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Contrasting alterations in pulmonary gas exchange during acetate and bicarbonate hemodialysis.

We studied 10 patients during acetate and 10 patients during bicarbonate hemodialysis to assess changes of minute ventilation; oxygen consumption (VO2); and carbon dioxide production (VCO2) as well as pO2, pCO2 and pH. We also measured the extent of pulmonic shunting by administering 100% O2. Our studies revealed that VO2 increased significantly during acetate dialysis, while it decreased slightly during bicarbonate dialysis. Since VCO2 decreased with both baths, the respiratory exchange ratio (R) decreased during acetate dialysis but did not change during bicarbonate dialysis. By the alveolar gas equation, these changes in R could account for a difference in alveolar pO2 and consequently arterial pO2. The fact that pO2 fell during bicarbonate dialysis may relate to decreased minute ventilation paralleling decreases in VCO2. The degree of intrapulmonic shunting was not altered during dialysis with either bath. We conclude that hypoxemia during dialysis relates to decreases in minute ventilation and that a greater decrease during acetate dialysis is a consequence of enhanced VO2 and its effect on R. Bicarbonate dialysis does not increase VO2.

Acetates↗

Effect of luminal calcium on proximal tubule bicarbonate reabsorption in the rat.

In previous investigations, it was found that rats depleted in parathyroid hormone (TPTX rats) had reduced rates of proximal bicarbonate reabsorption independent on blood calcium levels. In the present work, the role of calcium (Ca2+) in rat proximal tubule bicarbonate reabsorption was studied by in vivo stationary microperfusion. Tubules were perfused at different lumen Ca2+ concentrations in the presence and absence of the calcium ionophore A23187. Bicarbonate reabsorption was not affected by Ca2+ in the range of 0 to 1 mM, but was significantly reduced when 0.5 mM EGTA was added to the 0 Ca2+ perfusates, indicating that only at very low luminal Ca2+ levels, bicarbonate reabsorption ( = H+ secretion) was impaired. These observations indicate that Ca2+ in the tubule lumen is important for the maintenance of normal proximal bicarbonate transport, but the low Ca2+ level necessary to impair this transport mechanism is achieved only in the presence of EGTA, a condition that simulates the absence of parathyroid hormone.

Absorption↗

Duodenal bicarbonate secretion induced by human epidermal growth factor in rats is partially mediated by prostaglandins.

In the present study, the effect of graded intravenous infusions of human epidermal growth factor (hEGF) 0.005, 0.05 and 0.25 micrograms/ml, with or without 4 mg/kg i.p. indomethacin pretreatment, on rat duodenal bicarbonate secretion was investigated. Perfused duodenal loops were prepared in rats which were given intravenous infusions of hEGF with or without indomethacin. Duodenal pH and pCO2 were measured at 5-min intervals for 45 min, and bicarbonate secretion was calculated. Compared to control, each dose of hEGF caused a significant dose/response rise of duodenal bicarbonate secretion. Prostaglandin release was abolished by indomethacin pretreatment. Indomethacin-pretreated rats had a significant reduction of bicarbonate secretion which was still higher than in controls. These results provide evidence that duodenal bicarbonate secretion induced by hEGF is only partly accounted for by a prostaglandin-dependent mechanism.

Animals↗

Effects of sodium bicarbonate dentifrices on the levels of cariogenic bacteria in human saliva.

This investigation evaluated the efficacy of two bicarbonate-containing dentifrices (one with fluoride and one without) against one placebo dentifrice (containing neither fluoride nor bicarbonate) in vivo in a panel of human volunteers to determine whether or not sodium bicarbonate would affect salivary mutans streptococci and lactobacilli. Ten caries-inactive adults were divided randomly into three groups, each of which was exposed to all three dentifrices, in a crossover manner, during three 4-week test periods. Saliva samples were taken at 1-week intervals. Samples were stored on ice, and microbiological analyses were conducted. The statistical analyses showed that, over a 4-week period, there was a statistically significant (p < 0.05) reduction in numbers of mutans streptococci with the two bicarbonate dentifrices as compared with the placebo dentifrice. Although not statistically significant, a similar trend was observed with lactobacilli. Longer-term, large-scale studies need to be conducted to investigate the possible mechanisms of action of sodium bicarbonate on these organisms and to relate the results to possible cariostatic effects in humans.

