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PubMed1989

Metabolic acidosis stimulates bicarbonate reabsorption in the early proximal tubule.

The early proximal tubule is the major site for renal bicarbonate reabsorption but little is known about the influence of acidosis on transport in this segment. This study examined early proximal bicarbonate reabsorption in rats with chronic metabolic acidosis (MA) (induced by NH4Cl administration). Rats were studied by free-flow micropuncture techniques, after varying degrees of plasma volume expansion to vary the filtered load of bicarbonate (FLHCO3). At FLHCO3 less than 700 pmol/min, both control and acidotic animals reabsorbed greater than 80% of the filtered load by 2 mm from Bowman's space. At higher FLHCO3 (700-1,100 pmol/min), reabsorption in the early proximal tubule was significantly greater in MA rats vs. control (633 +/- 26 vs. 449 +/- 24 pmol/min, between 1 and 2 mm from Bowman's space, P less than 0.001). This MA-induced stimulation of early proximal bicarbonate reabsorption was completely reversed by restoring systemic pH to normal either by acute hypocapnia or alkali infusion. Thus bicarbonate reabsorption in the early proximal tubule correlated closely with changes in systemic pH in rats with MA when bicarbonate delivery was increased by plasma expansion. The mechanism of this effect remains to be determined.

Absorption↗
PubMed1989

Neural control of distal tubular bicarbonate and fluid transport.

Although previous studies have shown that inhibition of proximal tubular reabsorption of bicarbonate and fluid partially accounts for bicarbonaturia and diuresis observed in the denervated kidney, the role of the distal convoluted tubule in the neural regulation of electrolyte excretion has not been defined. This study was designed to examine the effects of denervation on bicarbonate and fluid reabsorption in the distal convoluted tubules by using in situ microperfusion methods. Early distal tubules were perfused with a solution containing 15 mM bicarbonate at a rate of 12 nl/min, and fluid samples were collected from the late distal tubule. Bicarbonate concentrations were measured as total CO2 by microcalorimetry. The rate of fluid absorption (Jv) was determined using [methoxy-3H]inulin as a volume marker. Before denervation, the rate of bicarbonate absorption (JHCO3-) was 24.7 +/- 2.6 peq.min-1.mm-1, and Jv was 1.80 +/- 0.14 nl.min-1.mm-1. After denervation, marked reductions in JHCO3- (51%) and Jv (60%) were observed. In contrast, sham denervation did not affect JHCO3- or Jv significantly. Our results indicate that the distal convoluted tubule can reabsorb bicarbonate and fluid under physiological conditions. We conclude that the transport processes in this segment of the nephron are regulated by renal nerve activity.

Absorption↗
PubMed1976

Rate of bicarbonate-chloride exchange in human red cells at 37 degrees C.

The rate of exchange of bicarbonate and chloride ions across the red cell membrane was studied in a continuous flow rapid reaction apparatus at 37 degrees C. A transmembrane gradient both ions was produced by mixture of cells suspended in a solution of one ion with an isosmotic solution of the other ion. Carbonic anhydrase activity was inhibited by acetazolamide to prevent changes in CO2 concentration during the experiments. Chloride and bicarbonate efflux from cells were studied in separate experiments at each experimental pH. Using a least squares technique, values of chloride and bicarbonate permeabilities were fitted to each pair of independent experiments. Chloride permeability averaged 1.1 (+/- 0.2 SD) X 10-4 cm/s and was not affected by change in pH. Recovered bicarbonate permeabilities varied widely, always remaining at least fivefold greater than chloride permeability. While bicarbonate permeability could not be accurately characterized, it appears to be greater than chloride permeability. Analysis of CO2 transfer with the estimated permeabilities indicates that the bicarbonate-chloride exchange by itself probably does not limit CO2 transfer.

Bicarbonates↗
PubMed2001

First-pass effect of an intravenous bolus of [13C]bicarbonate displayed breath-by-breath.

