with the abilities to reduce oxygen consumption in isolated rat hepatocytes. When rats were given each of these biguanides, the lactate concentration increased significantly. This effect was dose-dependent, and the EC(50) values of metformin, buformin, and phenformin were 734, 119, and 4.97 microM, respectively. All of these biguanides reduced the oxygen consumption by isolated rat hepatocytes in a concentration-dependent manner. When the concentration required to reduce the oxygen consumption to 75% of the control value (from 0.40 to 0.29 micromol/min/mg protein) was compared with the EC(50) value obtained in vivo, a clear correlation was observed among the three biguanides, suggesting that oxygen consumption in isolated rat hepatocytes can be used as an index of the incidence of lactic acidosis.

Acidosis, Lactic↗
PubMed2005

Hyperchloraemic metabolic acidosis following open cardiac surgery.

AIMS: To describe acid-base derangements in children following open cardiac surgery on cardiopulmonary bypass (CPB), using the Fencl-Stewart strong ion approach. METHODS: Prospective observational study set in the paediatric intensive care unit (PICU) of a university children's hospital. Arterial blood gas parameters, serum electrolytes, strong ion difference, strong ion gap (SIG), and partitioned base excess (BE) were measured and calculated on admission to PICU. RESULTS: A total of 97 children, median age 57 months (range 0.03-166), median weight 14 kg (range 2.1-50), were studied. Median CPB time was 80 minutes (range 17-232). Predicted mortality was 2% and there was a single non-survivor. These children showed mild metabolic acidosis (median standard bicarbonate 20.1 mmol/l, BE -5.1 mEq/l) characterised by hyperchloraemia (median corrected Cl 113 mmol/l), and hypoalbuminaemia (median albumin 30 g/l), but no significant excess unmeasured anions or cations (median SIG 0.7 mEq/l). The major determinants of the net BE were the chloride and albumin components (chloride effect -4.8 mEq/l, albumin effect +3.4 mEq/l). Metabolic acidosis occurred in 72 children (74%) but was not associated with increased morbidity. Hyperchloraemia was a causative factor in 53 children (74%) with metabolic acidosis. Three (4%) hyperchloraemic children required adrenaline for inotropic support, compared to eight children (28%) without hyperchloraemia. Hypoalbuminaemia was associated with longer duration of inotropic support and PICU stay. CONCLUSIONS: In these children with low mortality following open cardiac surgery, hypoalbuminaemia and hyperchloraemia were the predominant acid-base abnormalities. Hyperchloraemia was associated with reduced requirement for adrenaline therapy. It is suggested that hyperchloraemic metabolic acidosis is a benign phenomenon that should not prompt escalation of haemodynamic support. By contrast, hypoalbuminaemia, an alkalinising force, was associated with prolonged requirement for intensive care.

Acidosis↗
PubMed2004

Is lactic acidosis a cause of exercise induced hyperventilation at the respiratory compensation point?

OBJECTIVES: The respiratory compensation point (RCP) marks the onset of hyperventilation ("respiratory compensation") during incremental exercise. Its physiological meaning has not yet been definitely determined, but the most common explanation is a failure of the body's buffering mechanisms which leads to metabolic (lactic) acidosis. It was intended to test this experimentally. METHODS: During a first ramp-like exercise test on a cycle ergometer, RCP (range: 2.51-3.73 l x min(-1) oxygen uptake) was determined from gas exchange measurements in five healthy subjects (age 26-42; body mass index (BMI) 20.7-23.9 kg x m(-2); Vo(2peak) 51.3-62.1 ml x min(-1) x kg(-1)). On the basis of simultaneous determinations of blood pH and base excess, the necessary amount of bicarbonate to completely buffer the metabolic acidosis was calculated. This quantity was administered intravenously in small doses during a second, otherwise identical, exercise test. RESULTS: In each subject sufficient compensation for the acidosis, that is, a pH value constantly above 7.37, was attained during the second test. A delay but no disappearance of the hyperventilation was present in all participants when compared with the first test. RCP occurred on average at a significantly (p = 0.043) higher oxygen uptake (+0.15 l x min(-1)) compared with the first test. CONCLUSIONS: For the first time it was directly demonstrated that exercise induced lactic acidosis is causally involved in the hyperventilation which starts at RCP. However, it does not represent the only additional stimulus of ventilation during intense exercise. Muscle afferents and other sensory inputs from exercising muscles are alternative triggering mechanisms.

Acidosis, Lactic↗
PubMed1970

Hyperglobulinaemic renal tubular acidosis: a report of nine cases.