Adult↗

Placental clearance of lactate and bicarbonate in sheep.

To determine the placental clearance of lactate and bicarbonate in sheep, the fetal side of an isolated cotyledon and the umbilical circulation of the total placenta were artificially perfused. The release and uptake of lactate and bicarbonate by the perfusion fluid and the fetomaternal concentration differences of these substances were measured. From these data, the clearance of lactate and bicarbonate was determined to be 0.9 (SE = 0.2) ml/h/g of placental tissue. The production of lactate by the placenta was calculated to be about 30 mumol/min, the placental permeability of lactate was evaluated to be about 1.3 ml/h/g of placental tissue. These results indicate that fetal concentration changes of lactate and bicarbonate due to placental transfer occur with a half time of about 4 h. It is concluded that the lactate and bicarbonate permeability of the syndesmochorial placenta of the sheep is about 20 times smaller than the placental permeability of the hemochorial placenta of the guinea pig. It seems unjustified to draw any conclusions from experimental data obtained in the sheep placenta for the transplacental acid-base balance between mother and fetus in human beings.

Animals↗

Relative role of alkalosis and sodium ions in reversal of class I antiarrhythmic drug-induced sodium channel blockade by sodium bicarbonate.

BACKGROUND: Hypertonic sodium salts are used to treat sodium channel-blocking drug cardiotoxicity. The relative roles of alkalinization and increased sodium concentration ([Na+]o) for various drugs are incompletely known. METHODS AND RESULTS: The effects of four class I drugs on action potential characteristics of canine Purkinje fibers at equieffective concentrations (disopyramide 30 mumol/L, mexiletine 80 mumol/L, flecainide 7 mumol/L, imipramine 5 mumol/L) were studied in the presence of normal Tyrode solution and one altered solution (increased [Na+]o, increased bicarbonate concentration, or both) in each experiment. Combined increases in sodium and bicarbonate concentration significantly reduced the depressant effects of flecainide, imipramine, and mexiletine on phase 0 upstroke (Vmax) but did not alter the effects of disopyramide. The effects of sodium bicarbonate were entirely due to alkalinization in the case of imipramine, but both alkalinization and increased [Na+]o contributed to the interaction with flecainide and mexiletine. The reversal of Vmax depression by increased [Na+]o and pH was due in part to hyperpolarization. In addition, alkalosis directly reversed the hyperpolarizing shift in Vmax inactivation caused by flecainide and imipramine without altering the shift caused by disopyramide and mexiletine. CONCLUSIONS: Increases in sodium bicarbonate concentration reverse the effects of class I antiarrhythmic drugs to a varying extent, with drug-specific contributions of the sodium and bicarbonate moiety. The molecular basis for this drug specificity remains to be elucidated, but it has important potential implications for the use of hypertonic sodium salts to treat cardiotoxicity caused by sodium channel-blocking drugs.

Alkalosis↗

Bicarbonate does not increase left ventricular contractility during L-lactic acidemia in pigs.

