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[Incidence of stomach ruptures after ingestion of sodium bicarbonate-containing or carbonated beverages].

SUBJECT: Spontaneous rupture of the stomach is an uncommon condition with a usually poor prognosis. The questions of pathophysiologic factors and the possible role of carbonated or bicarbonate-containing beverages were addressed. METHODS AND RESULTS: A review of the literature based on a search of MEDLINE (1966-1998) was performed. Using the key word 'stomach rupture', we found 675 publications. 279 publications dealt with etiologic factors 15 of which mentioned the ingestion of bicarbonate preparations. No record of carbonated or bicarbonate-containing beverages as a single etiologic factor could be found. CONCLUSION: These beverages do not seem to play a significant role in the pathogenesis of stomach rupture, whereas in rare cases bicarbonate preparations can cause rupture of the previously overdistended stomach.

Carbonated Beverages↗

Does bicarbonate transfer have relevant hemodynamic consequences in standard hemodialysis?

BACKGROUND: In a previous study we demonstrated that mild metabolic alkalosis resulting from standard bicarbonate hemodialysis induces hypotension. This study aimed to compare hemodynamic consequences of either a decrease in the dialysate bicarbonate from 32 to 26 mmol/l or an increase in the dialysate calcium of 0.25 mmol/l and to verify whether the calcium shift secondary to alkalemia explains the consequences on blood pressure. METHODS: In this randomized controlled trial with a single-blind, cross-over design, we used dialysis liquids with two different bicarbonate (32 mmol/l in modalities A and C, and 26 mmol/l in modality B) and calcium (1.25 mmol/l in modalities A and B, and 1.50 mmol/l in modality C) concentrations, and in 27 patients, 243 dialysis sessions, compared blood pressure, heart rate and the incidence of hypotension. RESULTS: No significant differences were seen between A and B while an increase in systolic and diastolic blood pressures and a decrease in the incidence of hypotension (10.5 vs. 1.2%, p < 0.05) were documented in C. The subgroup of patients who with A showed a lower mean systolic blood pressure received more angiotensin-converting enzyme inhibitors or angiotensin II type-1 receptor blockers (36 vs. 0%, p<0.05) and in C showed a less important increase in systolic and diastolic pressures, but the incidence of hypotensive episodes between A and B was not significantly different (9.1 vs. 15.1%). CONCLUSIONS: In the present study it was not possible to demonstrate hemo dynamic instability associated with mild metabolic alkalosis. Even in the subgroup showing a lower blood pressure with a higher dialysate bicarbonate, significant hemodynamic or clinical consequences were not noticed. The calcium shift (0.05 mmol/l) related to alkalemia would justify a mean decrease in systolic blood pressure of only about 1 mm Hg.

Aged↗

Bicarbonate secretion in the guinea pig duodenum: functional characterization of peptide hormone receptors in duodenal enterocytes.

To get information about the peptide hormone receptors involved in duodenal bicarbonate secretion (DBS) and their cellular location, we determined DBS and adenylate cyclase (AC) activity in response to hormones of the vasoactive intestinal polypeptide (VIP)/secretin family of peptides. DBS was determined in an isolated, perfused (24 mmol/1 NaHCO3) loop of the proximal duodenum in urethane- and indometacin-treated guinea pigs. AC stimulation was measured in isolated, homogenized duodenal enterocytes, the histological evaluation of which revealed their villous origin. VIP (10(-9) to 10(-7) mol x kg-1) dose-dependently increased DBS 3.5-fold (p < 0.01); this effect was completely inhibited by the VIP antagonist [D-p-Cl-Phe6,Leu17]VIP (10(-6) mol x kg-1). Glucagon (10(-8) to 10(-6) mol x kg-1) increased DBS 2.1-fold, while secretin (10(-9) to 10(-6) mol x kg-1) had no effect on DBS, but stimulated pancreatic bicarbonate secretion. VIP concentration-dependently increased AC activity 5.6-fold with an EC50 of 1.3 x 10(-9) mol/l. [D-p-Cl-Phe6,Leu17]VIP caused a rightward shift of the VIP concentration-response curve. A Schild plot analysis yielded a slope of 0.85 +/- 0.11, indicating competitive inhibition. While secretin also stimulated AC activity, although 1,000-fold less potent than VIP, glucagon was ineffective. These data indicate that specific VIP receptors, which mediate VIP-stimulated bicarbonate secretion, are present on villous enterocytes. Stimulation of AC by secretin seems to be of pharmacological relevance only and is consistent with the lack of effect of this hormone on DBS. Glucagon likely activates a second transmitter of bicarbonate secretion, or works independently of AC.