Of nine women with hyperglobulinaemic renal tubular acidosis four presented with acidosis and five had the "incomplete" form of the disorder. Seven patients had nephrogenic diabetes insipidus, but none had the Fanconi syndrome. Investigation showed abnormal immunoglobulins and autoantibodies in all nine patients. Diseases coexisting with renal tubular acidosis were Sjögren's syndrome, hyperglobulinaemic purpura, autoimmune liver and thyroid disease, diffuse pulmonary fibrosis, and a peripheral neuropathy. It is suggested that this type of renal tubular acidosis might be due to an autoimmune process.

Acidosis, Renal Tubular↗
PubMed1984

Oral rehydration therapy: efficacy of sodium citrate equals to sodium bicarbonate for correction of acidosis in diarrhoea.

Forty patients with moderate degrees of dehydration and acidosis because of acute watery diarrhoea were successfully treated randomly with either WHO recommended oral rehydration solution containing 2.5 g sodium bicarbonate or an oral solution containing 2.94 g sodium citrate in place of sodium bicarbonate per litre of oral rehydration rehydration solution. Efficacies were compared by measuring oral fluid intake, stool and vomitus output, change in body weight, hydration status, and rate of correction of acidosis during a period of 48 hours. Seventy five per cent (21 cases) in the citrate group and 83% (19 cases) in the bicarbonate group were successfully rehydrated (p greater than 0.05). There were no significant differences in intake, output, gain in body weight, fall in haematocrit and plasma specific gravity, and correction of acidosis between the two groups of patients within 48 hours after initiation of therapy. The solution with sodium citrate base was as effective as WHO-oral rehydration solution for management of diarrhoea. This study shows the efficacy, safety, and acceptability of citrate containing oral rehydration solution for rehydration and correction of acidosis in diarrhoea.

Acidosis↗
PubMed2004

Statin precipitated lactic acidosis?

An 82 year old woman was admitted with worsening dyspnoea. Arterial blood gases were taken on air and revealed a pH of 7.39, with a partial pressure of CO2 (pCO2) of 1.2 kPa, pO2 of 19.3 kPa, HCO3 of 13.8 mmol/litre, and base excess of -16.3 mmol/litre: a compensated metabolic acidosis with hyperventilation induced hypocapnia, which is known to be a feature of lactic acidosis. There was also an increased anion gap ((Na140 + K4.0) - (Cl 106 + HCO3 13.8) = 24.2 mEq/litre (reference range, 7-16)), consistent with unmeasured cation. Lactate was measured and found to be raised at 3.33 mmol/litre (reference range, 0.9-1.7). After exclusion of common causes of lactic acidosis Atorvastatin was stopped and her acid-base balance returned to normal. Subsequently, thiamine was also shown to be deficient. The acidosis was thought to have been the result of a mitochondrial defect caused by a deficiency of two cofactors, namely: ubiquinone (as a result of inhibition by statin) and thiamine (as a result of dietary deficiency).

Acidosis, Lactic↗
PubMed1982

Acidosis and severe megaloblastic anaemia.

Ten patients with severe megaloblastic anaemia were studied to investigate whether the causative metabolic defects might predispose them to lactic or other acidosis. One patient had compensated acidosis with hyperlactataemia before treatment but there were obvious causes other than anaemia. No other patient developed an acidosis. Neither anaemia per se nor the metabolic defects of vitamin B(12) or folic acid deficiency are likely to cause clinically significant lactic acidosis or hyperlactataemia.

Acidosis↗
PubMed2003

Role of the Na+-H+ exchanger (NHE1) in heart muscle function during transient acidosis. A study in papillary muscles from rat and guinea pig hearts.

The sodium-hydrogen exchanger (NHE) helps the cell to recover from intracellular acidosis. In this study, we have investigated the effect of HOE 642 (a specific NHE1 blocker) on papillary muscles from rats and guinea pigs during transient acidosis and PKC activation by recording developed force (DF), action potential characteristics, and electrical conductance (stimulus-response interval). Two protocols were used, with or without HOE 642 (10(-5) mol/L): papillary muscle was exposed (i) for 15 min to a glucose-free, nonoxygenated HEPES buffer containing lactate (20 mmol/L) (pH 6.8) followed by 15 min recovery or (ii) to a PKC activator (phorbolmyristate acetate (PMA) (10(-9) mol/L)) for 30 min. The DF after acidification remained significantly decreased in the NHE-blocked papillary muscles. During recovery from acidosis, papillary muscles exposed to HOE 642 remained at a higher electrical resistance. The present study shows that post-acidotic continued depression of DF and change in tissue electrophysiological properties might occur as a result of blocking the NHE. During infarct development, the tissue-protecting effect of NHE blockade has been well documented. When acidosis or reduced contractile function is present, however, blocking NHE by HOE 642 might not improve the situation.