Lactic acidosis decreases left ventricular contractility, but whether bicarbonate increases left ventricular contractility during lactic acidosis in vivo is controversial. Therefore, we measured hemodynamics and left ventricular mechanics before and after bicarbonate administration during L-lactic acid infusion in 15 anesthetized pigs. The pigs were beta-blocked and atrially paced to minimize indirect effects of acidosis on contractility. We measured mean arterial pressure, left ventricular end-diastolic pressure, thermodilution cardiac output, left ventricular pressure (Miller catheter), and left ventricular volume (three orthogonal pairs of ultrasonic crystals). Left ventricular contractility was assessed primarily using the slope (Emax) of the end-systolic pressure-volume relationship. While PCO2 was kept constant, 0.2 M L-lactic acid was infused, which reduced arterial pH to 7.05 +/- 0.06. Animals were then randomized to receive either 1 M NaHCO3 (n = 8), which increased pH to 7.45 +/- 0.11, or an equivalent amount of 1 M NaCl (n = 7). Bicarbonate decreased mean arterial pressure (105 +/- 20 to 95 +/- 39 mm Hg, p < 0.05) but did not increase cardiac output. These effects were not significantly different from the effects of saline. Bicarbonate did not significantly increase Emax (4.2 +/- 0.8 to 4.9 +/- 0.8 mm Hg/ml) and was indistinguishable from saline (5.0 +/- 0.7 to 5.2 +/- 0.7 mm Hg/ml). We conclude that bicarbonate infusion does not directly increase left ventricular contractility during lactic acidemia in pigs within this pH range.

Acidosis, Lactic↗

Role of the Na+/H+ antiporter in rat proximal tubule bicarbonate absorption.

Amiloride and the more potent amiloride analog, 5-(N-t-butyl) amiloride (t-butylamiloride), were used to examine the role of the Na+/H+ antiporter in bicarbonate absorption in the in vivo microperfused rat proximal convoluted tubule. Bicarbonate absorption was inhibited 29, 46, and 47% by 0.9 mM or 4.3 mM amiloride, or 1 mM t-butylamiloride, respectively. Sensitivity of the Na+/H+ antiporter to these compounds in vivo was examined using fluorescent measurements of intracellular pH with (2', 7')-bis(carboxyethyl)-(5,6)-carboxyfluorescein (BCECF). Amiloride and t-butylamiloride were shown to be as potent against the antiporter in vivo as in brush border membrane vesicles. A model of proximal tubule bicarbonate absorption was used to correct for changes in the luminal profiles for pH and inhibitor concentration, and for changes in luminal flow rate in the various series. We conclude that the majority of apical membrane proton secretion involved in transepithelial bicarbonate absorption is mediated by the Na+-dependent, amiloride-sensitive Na+H+ antiporter. However, a second mechanism of proton secretion contributes significantly to bicarbonate absorption. This mechanism is Na+-independent and amiloride-insensitive.

Absorption↗

Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis.

In the intact rat kidney, bicarbonate reabsorption in the early proximal tubule (EP) is strongly dependent on delivery. Independent of delivery, metabolic acidosis stimulates EP bicarbonate reabsorption. In this study, we investigated whether systemic pH changes induced by acute or chronic respiratory acid-base disorders also affect EP HCO3- reabsorption, independent of delivery (FLHCO3, filtered load of bicarbonate). Hypercapnia was induced in rats acutely (1-3 h) and chronically (4-5 d) by increasing inspired PCO2. Hypocapnia was induced acutely (1-3 h) by mechanical hyperventilation, and chronically (4-5 d) using hypoxemia to stimulate ventilation. When compared with normocapneic rats with similar FLHCO3, no stimulation of EP or overall proximal HCO3 reabsorption was found with either acute hypercapnia (PaCO2 = 74 mmHg, pH = 7.23) or chronic hypercapnia (PaCO2 = 84 mmHg, pH = 7.31). Acute hypocapnia (PaCO2 = 29 mmHg, pH = 7.56) did not suppress EP or overall HCO3 reabsorption. Chronic hypocapnia (PaCO2 = 26 mmHg, pH = 7.54) reduced proximal HCO3 reabsorption, but this effect was reversed when FLHCO3 was increased to levels comparable to euvolemic normocapneic rats. Thus, when delivery is accounted for, we could find no additional stimulation of proximal bicarbonate reabsorption in respiratory acidosis and, except at low delivery rates, no reduction in bicarbonate reabsorption in respiratory alkalosis.