Adenylyl Cyclases↗

Comparison between acetate and bicarbonate dialysis for the treatment of lithium intoxication.

Lithium is used to treat manic-depressive disorders, but toxic side effects commonly occur. The preferred treatment of severe lithium intoxication is hemodialysis. No data, however, exist comparing the effectiveness of acetate to bicarbonate dialysis for the removal of lithium. We present a case of lithium intoxication treated with both. During acetate dialysis, lithium removal occurred exclusively from the extracellular fluid space, while during bicarbonate dialysis, lithium removal occurred equally from both the extracellular and intracellular fluid spaces. We hypothesize that acetate but not bicarbonate activates the sodium-hydrogen antiporter on cell membranes, and that lithium, substituting for sodium, is driven into cells. This may explain the rebound in lithium levels commonly noted after conventional dialysis. We recommend bicarbonate hemodialysis as the therapy of choice for severe lithium intoxication.

Acetates↗

Glomerular-tubular balance for bicarbonate in man.

We recently showed in dogs that there is a close relationship between bicarbonate reabsorption and glomerular filtration rate (GFR). The present studies were designed to confirm these findings in five normal men. Bicarbonate titrations were done after ingesting a low protein diet for one week and were repeated following elevation of GFR 11-29 per cent by high protein diet and dexamethazone ingestion. In every casetubular reabsorption of bicarbonate increased in proportion to the increases in GFR. We conclude that glomerular-tubular balance for bicarbonate reabsorption is a characteristic of human, as well as canine kidneys.

Absorption↗

Effect of bicarbonate or base precursor on water and solute absorption from a glucose-electrolyte solution in the human jejunum.

A modified perfusion technique was used to examine the effect on water and solute absorption in the healthy human jejunum of replacing bicarbonate (18 mmol/l) by equivalent amounts of different base precursors in a glucose-electrolyte solution. Acetate, citrate and lactate were absorbed from the perfusion solutions. Absorption of these base precursors appeared to have no effect on water uptake, but greater sodium (p less than 0.05) absorption occurred from solutions containing either acetate or lactate compared with the bicarbonate-containing solution. These data suggest that oral rehydration solutions with base precursors other than bicarbonate are as effective as bicarbonate-containing solutions in promoting absorption of water and electrolytes.

Acetates↗

The influence of the carbonic anhydrase inhibitor, benzolamide (CL-11,366), on the reabsorption of chloride, sodium, and bicarbonate in the proximal tubule of the rat.

Benzolamide (CL-11,366), a potent carbonic anhydrase inhibitor, was used to examine the influence of carbonic anhydrase inhibition on the reabsorption of chloride, sodium, and bicarbonate in the rat proximal convoluted tubule. Administration of 2 mg/kg benzolamide was associated with a decrease in the tubular fluid/plasma (TF/P) chloride ratio from 1.19+/-0.10 (SEM) to 1.06+/-0.01, and an increase in the TF/P bicarbonate ratio from 0.181+/-0.02 to 0.584+/-0.02. This dose of benzolamide significantly reduced proximal fractional reabsorption of chloride by 29.14%, of sodium by 34.3%, and of bicarbonate by 35.64%. These results indicate that benzolamide administration inhibits the reabsorption of all three electrolytes in the proximal convoluted tubule. Although 20 mg/kg benzolamide accentuated the changes in fractional reabsorption, the differences between 2 and 20 mg/kg were not statistically significant. Inhibition of proximal tubular cytoplasmic and luminal carbonic anhydrase could well explain the diminished bicarbonate reabsorption and a fraction of the diminished sodium reabsorption noted in these studies. The fall in chloride reabsorption, and a portion of the fall in sodium reabsorption, however, may be a direct or indirect consequence of carbonic anhydrase inhibition or of an influence of benzolamide on a transport mechanism not dependent upon carbonic anhydrase.

