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At least 667 records · Page 37Linked to original sources
PubMed1988

Stimulation of amphibian gastroduodenal bicarbonate secretion by sucralfate and aluminium: role of local prostaglandin metabolism.

The present studies were designed to explore the possible mode of protective and ulcer healing actions of sucralfate by examining its effect on gastroduodenal bicarbonate secretion by isolated amphibian mucosa. Luminal sucralfate (0.5 g/l) significantly increased bicarbonate secretion by fundic and antral mucosa without influencing transmucosal potential difference. Significant stimulation of duodenal bicarbonate secretion occurred only at 1.0 g/l without change in potential difference. Aluminium, a component of sucralfate, produced similar increases in bicarbonate secretion, while the sucrose and sulphate components were without effect. Pretreatment of mucosae with the cyclooxygenase inhibitor, indomethacin (10 5M) did not abolish the secretory response to sucralfate or aluminium. The results suggest that stimulation of gastroduodenal bicarbonate secretion, possibly by the aluminium moiety of sucralfate, may play a role in its protective and ulcer healing actions.

Aluminum↗
PubMed1980

The effect of bicarbonate concentration on fatigue and recovery in isolated rat diaphragm muscle.

Diaphragm strips from young rats (45--60 g) about 0.3 mm thick were fatigued by tetanic stimulation at a train repetition rate of 2 HZ for 3 min. The isometric tension developed was measured during fatigue and recovery in solutions containing 25, 10, or 2 mM bicarbonate at both 37 and 30 degrees C. Tension fell during fatigue to between 20 and 30% of the initial value and this was not significantly influenced by external bicarbonate concentration or temperature over the range considered. Recovery of tension was complete and rapid (t1/2 < 1 min) in 25 mM bicarbonate at both temperatures. In 10 and 2 mM bicarbonate recovery was slowed (t1/2 3.5 and 7 min, respectively, at 30 degrees C, 1.6 and 4.5 min at 37 degrees C) and incomplete (85 and 72% at 30 degrees C, 82 and 61% at 37 degrees C). Muscle creatine phosphate fell during fatigue but was completely restored within 4 min at 30 degrees C in either 2 or 25 mM HCO3. Lactate increased less in muscles fatigued in 2 mM HCO3 and fell at a slower rate during recovery. The results seem to exclude intracellular creatine phosphate concentration as a major determinant in recovery. The evidence suggests that external bicarbonate can affect the recovery of tension following fatigue by altering intracellular acid-base balance.

Adenosine Triphosphate↗
PubMed2005

Gastroduodenal mucus bicarbonate barrier: protection against acid and pepsin.

Secretion of bicarbonate into the adherent layer of mucus gel creates a pH gradient with a near-neutral pH at the epithelial surfaces in stomach and duodenum, providing the first line of mucosal protection against luminal acid. The continuous adherent mucus layer is also a barrier to luminal pepsin, thereby protecting the underlying mucosa from proteolytic digestion. In this article we review the present state of the gastroduodenal mucus bicarbonate barrier two decades after the first supporting experimental evidence appeared. The primary function of the adherent mucus gel layer is a structural one to create a stable, unstirred layer to support surface neutralization of acid and act as a protective physical barrier against luminal pepsin. Therefore, the emphasis on mucus in this review is on the form and role of the adherent mucus gel layer. The primary function of the mucosal bicarbonate secretion is to neutralize acid diffusing into the mucus gel layer and to be quantitatively sufficient to maintain a near-neutral pH at the mucus-mucosal surface interface. The emphasis on mucosal bicarbonate in this review is on the mechanisms and control of its secretion and the establishment of a surface pH gradient. Evidence suggests that under normal physiological conditions, the mucus bicarbonate barrier is sufficient for protection of the gastric mucosa against acid and pepsin and is even more so for the duodenum.

Animals↗
PubMed1978

Importance of bicarbonate in bile salt independent fraction of bile flow.