Acidosis, Respiratory↗

Effects of osmolality on bicarbonate absorption by medullary thick ascending limb of the rat.

UNLABELLED: Previously we demonstrated that arginine vasopressin (AVP) directly inhibits bicarbonate absorption (JHCO3, pmol/min per mm) in the medullary thick ascending limb (MTAL) of the rat. To determine whether changes in osmolality also may affect bicarbonate absorption, MTAL were studied in vitro with 25 mM HCO3- solutions. Control osmolality was 290 mosmol/kg H2O. In the absence of AVP, increasing osmolality to 560 in perfusate and bath by addition of 150 mM NaCl reduced JHCO3 from 13.7 to 4.5. With 2 x 10(-10) M AVP in the bath, adding 150 mM NaCl to perfusate and bath reduced JHCO3 from 6.9 to 0.6, while adding NaCl to the bath alone reduced JHCO3 from 7.1 to 0.5. Adding 150 mM NaCl to perfusate and bath caused a similar inhibition of JHCO3 in MTAL perfused with furosemide to inhibit net NaCl absorption. In the presence of AVP, adding 600 mM urea to perfusate and bath inhibited JHCO3 by 55%; adding 300 or 600 mM mannitol to perfusate and bath inhibited JHCO3 by 75%. The effects on JHCO3 were reversible and dissociable from changes in transepithelial voltage. CONCLUSIONS: (1) osmolality is a factor capable of regulating renal tubule bicarbonate absorption; (2) hypertonicity produced with NaCl, urea, or mannitol markedly inhibits bicarbonate absorption in the MTAL; (3) this inhibition occurs independent of, and is additive to, inhibition by vasopressin. Hypertonicity may shift TAL HCO3- absorption from medulla to cortex, thereby limiting delivery of bicarbonate to the medullary interstitium during antidiuresis.

Animals↗

Bicarbonate transport along the loop of Henle. II. Effects of acid-base, dietary, and neurohumoral determinants.

The loop of Henle contributes to renal acidification by reabsorbing about 15% of filtered bicarbonate. To study the effects on loop of Henle bicarbonate transport (JHCO3) of acid-base disturbances and of several factors known to modulate sodium transport, these in vivo microperfusion studies were carried out in rats during: (a) acute and chronic metabolic acidosis, (b) acute and chronic (hypokalemic) metabolic alkalosis, (c) a control sodium diet, (d) a high-sodium diet, (e) angiotensin II (AII) intravenous infusion, (f) simultaneously intravenous infusion of both AII and the AT1 receptor antagonist DuP 753, (g) acute ipsilateral mechanicochemical renal denervation. Acute and chronic metabolic acidosis increased JHCO3; acute metabolic alkalosis significantly reduced JHCO3, whereas chronic hypokalemic alkalosis did not alter JHCO3. Bicarbonate transport increased in animals on a high-sodium intake and following AII administration, and the latter was inhibited by the AII (AT1) receptor antagonist DuP 753; acute renal denervation lowered bicarbonate transport. These data indicate that bicarbonate reabsorption along the loop of Henle in vivo is closely linked to systemic acid-base status and to several factors known to modulate sodium transport.

Acid-Base Imbalance↗

Influence of acetate and bicarbonate dialysate on blood short- and long-chain acyl carnitine in adult pyelonephritis patients.