Animals↗

Sodium, phosphate, glucose, bicarbonate, and alanine interactions in the isolated proximal convoluted tubule of the rabbit kidney.

Interactions among the transport systems involved with sodium, bicarbonate, glucose, phosphate, and alanine absorption in isolated segments of the rabbit proximal convoluted tubule were examined with radioisotopic techniques to measure glucose, phosphate, and fluid absorption rates. The composition of the perfusate and bath varied from normal, physiological fluids to fluids deficient in a single solute. The deletion of glucose from the perfusate increased the lumen-to-bath flux of phosphate from 5.51 +/- 1.15 to 8.32 +/- 1.34 pmol/mm-min (P less than 0.01). Similar changes occurred when glucose transport was inhibited by phlorizin 10 micron in the perfusate, The deletion of alanine from the perfusate increased the lumen-to-bath flux of phosphate from 6.55 +/- 1.08 to 9.00 +/- 1.30 pmol/mm-min (P less than 0.01) but did not affect glucose transport significantly, 80.1 +/- 10.1 vs. 72.5 +/- 5.4 pmol/mm-min. Replacement of intraluminal sodium with choline, elimination of potassium from the bath, and removal of bicarbonate from the lumen and bath each reduced glucose, phosphate, and fluid absorption. These data indicate that the proximal absorptive processes for glucose and for phosphate include elements that are dependent upon some function of sodium transport. Additionally, the effects on phosphate transport of deleting glucose or alanine occur independent of any changes in net sodium transport and are opposite the effects of deleting bicarbonate. These differences may relate to the observations that the transport of glucose and alanine is electrogenic while that of bicarbonate is not. Regardless of possible mechanisms, the data demonstrate that important changes in the absorption rates of different solutes handled significantly by the proximal convoluted tubule may occur in response to changes in specific components of proximal sodium transport.

Alanine↗

Chronic hypercapnia stimulates proximal bicarbonate reabsorption in the rat.

The hyperbicarbonatemia of chronic respiratory acidosis might be maintained by a reduction in filtration rate or an enhancement of tubular bicarbonate reabsorption. To investigate this question, 12 Munich-Wistar rats were exposed to a 10% CO2 atmosphere for 6-8 d. Chronic respiratory acidosis developed, with arterial pH 7.30 +/- 0.01, partial pressure of CO2 (pCO2) 80 +/- 2 mmHg, and total CO2 concentration 45 +/- 1 mM. Single nephron glomerular filtration rate was normal (42 +/- 1 nl/min). Chronic hypercapnia caused absolute proximal reabsorption to be significantly stimulated (1,449 +/- 26 pmol/min) as compared with reabsorption previously observed in normal animals (1,075 +/- 74 pmol/min) or in animals subjected to acute hypercapnia (1,200 +/- 59 pmol/min). This is the first demonstration that proximal bicarbonate reabsorption can be stimulated above normal euvolemic values. When eight animals were subsequently allowed to return toward a normocapnic state (arterial pCO2 46 +/- 1 mmHg) over the course of 1-1.5 h, bicarbonate reabsorption was still significantly higher (1,211 +/- 34 pmol/min) than in similarly alkalotic, normocapnic control groups (994 +/- 45 pmol/min). In conclusion, chronic, but not acute, hypercapnia stimulates absolute proximal bicarbonate reabsorption to exceed the level found in normal euvolemic rats.

Absorption↗

An in vivo microperfusion study of distal tubule bicarbonate reabsorption in normal and ammonium chloride rats.