The dilution of an intravenous bolus dose of [13C]bicarbonate is used as an estimate for the metabolic rate under certain conditions. It is a consistent finding in all studies that the total amount of intravenous [13C]bicarbonate cannot be recovered as breath 13CO2. In this study, we used a breath-by-breath analysis of 13CO2 to depict the washout of 13CO2 at a high temporal resolution to analyze the extent to which a probable first-pass effect is responsible for the reduced recovery. Eight healthy men were tested at seated rest and with bicycle exercise at a constant load relative to 40 and 75% maximal O2 consumption VO2 max). [13C]bicarbonate (0.0125 g/kg body wt) was administered as an intravenous bolus in each test. Respiratory mass spectrometry was used to derive the course of the end-tidal 13CO2-to-12CO2 ratio from the breath-by-breath data. Approximately 2 min after 13C administration, the washout curve could be fitted well by a two-exponential curve describing a two-compartment mammillary model. Immediately after administration of the bolus dose, an excess peak in the end-tidal 13CO2-to-12CO2 ratio appeared. This peak could not be included in the two-exponential fitting. The area under the first peak resulted in 3.8 +/- 1.3% of the total [13C]bicarbonate dose at rest, 11.5 +/- 2.9% at moderate exercise (40% VO2 max), and 16.9 +/- 4.0% at intensive exercise (75% VO2 max). The first-pass effect had an increasing impact of up to about two-thirds of the lacking bicarbonate with higher exercise intensity. The "loss" of tracer via this first-pass effect must be considered when the results of studies with parenteral administration of [13C]bicarbonate are considered, especially when it is given as a bolus dose and during exercise.

Adult↗
PubMed2000

Concentration dependence of bicarbonate-induced calcium current modulation.

High-voltage-activated calcium currents (HVA) of CA1 neurons are prominently attenuated following a switch from HEPES-buffered solution to one buffered with CO(2)/HCO(3)(-). In the present study we investigated whether bicarbonate ions or the dissolved CO(2) induce this alteration in current characteristic. The study was carried out on freshly isolated CA1 neurons using the whole cell patch-clamp technique. Maximal calcium conductance and the mean peak amplitude of the currents showed a concentration-dependent decrease when cells were consecutively bathed in solutions containing increasing amounts of bicarbonate and CO(2). This decrease is best described by the Hill equation, yielding a maximal attenuation of 69%, a half-maximal concentration (EC(50)) of 7.4 mM HCO(3-), and a Hill coefficient of 1.8. In parallel, the potentials of half-maximal activation (V(h,a)) and inactivation (V(h,i)) were linearly shifted in hyperpolarizing direction with a maximal shift, in the 10% CO(2)/37 mM HCO(3)(-) containing solution of 10 +/- 1 mV for V(h,a) (n = 23) and 17 +/- 1.4 mV for V(h,i) (n = 18). When currents were evoked in solutions containing equal concentrations of bicarbonate but different amounts of CO(2), only nonsignificant changes were observed, while marked alterations of the currents were induced when bicarbonate was changed and CO(2) held stable. The experiments suggest that bicarbonate is the modulating agent and not CO(2). This bicarbonate-induced modulation may be of critical relevance for the excitation level of the CNS under pathological situation with altered concentration of this ion, such as hyperventilation and metabolic acidosis.

Animals↗
PubMedDate not supplied

Evidence for an inhibitory effect of kallikrein on collecting duct bicarbonate secretion in rats and rabbits.

The luminal membrane of collecting duct cells, especially the intercalated cells, is normally exposed to active kallikrein. This is the consequence of the specific localization of this renal enzyme in the connecting tubule cells and its principal route of secretion being into the tubular lumen. It is conceivable that kallikrein acts downstream on a transporter involved in distal bicarbonate handling. To investigate this possibility, we estimated bicarbonate concentration and measured kallikrein amidolytic activity in urine fractions collected after a classical stop-flow experiment in rabbits. A highly significant inverse correlation was found between these parameters (r = -0.94, p < 0.001) in the peak kallikrein fractions. Neither sodium nor potassium concentration were correlated to kallikrein. This suggests that the physiological role of renal kallikrein may be to regulate extracellular fluid pH by inhibiting collecting duct bicarbonate secretion. To test the hypothesis that tubular fluid kallikrein activity and bicarbonate secretion are causally related, we developed a novel in vivo stop-flow injection model ('orthograde stop-flow'). A hog-kallikrein containing solution (0.5 microgram/ml) was injected through the abdominal aorta into the renal tubular system of one kidney of barbiturate-anesthetized rats, while the renal blood supply was interrupted. The ureter was then occluded and renal blood perfusion reinitiated. After a 2-min contact time five 125-microliters urine fractions were collected. Bicarbonate secretion was clearly detected in the second and third fractions (i.e. those coming from the collecting ducts) of the control animals, which had received only the vehicle. There was no bicarbonate secretion peak in the corresponding urine fractions collected from kallikrein-injected animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1977

Relationship between serum phosphate concentration and proximal tubular bicarbonate transport.