The effect of acetate and bicarbonate haemodialysis (HD) on the concentrations of erythrocyte, whole-blood and plasma total carnitine (TC), free carnitine (FC), short- (SC) and long-chain acylcarnitine (LC) and acylcarnitine (AC) as well as the ratio of AC to FC was investigated in 30 healthy subjects (15 men and 15 women) and 27 patients (10 men and 17 women) with chronic pyelonephritis (CPN) undergoing chronic HD. Fourteen patients (5 men and 9 women) used acetate HD and the remainder (5 men and 8 women) used bicarbonate HD. The mean predialysis erythrocyte, whole-blood and plasma concentrations of TC, FC, SC, LC and AC as well as the ratio of AC to FC were not significantly different from those in healthy controls (P > 0.05). However, after acetate or bicarbonate HD, a significant decrease in erythrocyte, whole-blood and plasma concentrations of TC, FC, SC, LC and AC were found, compared with either predialysis or healthy control values (P < 0.001). Furthermore, the ratio of AC to FC was significantly higher following acetate HD as compared with either acetate or bicarbonate predialysis values (P < 0.001). The observed variations in response between acetate and bicarbonate HD may be due to enhanced formation of acetyl-coenzyme A and fatty acid synthesis during acetate HD.

Acetates↗

Agreement between two plasma bicarbonate assays in critically ill patients.

Previous studies have suggested that measurement of plasma bicarbonate concentration using the Henderson-Hasselbalch equation may be unreliable, particularly in critically ill patients. We examined the agreement between two plasma bicarbonate concentration assays in critically ill patients. Data were collected from records of routine daily blood samples. Paired samples were taken at the same time from arterial lines. A Bland-Altman analysis was used to compare two bicarbonate assays in clinical use. The first used the Henderson-Hasselbalch equation for blood-gas machine calculations. The second used a spectrophotometric enzymatic technique. Comparing the enzymatic method to the calculated method (enzymatic minus calculated) the bias was -1.6 mmol/l (95% CI: -1.2 to -2.0 mmol/l). The limits of agreement were -5.85 mmol/l to 2.65 mmol/l. This study found poor agreement between the two bicarbonate assays. This poor agreement is clinically important but the causes are unclear. We suggest further investigation of the reliability of bicarbonate assays.

Bicarbonates↗

Effects of the infusion mode on bicarbonate balance in on-line hemodiafiltration.

BACKGROUND: Electrolyte and acid-base balance may be differently affected by the infusion mode in on-line hemodiafiltration (HDF). We studied the effects of the different infusion modes on bicarbonate transport across the dialyzer membrane, and thus on the final bicarbonate balance of the HDF sessions. METHODS: Instantaneous HCO3- transfer across the dialyzer membrane, blood bicarbonate profile and the total balance of the sessions were studied in six dialysis patients under the same operating conditions over 36 HDF sessions, in order to compare the effects of predilution HDF (pre-HDF), postdilution HDF (post-HDF), and mixed HDF on the final bicarbonate balance. RESULTS: The final HCO3- balance was more positive in post-HDF vs pre-HDF (142 +/- 36 vs 99 +/- 41 mmol/session, p<0.05), with a final blood HCO3- concentration of 26.6 +/- 1.0 vs 25.4 +/- 1.1 mmol/L, (p<0.05). Mixed HDF yielded intermediate results (balance: 119 +/- 42 mmol/session, final HCO3- 26.2 (1.2 mmol/L). These differences were seen to result from the increased HCO3- concentration of blood entering the filter in predilution, due to the infused HCO3-, enhancing convective loss and reducing the driving force for diffusive HCO3- gain. CONCLUSIONS: Bicarbonate concentration in dialysate-reinfusate is critical in order to obtain an adequate end of session HCO3- balance in on-line HDF. The predilution method produced the lowest cumulative net HCO3- gain between the three studied infusion modes. Our data suggest that, under the same operating conditions and excluding the effect of ultrafiltration, dialysate HCO3- should be increased by about 2 mmol/L in pre-HDF, and 1 mmol/L in mixed HDF, to yield the same final balance as in post-HDF.

Acid-Base Equilibrium↗

Continuous renal replacement therapy: does technique influence electrolyte and bicarbonate control?