For many years it has been thought that distal nephron hydrogen ion secretion can be importantly modulated by factors such as sodium delivery, sodium avidity, and potassium stores. Free flow micropuncture studies have also indicated that the rate of bicarbonate delivery may also alter the rate of bicarbonate reabsorption. The present studies were undertaken to examine possible luminal influences on total CO2 reabsorption in microperfused distal tubules in the rat in vivo. Tubules from normal and acidotic rats were perfused with five solutions in a manner that induced changes in bicarbonate load, sodium and potassium fluxes (JNa, JK), and luminal sulfate concentration. in each collected perfusate, simultaneous analyses were undertaken to determine water reabsorption, Na, and K concentrations using graphite furnace atomic absorption spectroscopy and total CO2 by microcalorimetry. Using factorial analysis of covariance to account for confounding effects on total CO2 flux (JtCO2) such as water reabsorption, distal tubules of acidotic rats reabsorbed CO2 in the range of 50-112 pmol X min-1 X mm-1 X These JtCO2 values were not significantly correlated with HCO3 load, JNa, or JK despite changes in the latter from net reabsorption to net secretion. Distal tubules of rats with normal acid-base status had JtCO2 values which were neither significantly different from zero nor correlated with changes in JK and JNa. Further, doubling the load from 250-500 pmol/min (by doubling the perfusion rate of 25-mM HCO3 solutions) did not stimulate JtCO2 in these normal animals. Accordingly, these acute in vivo microperfusion studies indicate for the first time that neither load nor potassium or sodium fluxes are important modulators of distal tubule bicarbonate reabsorption.

Absorption↗

Effects of antidiuretic hormone on urinary acidification and on tubular handling of bicarbonate in the rat.

Paired micropuncture experiments were carried out in plasma-replete volume-expanded rats to examine the acute effects of 1-desamino-8-D-arginine vasopressin (dDAVP) on urinary acidification and tubular handling of bicarbonate and chloride. No effect was detected on the fractional absorption of water, total CO2, and chloride at end-proximal and early distal sites of superficial nephrons in intact animals; dDAVP, however, inhibited the fractional absorption of total CO2 in Henle's loop while stimulating that of chloride in thyroparathyroidectomized (TPTX) somatostatin-infused rats. In the distal tubule accessible to micropuncture, net total CO2 secretion was observed during hypotonic volume expansion, which reversed to net total CO2 absorption during dDAVP infusion in intact Wistar rats. Marked stimulation of urinary acidification occurred in all animals as attested by a fall in urine pH and bicarbonate excretion. Net acid excretion almost doubled in intact rats. We conclude that (a) antidiuretic hormone (ADH) inhibits fractional bicarbonate absorption in the thick ascending limb while stimulating that of chloride at least in TPTX somatostatin-infused rats, and (b) ADH stimulates proton secretion (or inhibits bicarbonate secretion) in the distal tubule and cortical collecting ducts, which leads to enhanced urinary acidification.

Acids↗

Peripheral melatonin mediates neural stimulation of duodenal mucosal bicarbonate secretion.

Melatonin is released from intestinal enterochromaffin cells and from the pineal gland, but its role in gastrointestinal function is largely unknown. Our aim was to study the involvement of intestinal and central nervous melatonin in the neurohumoral control of the duodenal mucosa-protective bicarbonate secretion. Working in anesthetized rats, we cannulated a 12-mm segment of duodenum with an intact blood supply and titrated the local bicarbonate secretion with pH-stat. Melatonin and receptor ligands were supplied to the duodenum by close intra-arterial infusion. Even at low doses, melatonin and the full agonist 2-iodo-N-butanoyl-5-methoxytryptamine increased duodenal bicarbonate secretion. Responses were inhibited by the predominantly MT2-selective antagonist luzindole but not by prazosin, acting at MT3 receptors. Also, luzindole almost abolished the marked rise in secretion induced by intracerebroventricular infusion of the adrenoceptor agonist phenylephrine. This response was also abolished by sublaryngeal ligation of all nerves around the carotid arteries. However, it was insensitive to truncal vagotomy alone or sympathectomy alone and was unaffected by removal of either the pineal gland or pituitary gland. Thus, melatonin stimulates duodenal bicarbonate secretion via action at enterocyte MT2-receptors and mediates neural stimulation of the secretion.

Adrenocorticotropic Hormone↗

The prevention of pain from injection of rocuronium by magnesium sulphate, lignocaine, sodium bicarbonate and alfentanil.