Micropuncture studies were performed in intact and thyroparathyroidectomized (TPTX) dogs to evaluate the relationship between the absolute level of serum ultrafilterable phosphate concentration (SUFP) and proximal bicarbonate reabsorption. In both groups of animals, a reverse linear relationship was noted between the serum phosphate level and the tubular fluid bicarbonate concentration (TFHCO3). For the intact dogs, TFHCO3=32.27 SUFP+/-2.17, r=0.715, p=0.02, and for the TPTX dogs, TFHCO3=35.68-2.39 SUFP+/-2.26; r=0.619, p less than 0.02. Furthermore, when late-proximal tubular values for absolute bicarbonate reabsorptive rate (THCO3)/100 nl single nephron filtrate were plotted against SUFP, a direct relationship was found for both groups; intact dogs: THCO3=205 SUFP-169+/-136, r=0.707, p less than 0.05; TPTX dogs: THCO3=224 SUFP-882+/-221, r=0.625, p less than 0.01. Variations in plasma bicarbonate concentration or PCO2 did not contribute to the relationship between SUFP and bicarbonate reabsorption. The data suggest that extracellular fluid phosphate concentration is an important modulator of proximal bicarbonate transport, independent of the action of parathyroid hormone.

Animals↗
PubMed1991

Bicarbonate and calcium kinetics in postdilutional hemodiafiltration.

Hemodiafiltration (HDF) is a very effective blood treatment resulting from the coupling of dialysis and hemofiltration and leading to reduction of dialysis time. The aim of this study was to evaluate the balance of bicarbonate and calcium through the filter during postdilutional HDF (with an ultrafiltration flow rate of 70 ml/min) and to verify the effect of ultrafiltration on the kinetics of these two solutes. The study was performed by simultaneously collecting three blood samples (at filter inlet and outlet and after reinfusion) at different ultrafiltration flow rates (12.5-90 ml/min), to measure blood pH, pCO2, plasma total CO2(TCO2), total calcium, ionized calcium and plasma protein concentration. Plasma bicarbonate concentration was calculated by measuring plasma TCO2. The results showed an inverse linear relationship between bicarbonate (r: -0.7938; p less than 0.001) and calcium (r: -0.8731; p less than 0.001) balance and ultrafiltration flow rate. In particular, in postdilutional HDF both bicarbonate and calcium balances through the filter were negative at ultrafiltration flow rates greater than 40 and 55 ml/min, respectively. The negative bicarbonate balance, however, was corrected by reinfusing a substituting solution containing bicarbonate (40 mmol/l). By contrast, the negative calcium balance cannot be corrected by reinfusion and requires a greater calcium concentration in the dialysate and oral calcium supplements.

Bicarbonates↗
PubMed1994

Comparative activities of agonists of active duodenal bicarbonate secretion in the guinea pig.

The comparative activity of agonists of duodenal bicarbonate secretion was studied in the anesthetized guinea pig, where the duodenal lumen was perfused with 24 mmol/l NaHCO3 to ensure active secretion of bicarbonate. Agonists were infused alone and in combination. Dibutyryl 3',5'-cyclic adenosine monophosphate, vasoactive intestinal polypeptide (VIP) and prostaglandin E2 (PGE2) were strong stimulants of bicarbonate secretion. Theophylline, dibutyryl 3',5'-cyclic guanosine monophosphate, glucagon and prostaglandin F2 alpha (PGF2 alpha) were weaker agonists, and secretin had no effect. Combinations of any two of VIP, PGE2 and glucagon depressed bicarbonate secretion, whereas combinations of PGE2 and PGF2 alpha, VIP and PGE2, and glucagon and PGF2 alpha increased bicarbonate secretion. The data indicate that cAMP and other secondary messengers may mediate duodenal bicarbonate secretion.

Adenosine Monophosphate↗
PubMed1972

Renal tubular acidosis in infants: the several kinds, including bicarbonate-wasting, classic renal tubular acidosis.