The bile salt independent fraction (BSIF) of canalicular bile flow from the isolated rat liver perfused with bicarbonate-free perfusate is 50% of that from the liver perfused with bicarbonate-containing perfusate. HCO3-excretion is nearly eliminated and Na+ and Cl- excretion is reduced 50%. Replacement of HCO3- into perfusate increased bile flow by 0.3 microliter/g.min without changing bile acid excretion rate. 5.5-Dimethyl-2,4-oxazolidinedione (DMO) produced a similar effect. DMO was passively distributed between bile and plasma. The data indicate that a bicarbonate transport mechanism is responsible for production of up to 50% of the BSIF. Another weak acid, N-5[5-(2-methoxyethoxy)-2-pyrimidinyl]sulfamoylbenzene (glymidine), was rapidly excreted into bile and increased bile flow by over 2.0 microliter/g.min. Glymidine is probably excreted by an independent organic anion transport mechanism, and any effect on the bicarbonate transport mechanism is obscured. Canaliculus-enriched hepatocyte membrane fractions contained no HCO3-stimulated ATPase activity. Either this enzyme is unimportant in hepatocyte bicarbonate transport or transport occurs across membranes other than the bile canalicular membrane.

Adenosine Triphosphatases↗
PubMed1996

Mechanisms behind changes in gastric acid and bicarbonate outputs during the human interdigestive motility cycle.

Human gastric interdigestive acid and bicarbonate outputs vary cyclically in association with the migrating motor complex (MMC). These phenomena were studied in 26 healthy volunteers by constant-flow gastric perfusion, with continuous recording of pH and Pco2 in mixed gastric effluent and concomitant open-tip manometry of gastroduodenal motility. Stable acid and bicarbonate outputs were registered during less than 50% of the MMC cycle. Acid secretion started to increase 71 +/- 3% into the cycle, with maximum output during antral phase III. Bicarbonate output increased biphasically 1) 40 +/- 5% into the cycle, coinciding with reflux of bile, and 2) at the end of duodenal phase III when the aspirate was devoid of bile. The bicarbonate peak associated with phase III was abolished by atropine (0.01 mg/kg iv, n = 8) and by pyloric occlusion (n = 9) but remained unchanged after omeprazole (n = 10). The acid peak was abolished by both atropine and omeprazole. It is concluded that the MMC-related changes in acid and alkaline outputs represent two different and independent phenomena. Acid secretion cyclicity is due to periodical variations in cholinergic stimulation of the parietal cells. In contrast, the phase III-associated increase in bicarbonate output is due to duodenogastric reflux.

Adolescent↗
PubMed1997

Neurokinin A increases duodenal mucosal permeability, bicarbonate secretion, and fluid output in the rat.

The aim of this study was to examine the integrative response to neurokinin A (NKA) on duodenal mucosal permeability, bicarbonate secretion, fluid flux, and motility in an in situ perfusion model in anesthetized rats. Intravenous infusion of NKA (100, 200, and 400 pmol.kg-1.min-1) induced duodenal motility. Furthermore, duodenal mucosal bicarbonate secretion, fluid output, and mucosal permeability increased in response to NKA. Pretreatment with the nicotinic antagonist hexamethonium did not change the response in any of the parameters investigated, whereas the NK2-receptor antagonist MEN 10,627 effectively inhibited all responses to NKA. Indomethacin induced duodenal motility and stimulated bicarbonate secretion. In indomethacin-treated rats, NKA further increased motility but decreased indomethacin-stimulated bicarbonate secretion by 70%. The NKA-induced increase in mucosal permeability was unaltered by indomethacin. It is concluded that NKA not only induces motility but also increases mucosal permeability and fluid output. Furthermore, the neuropeptide may have both stimulative and inhibitory effects on bicarbonate secretion. All responses to NKA are dependent on NK-2 receptor activation but are not mediated through nicotinic receptors.

Animals↗
PubMed1983

[13C]bicarbonate kinetics in humans: intra- vs. interindividual variations.