BACKGROUND AND OBJECTIVES: Different techniques of continuous renal replacement therapy (CRRT) might have different effects on electrolyte and acid-base control. The aim of this study was to determine whether continuous veno-venous hemodiafiltration (CVVHDF) or continuous veno-venous hemofiltration (CVVH) achieve better control of serum sodium, potassium and bicarbonate concentrations. DESIGN: Retrospective controlled study. SETTING: Two tertiary intensive care units. PATIENTS: Critically ill patients with acute renal failure (ARF) treated with CVVHDF (n=49) or CVVH (n=50). INTERVENTIONS: Retrieval of daily morning sodium and potassium values and arterial bicarbonate levels from computerized biochemical records before and after the initiation of CRRT for up to 2 weeks of treatment. Statistical comparison of findings. MEASUREMENTS AND RESULTS: Before treatment, abnormal (high or low) values were frequently observed for sodium (65.1% for CVVHDF vs. 80.0% for CVVH; NS), potassium (45.9% vs. 34.0%; NS), and bicarbonate (73.3% vs. 68.0%; NS). After treatment, however, CVVHDF was more likely to achieve serum sodium concentrations within the normal range (74.1% vs. 62.9%; p=0.0026). Both treatments decreased the mean serum potassium concentration over the first 48 h (p=0.0059 and p<0.0001, respectively), but there was no difference in terms of the normalization of serum potassium concentration during the entire treatment period (88.3% vs. 90.5%; NS). Both treatments increased the mean arterial bicarbonate concentration over the first 48 hours (p=0.011 and p<0.0001, respectively). However, CVVH was associated with a lower incidence of metabolic acidosis (13.8% for CVVH vs. 34.5% for CVVHDF; p<0.0001) and a higher incidence of metabolic alkalosis (38.9% vs. 1.1%; p<0.0001) during the entire treatment period. CONCLUSIONS: CRRT strategies based on different techniques have a significantly different impact on sodium and bicarbonate control.

Acute Kidney Injury↗

The acid-base effects of continuous hemofiltration with lactate or bicarbonate buffered replacement fluids.

OBJECTIVE: To evaluate, quantify and compare the effects of continuous veno-venous hemofiltration (CVVH) with lactate or bicarbonate-buffered replacement fluids on acid-base balance. DESIGN: Randomized double crossover study. SETTING: Intensive Care Unit of Tertiary Medical Center. PARTICIPANTS: Eight patients with severe acute renal failure. INTERVENTIONS: Random allocation to either 2 hours of isovolemic lactate-buffered (treatment A) CVVH or 2 hours of bicarbonate-buffered (treatment B) CVVH with cross over and with same procedure repeated the following day (double cross over). MEASUREMENTS AND RESULTS: Timed collections of arterial blood and ultrafiltrate (UF), measurement of blood and UF gases and lactate concentrations and calculation of buffer-base mass balance. At baseline, both groups of patients had a similar, slight metabolic alkalosis (pH: 7.45 vs. 7.45; BE 3.9 mEq/L for treatment A and 4.0 for treatment B) and a serum bicarbonate of 28.1 mmol/L for treatment A vs. 28.3 mmol/L for treatment B; all NS. This alkalosis was present despite slight hyperlactatemia in both groups (A: 2.4 mmol/L vs. B 2.8 mmol/; NS). Within 60 minutes of treatment, however, treatment A led to a significantly higher lactate concentration (3.9 vs 2.5 mmol/L; p = 0.0011), a significantly lower BE (2.3 vs 4.1 mEq/L; p = 0.0019) and a significantly lower bicarbonate concentration (26.7 vs. 28.3 mmol/L; p = 0.0038) in the presence of an unchanged PaCO2. These differences persisted during the study period. The UF of patients receiving treatment A contained more lactate (10.2 vs 2.9 mmol/L; p < 0.0001) and less bicarbonate (25.6 vs. 30.8 mmol/L; p < 0.0001) than treatment B resulting in a mean buffer-base balance of +20.4 mEq/h compared to -2.6 mEq/h for treatment B; p < 0.0001). CONCLUSIONS: CVVH with lactate-buffered replacement fluids induces iatrogenic hyperlactatemia. Such hyperlactatemia is associated with an acidifying effect despite a positive buffer-base balance.