In four infants with renal tubular acidosis (RTA), including three with apparently classic RTA and one with Fanconi syndrome (FS), the physiologic character of the renal acidification defect was investigated. In two of the infants with apparently classic RTA, the acidification defect was physiologically separable from that described in both adult patients and children with classic RTA (type 1 RTA) in the following ways. (a) The fractional excretion of filtered bicarbonate (C(HCO3)/C(ln)) was not trivial but substantial (6-9%), as well as relatively fixed, over a broad range of plasma bicarbonate concentrations (15-26 mmoles/liter). (b) This value of C(HCO3)/C(ln), combined with a normal or near normal glomerular filtration rate, translated to renal bicarbonate wasting (RBW). (c) RBW at normal plasma bicarbonate concentrations was the major cause of acidosis, and its magnitude was the major determinant of corrective alkali therapy (5-9 mEq/kg per day), just as in the patient with FS, who was found to have type 2 ("proximal") RTA. (d) Persistence of RBW at substantially reduced plasma bicarbonate concentrations, which did not occur in FS, accounted for the spontaneous occurrence of severe acidosis and its rapid recurrence after reduction in alkali therapy. (e) During severe acidosis the urinary pH was >7, a finding reported frequently in infants with apparently classic RTA and "alkali-resistant" acidosis but rarely in adult patients with classic RTA. Continued supplements of potassium were required to maintain normokalemia during sustained correction of acidosis with alkali therapy. Yet, in at least two of the three infants with apparently classic RTA, but in distinction from the patient with FS and other patients with type 2 RTA, fractional excretion of filtered potassium decreased when plasma bicarbonate was experimentally increased to normal values. In one of the two infants with apparently classic RTA and RBW, C(HCO3)/C(ln) and the therapeutic alkali requirement decreased concomitantly and progressively over 2 yr, but RBW continued. Renal tubular acidosis has persisted in all four patients for at least 3 yr, and in three for 4 years.

Acidosis, Renal Tubular↗
PubMed1988

Interaction of chloride and bicarbonate transport across the basolateral membrane of rabbit proximal straight tubule. Evidence for sodium coupled chloride/bicarbonate exchange.

The existence of chloride/bicarbonate exchange across the basolateral membrane and its physiologic significance were examined in rabbit proximal tubules. S2 segments of the proximal straight tubule were perfused in vitro and changes in intracellular pH (pHi) and chloride activity (aCli) were monitored by double-barreled microelectrodes. Total peritubular chloride replacement with gluconate increased pHi by 0.8, and this change was inhibited by a pretreatment with an anion transport inhibitor, SITS. Peritubular bicarbonate reduction increased aCli, and most of this increase was lost when ambient sodium was totally removed. The reduction rates of pHi induced by a peritubular bicarbonate reduction or sodium removal were attenuated by 20% by withdrawal of ambient chloride. SITS application to the bath in the control condition quickly increased pHi, but did not change aCli. However, the aCli slightly decreased in response to SITS when the basolateral bicarbonate efflux was increased by reducing peritubular bicarbonate concentration. It is concluded that sodium coupled chloride/bicarbonate exchange is present in parallel with sodium-bicarbonate cotransport in the basolateral membrane of the rabbit proximal tubule, and it contributes to the basolateral bicarbonate and chloride transport.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1988

Secretion of bicarbonate by rat distal tubules in vivo. Modulation by overnight fasting.

We have performed microperfusion studies on distal tubule bicarbonate reabsorption (JtCO2) of fed and fasted rats to extend our previous observations of in vivo bicarbonate secretion and to resolve certain discrepancies between free-flow and microperfusion data. When rats are fasted overnight, as in previous free-flow studies, distal tubule microperfusion with a 28-mM tCO2 solution results in significant JtCO2 (53 +/- 6 pmol.min-1.mm-1) at normal flow and increases briskly (91 +/- 16 pmol.min-1.mm-1) with bicarbonate load. This response is not influenced by the addition of other normal tubular fluid constituents. However, when normally fed rats are used, as in our previous microperfusion studies, distal tubule JtCO2 is not different from zero when a 28-mM tCO2 solution is perfused at normal flow rates but becomes negative (-54 +/- 13 pmol.min-1.mm-1) at high flow rates, which indicates the existence of bicarbonate secretion against a concentration gradient. Alkali loading of fasted rats also elicits bicarbonate secretion at high flow. These results demonstrate for the first time that normal feeding or alkali loading can induce bicarbonate secretion in a mammalian nephron segment in vivo, and resolves previous discrepancies between free-flow and microperfusion data.

Absorption↗
PubMed1989

Angiotensin II stimulates early proximal bicarbonate absorption in the rat by decreasing cyclic adenosine monophosphate.