A comprehensive multicompartmental analysis of HCO-3 kinetics was carried out on five normal, resting, fasted adults on three separate occasions at 1-wk to 1-mo intervals to obtain a set of bicarbonate kinetic parameters and estimates of their inter- and intraindividual variations for use in the design and analysis of future nutrient oxidation studies. Following a rapid bolus of NaH13CO3 (10 mumol . kg-1 iv), the decay of 13C enrichment of breath CO2 could be described by a three-exponential decay process and a linearly time-dependent term that accounted for changes in the 13C enrichment of metabolic fuels. The data were fitted subsequently to a mammillary multicompartmental model that consisted of a central pool and two peripheral pools of 3,310, 3,490, and 8,070 mumol . kg-1 HCO-3-CO2. Labeled CO2 was eliminated from the central pool by respiratory and nonrespiratory routes at rates of 101 and 97 mumol . kg-1 . min-1, respectively. The within-subject and among-subject variances were similar for the amount of freely exchangeable bicarbonate (14,870 mumol . kg-1), CO2 output (101 mumol . kg-1 . min-1), bicarbonate flux (198 mumol . kg-1 . min-1), and the fraction of administered bicarbonate recovered in breath (0.51). Comparison of variances associated with the assignment of a population mean value to a new subject and the variance associated with the use of a value obtained in the same individual on another day indicated that there was no advantage to making a determination on an alternate day over using a population value. Efforts should be made to compile population values for bicarbonate kinetics in different age groups and metabolic, nutritional, and pathological states for use in interpretation of nutrient oxidation data.

Adult↗
PubMed1977

Bicarbonate transport by isolated perfused rabbit proximal convoluted tubules.

Proximal convoluted tubules were dissected from rabbit kidneys and perfused in vitro in order to investigate the relationship between the reabsorption of fluid and of bicarbonate. Bicarbonate was absorbed when it was initially present in the perfusate. At slow rates of perfusion the mean concentration of total CO2 was 9 mM in collected fluid with 25 mM bicarbonate in the bath. At faster rates of perfusion the mean rate of reabsorption was 13.6 pmol cm-1 tubule length s-1. Absorption of bicarbonate was inhibited to a large but not complete extent by elimination of sodium from the perfusate and bath or potassium from the bath, and by addition of ouabain. It was not inhibited by elimination of the organic solutes from the perfusate nor by elimination of chloride from the perfusate and bath. Considered with previous measurements of fluid absorption these results are consistent with the existence of a linked sodium-for-hydrogen ion exchange mechanism at the luminal border of the tubule cells, but there are other possibilities which are discussed. Additionally, the effect of acetazolamide was investigated. The drug virtually completely inhibited bicarbonate absorption and inhibited fluid absorption by 30-40%.

Acetazolamide↗
PubMed1978

Uncoupling of proximal sodium bicarbonate from sodium phosphate transport by bumetanide.

Re-collection micropuncture of late proximal tubular segments and simultaneous clearance studies were performed in chronically thyroparathyroidectomized dogs before and after the intravenous administration of bumetanide. The drug, a new sulfonamide-derivative diuretic, inhibited proximal fractional sodium and fluid transport by 0.12 (from 0.44 +/- 0.04 to 0.32 +/- 0.04, P less than 0.05) and that of bicarbonate by 0.14 (from 0.43 +/- 0.05 to 0.29 +/- 0.07, P less than 0.02). Tubular fluid bicarbonate concentration was unchanged, indicating a reduction in the transport of this ion proportionate to that of tubular fluid. However, unlike sodium and bicarbonate reabsorption, fractional proximal phosphate transport was unaltered (from 0.65 +/- 0.04 to 0.62 +/- 0.04, P greater than 0.40). The drug induced a substantial natriuresis; the percentage of filtered sodium excreted rose from 0.4 +/- 0.1 to 13.1 +/- 2.4% (P less than 0.005). Bicarbonate and phosphate excretion rose more modestly: the percentage excretion of the former ion increased from 0.9 +/- 0.3 to 3.7 +/- 0.08% (P less than 0.005) and that for phosphate doubled (from 3.4 +/- 1.0 to 6.8 +/- 1.3%, P less than 0.025). However, urinary pH did not change. Accordingly, bumetanide uncoupled the transport of sodium bicarbonate from that of sodium phosphate in the proximal convoluted tubule. It is concluded from these data that the action of bumetanide in the proximal convoluted tubule is probably not related either to carbonic anhydrase inhibition or to the impairment of sodium-phosphate-linked transport.

Animals↗
PubMed1979

Impaired renal bicarbonate reabsorption in the hypothyroid rat.