Acidosis↗
PubMed1985

In vitro effects of hypoxia and (or) hypercapnic acidosis on the myocardial uptake of digoxin.

A recent study has shown in the conscious dog that hypoxia associated with respiratory acidosis could increase the in vivo distribution of digoxin in the myocardium. The aim of the present study was to evaluate in vitro the effects of hypoxia and (or) hypercapnic acidosis on the digoxin uptake. For this purpose, rat myocardium was incubated for 180 min with radiolabelled [3H]digoxin. The uptake of digoxin which was expressed in nanograms of digoxin bound per 100 mg of myocardium was decreased by hypoxia and increased by hypercapnic acidosis. The association of hypoxia and hypercapnic acidosis had no effect on the digoxin uptake, suggesting that in vitro hypoxia acts in an opposite way to hypercapnia.

Acidosis↗
PubMed1994

Intracellular pH recovery during respiratory acidosis in perfused hearts.

Na(+)-H+ exchange and Na(+)-dependent HCO3- influx both contribute to recovery of intracellular pH (pHi) after an acidosis induced by using the NH4Cl prepulse technique in mammalian and avian cardiac tissue. We have investigated the relative contributions of these mechanisms to pHi recovery during respiratory acidosis in the Langendorff-perfused ferret heart with and without correction of extracellular pH (pHo). pHi was measured from the chemical shift of the exogenous 31P nuclear magnetic resonance pH indicator 2-deoxy-D-glucose 6-phosphate. Intrinsic intracellular buffering capacity, calculated from the change in intracellular HCO3- concentration after a change in CO2, was reduced from approximately 33 (no inhibitors of acid extrusion present) to 19 +/- 5 mM when H+ extrusion during the acid loading phase was inhibited. During respiratory acidosis (pHo approximately 6.95), the proton efflux rate (JH) calculated at pHi 6.85 was 0.30 +/- 0.04 mmol.l-1.min-1 (n = 9). When pHo was corrected by increasing external HCO3- concentration to 60 mM during respiratory acidosis (pHo approximately 7.33), JH was 1.11 +/- 0.11 mmol.l-1.min-1 (n = 7), and when pHo was partially corrected by the addition of 50 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid to the perfusion solution (pHo approximately 7.1), JH was 0.64 +/- 0.08 mmol.l-1.min-1 (n = 6). In all three groups Na(+)-H+ exchange and HCO3- influx each contributed approximately 50% to acid-equivalent efflux.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1995

Additive effects of acidosis and parathyroid hormone on mouse osteoblastic and osteoclastic function.

Patients with end-stage renal disease are acidotic and often develop secondary hyperparathyroidism. Whether acidosis contributes to the bone disease observed in these patients is not clear. To determine whether acidosis and parathyroid hormone (PTH) have additive effects on net calcium efflux (JCa+) from bone and on bone cell function, we measured JCa+, osteoblastic collagen synthesis, and osteoclastic beta-glucuronidase release from neonatal mouse calvariae cultured in control (Ctl, pH approximately 7.4) or acidified (Met, pH approximately 7.1) medium with or without a submaximal concentration of PTH (10(-10) M) for 48 h. Compared with Ctl, from 24 to 48 h JCa+ was increased with Met and with PTH, and the combination of Met + PTH increased JCa+ further. Compared with Ctl, collagen synthesis was decreased with Met and with PTH and decreased further with Met + PTH. There was an inverse correlation between percent collagen synthesis and JCa+. Compared with Ctl, beta-glucuronidase release into the medium was increased with Met and with PTH and increased further with Met + PTH. There was a direct correlation between medium beta-glucuronidase activity and JCa+. Osteoclastic beta-glucuronidase activity correlated inversely with osteoblastic collagen synthesis. During cultures to 96 h, there continued to be greater JCa+ from calvariae incubated with Met + PTH than from those with either treatment alone. Thus acidosis and PTH independently stimulated JCa+ from bone, inhibited osteoblastic collagen synthesis, and stimulated osteoclastic beta-glucuronidase secretion, whereas the combination had a greater effect on each of these parameters than either treatment alone. These findings indicate that acidosis and PTH can have an additive effect on bone cell function and suggest that uremic osteodystrophy may result from a combination of a low pH and an elevated PTH.

Acidosis↗
PubMed1980

Mithcondrial glutamine permeability and renal ammonia production in metabolic acidosis.