These studies explored the hypothesis that angiotensin II increases bicarbonate absorption in the proximal convoluted tubule (PCT) by decreasing intracellular cAMP. In vivo microperfusion was performed in rat PCT with measurements of bicarbonate absorption and of tubular fluid cAMP delivery, as a reflection of intracellular cAMP. Intravenous angiotensin II potently increased S1 PCT bicarbonate absorption (348 +/- 11 to 588 +/- 8 peq/min.min, P less than 0.001) and decreased tubular fluid cAMP (18 +/- 2 to 12 +/- 2 fmol/mm.min, P less than 0.05). Parathyroid hormone had the expected opposite effects, which were additive to those of angiotensin II. Over a wide range of hormonal activities, there was an excellent inverse relationship between hormonally modulated bicarbonate absorption and cAMP delivery. Pertussis toxin pretreatment significantly attenuated (by 35-45%) the angiotensin-induced increase in bicarbonate absorption and decrease in cAMP delivery, indicating Gi-protein intermediation. Luminal dibutyryl cAMP abolished the transport response to angiotensin II. In conclusion, these in vivo results suggest angiotensin II stimulates bicarbonate absorption in the S1 PCT by a G1-mediated depression in intracellular cAMP.

Adenylyl Cyclases↗
PubMed1989

Augmented bicarbonate reabsorption by both the proximal and distal nephron maintains chloride-deplete metabolic alkalosis in rats.

Whether augmented bicarbonate reabsorption by renal tubular epithelium contributes to the maintenance of chloride-deplete metabolic alkalosis is not clear. This study used free-flow micropuncture to investigate bicarbonate reabsorption by surface nephron segments in a rat model of diuretic-induced alkalosis compared to control. The proximal and distal nephron of the alkalotic animals had higher values for both delivered load to and absolute reabsorption from these segments. The proximal tubules of alkalotic and control animals had similar values for the slopes of the linear regression of delivered load vs. reabsorption and for the bicarbonate tubular fluid to plasma (TF/P) ratio at the late proximal tubule. By contrast, the corresponding analysis for the distal segment of alkalotic animals revealed a greater slope (0.98 vs. 0.81, P less than 0.003) and a smaller bicarbonate TF/P ratio at the late distal tubule (0.10 vs. 0.16, P less than 0.006). The data indicate that augmented bicarbonate reabsorption by both the proximal and distal nephron contributes to maintaining the alkalosis of this model. The data suggest primary stimulation of bicarbonate reabsorption in the distal nephron and load-dependent reabsorption in the proximal tubule.

Absorption↗
PubMed1990

Cerebroventricular calcitonin gene-related peptide inhibits rat duodenal bicarbonate secretion by release of norepinephrine and vasopressin.

Proximal duodenal bicarbonate secretion is an important factor in humans and animals protecting the mucosa against acid-peptic damage. This study examined the mechanisms responsible for the central nervous system regulation of duodenal bicarbonate secretion by calcitonin gene-related peptide (CGRP) in unrestrained rats. Cerebroventricular administration of rat CGRP significantly inhibited basal duodenal bicarbonate secretion as well as the stimulatory effects of vasoactive intestinal peptide, neurotensin, a luminal PGE1 analogue, misoprostol, and hydrochloric acid. The inhibitory effects of cerebroventricular CGRP were abolished by ganglionic blockade with chlorisondamine, significantly attenuated by noradrenergic blockade with bretylium, and enhanced by vagotomy. Inhibition of duodenal bicarbonate secretion induced by CGRP coincided with significant increases in plasma norepinephrine (NE) and vasopressin concentrations. The alpha adrenergic receptor antagonist, phentolamine, and the vasopressin V1 receptor antagonist, (1-deaminopenicillamine, 2-[O-methyl]Tyr, 8-Arg)-vasopressin, given intravenously reversed the central inhibitory effect of CGRP by approximately 50% each. Pretreatment of the animals with both phentolamine and the vasopressin antagonist completely abolished the central inhibitory effect of CGRP. Peripheral vasopressin and NE significantly decreased duodenal bicarbonate secretion, and their inhibitory effects were additive and prevented by phentolamine and the vasopressin antagonist, respectively. We conclude that cerebroventricular CGRP inhibits rat duodenal bicarbonate secretion by activation of sympathetic efferents and subsequent release of NE and vasopressin that act on alpha adrenergic and vasopressin receptors, respectively.

Adrenalectomy↗
PubMed1991

Participation of monocarboxylic anion and bicarbonate exchange system for the transport of acetic acid and monocarboxylic acid drugs in the small intestinal brush-border membrane vesicles.