Acid-Base Equilibrium↗

Validation of a [13C]bicarbonate tracer technique to measure neonatal energy expenditure.

The use of a stable isotope-labeled [13C]bicarbonate infusion to measure energy expenditure is advantageous, as a complete collection of expired air is not required. This technique allows for facile measurements of energy expenditure in intubated neonates. The aim of the present study was to determine the accuracy of energy expenditure estimates in postsurgical neonates by using the [13C]bicarbonate method compared with the current standard, indirect calorimetry. Eight neonates who were receiving total parenteral nutrition [98 +/- 21 (SD) kcal x kg(-1) x d(-1); 3.1 +/- 0.7 (SD) protein g x kg(-1) x d(-1)] were studied on postoperative d 15.5 +/- 11.9. A primed continuous 3-h intravenous infusion of NaH13CO3 and indirect calorimetry were performed simultaneously. Energy expenditure was calculated separately from the Weir equation and from the dilution of 13CO2 in the breath in combination with the individual energy equivalents of CO2 from the diet. The rate of CO2 appearance and energy expenditure calculated from the bicarbonate method (0.725 +/- 0.021 mol x kg(-1) x d(-1); 89.5 +/- 2.5 kcal x kg(-1) x d(-1)) highly correlated (r = 0.94 and 0.98, respectively) with the CO2 excretion and energy expenditure determined by indirect calorimetry (0.489 +/- 0.016 mol x kg(-1) x d(-1); 60.2 +/- 2.0 kcal x kg(-1) x d(-1)) when analyzed nonproportionately to weight. Bland-Altman analysis demonstrated the 95% confidence interval to be +/- 8.2 kcal x kg(-1) x d(-1). Linear regression analysis revealed a highly statistically significant equation relating the two energy expenditures: Indircal (kcal/d) = -9.341 + [0.705 x Bicarb (dcal/d)]; p < 0.001, r2 = 96.4%. We conclude that energy expenditure in neonates can be accurately determined using the [13C]bicarbonate method and a regression equation. Therefore, the bicarbonate method may be useful for determining energy expenditure in neonates not readily accessible to indirect calorimetry, such as those being mechanically ventilated or on extracorporeal life support.

Bicarbonates↗

Use of [13C]bicarbonate for metabolic studies in preterm infants: intragastric versus intravenous administration.

The metabolic fate of substrates in humans can be examined by the use of stable isotopes, one of which, [13C]bicarbonate, may serve to estimate CO2 production rate. In view of minimizing the burden of metabolic studies for preterm infants, the authors determined whether intragastric and intravenous infusions of [13C]bicarbonate would achieve the same 13CO2 enrichment in expired air during steady state. A second aim of this study was to determine the minimum time required to reach steady state during intragastric infusion. Ten preterm infants received a primed continuous [13C]bicarbonate infusion intragastrically, followed by an intravenous infusion the next day. Breath samples were obtained every 30 min by the direct sampling method. 13CO2 isotopic enrichment, expressed as atom percent excess, was measured by isotopic ratio mass spectrometry. Two-tailed t tests were used to detect statistically significant differences between the infusion routes. The isotopic enrichment at plateau did not differ between intragastric and intravenous infusion. A steady state of 13CO2 enrichment was achieved after 60 min of intravenous infusion and after 120 min of intragastric infusion. In conclusion, intragastric infusion of [13C]bicarbonate may serve to estimate the whole-body CO2 production rate in preterm infants. To reach 13CO2 steady state, a minimum of 120 min of bicarbonate administration is required.

Bicarbonates↗