We compared the efficacy of magnesium sulphate, lignocaine, sodium bicarbonate or alfentanil in minimizing pain due to injection of rocuronium in 250 patients. After tourniquet application on the forearm, the patients were given saline, magnesium sulphate, lignocaine, sodium bicarbonate 8.4% or alfentanil, diluted into a 3 ml solution. The occlusion was released after 20 seconds, and rocuronium was injected over 10 to 15 seconds. The patients were observed and asked immediately if they had pain in the arm and the response was assessed. Reactions such as discomfort and pain, withdrawal of the hand and screaming after the administering of the rocuronium were recorded as side-effects and patients were reassessed at 24 hours postoperatively. We concluded that magnesium sulphate, lignocaine, sodium bicarbonate or alfentanil decreased the level of rocuronium injection pain. Of these drugs, magnesium sulphate, lignocaine and sodium bicarbonate were the most effective while alfentanil was the least effective.

Adult↗

Effects of acetate or bicarbonate dialysis solutions on serum HDL and HDL subfractions of patients undergoing haemodialysis.

The aim of this study was to compare the effect of acetate- and bicarbonate-containing dialysis solutions (buffers) on serum lipid (triglyceride and total cholesterol) and lipoprotein (LDL, HDL and its subfractions as HDL2 and HDL3', Apolipoprotein A1 and Apolipoprotein B) values in patients undergoing haemodialysis. Lipid concentrations in 16 patients on bicarbonate and in 18 patients on acetate haemodialysis were investigated initially and after four weeks of dialysis treatment. Over four weeks of treatment both acetate and bicarbonate dialysis treatments had no negative effects on either HDL or HDL subfractions, and these buffering systems were indistinguishable from each other. We confirm that HDL is the major factor that is changed in the lipid profile in haemodialysis patients undergoing acetate or bicarbonate dialysis and suggest that the relation between LDL and HDL subfractions may be useful for monitoring the lipid changes in haemodialysis patients at risk of atherogenesis.

Acetates↗

Persistent and transient distal renal tubular acidosis with bicarbonate wasting.

Bicarbonate titration studies were performed on two patients with bicarbonate wasting distal renal tubular acidosis (RTA; patients 1 and 2) and on three patients (3,4, and 5) with classic distal RTA. Daily requirements of alkali were 4.5 mEq/kg body wt in patient 1, a 3-year-old boy, and 16 mEq/kg in patient 2, a 5-month-old male infant. In contrast, only 1.5-2 mEq/kg/24 hr alkali were required in the three patients with classic distal RTA (age 8 1/2- 22 years). Patient 1 had glucose-6-phosphate dehydrogenase deficiency and patient 3 had inner ear deafness as an associated anomaly. In patient 2, the acidification defect was transient. Mean fractional excretion of bicarbonate (ChCO3-/Cin) times 100 at a plasma concentration of HCO3 below 20 mmol/liter was 5.1% in patient 1, 11.6% in patient 2, and 1.7% in patients 3-5. Minimal urine pH during the study was 7.38 in patient 1, 7.66 in patient 2, and 6.78-6.97 in the other patients. Values of net acid excretion at plasma HCO3 = 16 mmol/liter were strongly negative in patients 1 and 2 (-75 and -195 mumol/100 ml glomerular filtrate (GF), respectively) but slightly positive in the three patients with classic RTA (+3 to +20 mumol/100 ml GF). The two patients with bicarbonate wasting distal RTA were thus clearly separated from the group of patients with classic distal RTA.

Acidosis, Renal Tubular↗

Bicarbonate reduces serum prolactin increase induced by exercise to exhaustion.

PURPOSE: The aim of the study was to examine the effect of acid-base status on serum prolactin (PRL) concentration postexercise. METHODS: Seven male recreational athletes participated in two experimental trials separated by 1 wk. In the respective trial, subjects received either a placebo infusion (normal isotonic saline) or an alkali infusion (isotonic sodium bicarbonate) before and during exercise. Venous and capillary blood samples were drawn at rest, immediately after a 10-min warm-up period, and after a maximal ramp test on a cycle ergometer, as well as at 3, 6, 10, and 15 min postexercise. RESULTS: Power output, HR, capillary blood lactate concentration, carbon dioxide pressure (PCO2), and partial oxygen pressure (PO2) did not differ between trials at any point in time. Capillary PO2 did not change from resting values, but a significant increase (P < 0.05) was found from the end of warm-up to 3 min of the recovery period. Exercise induced a significant (P < 0.01) decrease in capillary blood bicarbonate concentration (HCO3-), pH, base excess (BE), and PCO2 at exhaustion and during the recovery period. Significantly higher HCO3-, pH, and BE were found during bicarbonate infusion and postexercise in comparison with the placebo trial. Serum PRL concentration was significantly increased 3 min postexercise until the end of the placebo trial, whereas after bicarbonate infusion, serum PRL concentration did not change from values at rest. Significant (P < 0.01) differences between trials in serum PRL concentration were found 10 and 15 min postexercise. CONCLUSIONS: The present study suggests that acidosis is a stimulus for exercise-induced PRL secretion.