A participation of bicarbonate exchange system for the transport of acetic acid and the related monocarboxylic acid drugs in the intestinal brush-border membrane vesicles (BBMVs) was investigated. The uptake of [3H]acetic acid at 37 degrees C by BBMVs was markedly stimulated and showed a clear overshoot phenomenon in the presence of outward-directed bicarbonate gradient (pHin = 7.5, [KHCO3]in or [NaHCO3]in = 100 mM; pHout = 7.5, [K-gluconate]out or [Na-gluconate]out = 100 mM). This uptake process was saturable (Kt = 50.4 +/- 4.96 mM and Jmax = 11.6 +/- 0.61 nmol/mg protein/10 s) and was inhibited by DIDS (4,4-diisothiocyano-2,2'-disulfonic acid stilbene disodium salt) and furosemide, anion exchange inhibitors, and by many monocarboxylates. The initial uptake of [3H]acetic acid was competitively inhibited by salicylic acid, suggesting the common transport between acetic acid and salicylic acid. At lower extravesicular pHs and in the presence of outward-directed bicarbonate gradient (pHin = 7.5 [KHCO3]in = 100 mM; pHout = 6.0 or 5.0, [K-gluconate]out = 100 mM) where membrane potential was clamped to zero by K(+)-valinomycin, the uptake of [3H]acetic acid showed an overshoot phenomenon, whereas the uptake was significantly decreased in the presence of carbonyl cyanide p-trifluoromethoxyphenylhydrazone, a protonophore. It was concluded, therefore, that there are one or two mechanisms for the carrier-mediated transport of acetic acid and monocarboxylates related to bicarbonate exchange systems in rabbit intestinal BBMVs: 1) proton gradient independent and bicarbonate exchange system; 2) proton gradient dependent and bicarbonate exchange system.

Acetates↗
PubMed2006

N-acetylcysteine and sodium bicarbonate versus N-acetylcysteine and standard hydration for the prevention of radiocontrast-induced nephropathy following coronary angiography.

BACKGROUND: Radiocontrast-induced nephropathy (RCIN) is thought to be caused by renal ischemia and direct toxic effects on renal tubular cells brought on by contrast media. The combination of N-acetylcysteine (NAC) and hydration fluids (NaCl 0.9% or 0.45%) has been shown to reduce these deleterious effects and is commonly given prior to coronary angiography. The use of bicarbonate as the hydration anion has been shown to confer additional RCIN protection compared with that of saline. However, limited data are available regarding whether sodium bicarbonate hydration, proven to be beneficial alone, can further improve outcomes when given with NAC. OBJECTIVE: To compare the incidence of RCIN in patients undergoing coronary angiography after pretreatment with NAC plus sodium bicarbonate hydration or NAC plus standard hydration (NaCl 0.9% or 0.45%). METHODS: A retrospective, single-center study evaluated 96 patients who underwent coronary angiography from January 2002 to December 2005. Data were collected through electronic chart reviews. RESULTS: Forty-seven patients received NAC and sodium bicarbonate for hydration and 49 received NAC and standard hydration. Baseline characteristics between the 2 groups were similar. All patients received at least one 600 mg oral dose of NAC before angiography was performed. RCIN was defined as impairment of renal function occurring within 72 hours of administering contrast media, indicated by an absolute increase in the serum creatinine level of 0.5 mg/dL or more. A total of 12.2% of the patients receiving NAC and standard hydration developed RCIN, versus 14.9% of the patients in the NAC and sodium bicarbonate group (p = 0.713). CONCLUSIONS: The addition of sodium bicarbonate to NAC does not appear to confer additional protection against the development of RCIN. Prospective, randomized, placebo-controlled trials are warranted to definitively determine how this combination compares with NAC and standard hydration in preventing RCIN.

Acetylcysteine↗
PubMed2000

Sodium bicarbonate for the treatment of lactic acidosis.

Lactic acidosis often challenges the intensivist and is associated with a strikingly high mortality. Treatment involves discerning and correcting its underlying cause, ensuring adequate oxygen delivery to tissues, reducing oxygen demand through sedation and mechanical ventilation, and (most controversially) attempting to alkalinize the blood with IV sodium bicarbonate. Here we review the literature to answer the following questions: Is a low pH bad? Can sodium bicarbonate raise the pH in vivo? Does increasing the blood pH with sodium bicarbonate have any salutary effects? Does sodium bicarbonate have negative side effects? We find that the oft-cited rationale for bicarbonate use, that it might ameliorate the hemodynamic depression of metabolic acidemia, has been disproved convincingly. Further, given the lack of evidence supporting its use, we cannot condone bicarbonate administration for patients with lactic acidosis, regardless of the degree of acidemia.

Acidosis, Lactic↗