These experiments were undertaken to determine the correspondence between acidosis-induced in situ motochondrial glutamine uptake and the process by which glutamine moves across the mitochondrial membrane. Feeding rats 1.5% NH4Cl for 2 wk accelerated the in situ uptake rate from 0.12 +/- 0.08 to 1.89 +/- 0.28 mu mol/min or some 16-fold. To determine glutamine uptake independent of its metabolic conversion, D-glutamine was employed. In isolated mitochondria from non-acidotic rat kidneys, D-glutamine diffused into 71 +/- 10% of the mitochondria water volume; in acidotic mitochondria the diffusion volume increased to 127 +/- 16%. The reflection coefficients (sigma) for a series of amides, including glutamine, were determined by gravimetrically following volume decrements in increasing concentrations of solute; D-glutamine's sigma fell from 1.05 +/- 0.08 to 0.50 +/- 0.06 in acidotic rat kidney mitchondria, The permeability coefficients corresponding to the measured sigma were 10(-7) cm/s and 10(-5) cm/s in nonacidosis and acidosis, respectively. When viewed in situ proximal tubule mitochondria undergo dramatic alterations during chronic acidosis. These involved an enlargement in the mitochondria particularly in the basal region of the cell and a reduction in number. Furthermore, numerous autophagic vacuoles, containing mitochondria, appear in the basal region. The findings are consistent availability that becomes activated during acidosis as a consequence of mitochondrial glutamine permeability resulting in increased ammoniagenesis and accelerated organelle turnover.

Acidosis↗
PubMed1992

Ammonium chloride-induced acidosis increases protein breakdown and amino acid oxidation in humans.

The effect of acidosis on whole body protein turnover was determined from the kinetics of infused L-[1-13C]leucine. Seven healthy subjects were studied before (basal) and after (acid) the induction of acidosis with 5 days oral ammonium chloride (basal pH 7.42 +/- 0.01, acid pH 7.35 +/- 0.03). Bicarbonate recovery, measured from the kinetics of infused NaH13CO3, was increased in the acidotic state (basal 72.9 +/- 1.2 vs. acid 77.6 +/- 1.6%; P = 0.06). Leucine appearance from body protein (PD), leucine disappearance into body protein (PS), and leucine oxidation (O) increased significantly (PD: basal 120.5 +/- 5.6 vs. acid 153.9 +/- 6.2, P < 0.01; PS: basal 98.8 +/- 5.6 vs. acid 127.0 +/- 4.7, P < 0.01; O: basal 21.6 +/- 1.1 vs. acid 26.9 +/- 2.3 mumol.kg-1.h-1, P < 0.01). Plasma levels of the amino acids threonine, serine, asparagine, citrulline, valine, leucine, ornithine, lysine, histidine, arginine, and hydroxyproline increased significantly with the induction of acidosis. These results confirm that acidosis in humans is a catabolic factor stimulating protein degradation and amino acid oxidation.

Acidosis↗
PubMed2006

Isoflurane-induced acidosis depresses basal and PGE(2)-stimulated duodenal bicarbonate secretion in mice.

When running in vivo experiments, it is imperative to keep arterial blood pressure and acid-base parameters within the normal physiological range. The aim of this investigation was to explore the consequences of anesthesia-induced acidosis on basal and PGE(2)-stimulated duodenal bicarbonate secretion. Mice (strain C57bl/6J) were kept anesthetized by a spontaneous inhalation of isoflurane. Mean arterial blood pressure (MAP), arterial acid-base balance, and duodenal mucosal bicarbonate secretion (DMBS) were studied. Two intra-arterial fluid support strategies were used: a standard Ringer solution and an isotonic Na(2)CO(3) solution. Duodenal single perfusion was used, and DMBS was assessed by back titration of the effluent. PGE(2) was used to stimulate DMBS. In Ringer solution-infused mice, isoflurane-induced acidosis became worse with time. The blood pH was 7.15-7.21 and the base excess was about -8 mM at the end of experiments. The continuous infusion of Na(2)CO(3) solution completely compensated for the acidosis. The blood pH was 7.36-7.37 and base excess was about 1 mM at the end of the experiment. Basal and PGE(2)-stimulated DMBS were markedly greater in animals treated with Na(2)CO(3) solution than in those treated with Ringer solution. MAP was slightly higher after Na(2)CO(3) solution infusion than after Ringer solution infusion. We concluded that isoflurane-induced acidosis markedly depresses basal and PGE(2)-stimulated DMBS as well as the responsiveness to PGE(2), effects prevented by a continuous infusion of Na(2)CO(3). When performing in vivo experiments in isoflurane-anesthetized mice, it is recommended to supplement with a Na(2)CO(3) infusion to maintain a normal acid-base balance.

Acid-Base Equilibrium↗