Acid-Base Equilibrium↗

Impact of topiramate on serum bicarbonate concentrations in adults.

BACKGROUND: Topiramate is an antiepileptic medication with multiple pharmacologic effects, including inhibition of carbonic anhydrase activity. It is associated with metabolic acidosis in both children and adults. OBJECTIVE: To evaluate the incidence and magnitude of the effect of topiramate on serum bicarbonate concentrations in an adult population. METHODS: This was a retrospective cohort study. Data were evaluated to assess the relationship between serum bicarbonate concentrations before and during topiramate therapy. RESULTS: Fifty-four patients (40 females) with a mean age of 47.6 years (range 19-89) were included in the study. Mean +/- SD serum bicarbonate concentrations before and during topiramate therapy were 26.8 +/- 2.9 mEq/L (range 21-36) and 21.7 +/- 3.6 mEq/L (range 13-29), respectively, with a mean difference of 5.1 (95% CI 3.7 to 6.5; p < 0.001). Twenty-six patients (48%) had low serum bicarbonate concentrations while on topiramate, with a mean concentration of 18.8 mEq/L (range 13-21). CONCLUSIONS: Topiramate was associated with metabolic acidosis in 48% of the patients studied, which did not result in clinically significant problems.

Acidosis↗

Physicochemical effects of bicarbonate-buffered solution versus compound sodium lactate during major abdominal surgery: A randomized, open-label, non-inferiority trial.

INTRODUCTION: Bicarbonate-buffered crystalloids avoid exogenous lactate and have physicochemical properties distinct from compound sodium lactate (CSL), but direct comparative evidence during major abdominal surgery remains limited. METHODS: This single-center, open-label, randomized non-inferiority trial enrolled high-risk adults undergoing elective major abdominal surgery. Participants received bicarbonate-buffered solution or CSL as the allocated intraoperative crystalloid. The primary estimand was the arithmetic mean difference in standard base excess (SBE) at skin closure (bicarbonate-buffered solution minus CSL). The non-inferiority margin was -1.5 mEq/L. The trial was prospectively registered with the Australian New Zealand Clinical Trials Registry (ACTRN12619001228178). RESULTS: Fifty participants were randomized (25 per group) and received their allocated intervention. End-of-surgery arterial blood gas data were missing for two CSL participants. In the intention-to-treat analysis using multiple imputation, the estimated mean difference in end-of-surgery SBE was -0.42 mEq/L (95% confidence interval [CI], -1.92 to 1.09 mEq/L). The complete-case per-protocol estimate was -0.48 mEq/L (95% CI, -2.02 to 1.06 mEq/L). In both analyses, the lower CI bound was below the prespecified non-inferiority margin; non-inferiority was not established. Secondary outcomes were exploratory; observed end-of-surgery lactate was lower with bicarbonate-buffered solution (median 0.9 vs 1.2 mmol/L; unadjusted P&#x2009;=&#x2009;0.031), without a corresponding difference in SBE or pH. CONCLUSIONS: In this small trial of hemodynamically stable adults undergoing elective major abdominal surgery, the primary non-inferiority result was inconclusive. The data did not establish interchangeability, equivalence, superiority, or inferiority of the two fluids. As the trial was powered for a physiologic endpoint, no comparative inference can be made about organ dysfunction, postoperative complications, recovery, or mortality. Larger trials with standardized co-interventions and patient-important outcomes are required before routine substitution for CSL can be recommended.

Humans↗