We previously demonstrated a decrease of sodium reabsorption in the proximal superficial nephron of the hypothyroid rat. The present clearance studies were designed to examine the renal handling of bicarbonate in hypothyroid rats. Hypothyroidism was induced by the intraperitoneal injection of Na131I and the animals were studied 10 or more wk thereafter under anesthesia and compared to their age-matched litter-mates. As is characteristic of hypothyroid animals, insulin clearance was lower and fractional urine flow and sodium excretion rates were higher than in the control rats. At the peak of the bicarbonate diuresis and at similar blood pH, PCO2, and bicarbonate levels, fractional renal bicarbonate excretion was significantly higher in the hypothyroid animals: 22 +/- 2 vs. 15 +/- 1%, P less than 0.02. This perturbation of bicarbonate reabsorption of the hypothyroid rats was independent of the influence of extracellular fluid volume expansion and appears closely related to the impaired sodium reabsorptive capacity characteristic of experimental hypothyroidism.

Animals↗
PubMed1986

Chloride transport by rat renal proximal tubule: effects of bicarbonate absorption.

In the early part of the proximal tubule chloride concentration is increased above that in plasma, a change attributed to preferential absorption of bicarbonate with sodium and water. To determine the mechanism(s) of the preferential absorption of HCO3 over chloride, in vivo paired perfusions were done in surface proximal tubules of the rat kidney. Each tubule was perfused with a control bicarbonate solution, similar in ionic composition to the solution normally present in the early part of the proximal tubule, and one of the experimental solutions that were modified by either replacing all of bicarbonate with sulfate, N-2-hydroxyethylpiperazine-N'-ethanesulfonate (HEPES), or all bicarbonate with sulfate and sodium with lithium, or addition of acetazolamide (ATZ), or cyanide (CN). Sufficient mannitol was added to reduce net fluid flux to zero. When sulfate replaced bicarbonate in luminal fluid, net chloride absorption was enhanced, a change associated with low lumen HCO3 and low pH. ATZ inhibited HCO3 absorption, whereas net Cl absorption increased, an effect associated with high HCO3 and low pH. With HEPES-plus-ATZ solutions, chloride absorption also increased but, in contrast to SO4 or ATZ solutions, pH increased. With sulfate and lithium replacement chloride absorption also increased despite net sodium secretion. CN, a metabolic inhibitor, inhibited HCO3 and sodium absorption but stimulated net chloride absorption. The data indicate that HCO3 absorption inhibits chloride absorption, a process independent of luminal HCO3 per se, luminal pH, sodium absorption, and transepithelial volume flux and voltage.

Absorption↗
PubMed1986

Factors affecting renal handling of sodium, hydrogen ions, and bicarbonate by the fetus.

Renal excretion of acid and reabsorption of bicarbonate was studied in 17 chronically catheterized fetal sheep aged 121-143 days. The rates of excretion of titratable acid (0.16-6.2 mumol/min) and ammonium (1.2-9.7 mumol/min) were variable. Urinary phosphate excretion was significantly greater (P less than 0.001) than the excretion of titratable acid. Of the filtered bicarbonate load 80-100% was reabsorbed. In 9 of the 17 fetuses net acid excretion was positive. Bicarbonate, sodium, and chloride reabsorption were related to glomerular filtration rate (GFR) (P less than 0.0005). The increase of GFR results in an increase in the excretion of titratable acid (P less than 0.001), phosphate (P less than 0.0005), and ammonium (P less than 0.001). These relationships could account for the age-dependent increase in renal excretion of acid (P less than 0.0005), ammonium (P less than 0.025), and bicarbonate reabsorption (P less than 0.0005). Arterial pH affected the rates of excretion of titratable acid (P less than 0.005), ammonium ions (P less than 0.05), and net acid (P less than 0.025). It is concluded that the fetal kidneys can excrete protons and generate bicarbonate. This ability increases with age due mainly to the concomitant increase in GFR.

Acids↗
PubMed1988

Flow dependence of bicarbonate transport in the early (S1) proximal convoluted tubule.

We previously found, using an in vivo microperfusion pump rate of 30 nl/min, that proton secretion in the early (S1) proximal convoluted tubule (PCT) of the Munich-Wistar rat exhibited saturation kinetics. The maximal transport capacity was very high, approximately 500-600 peq.mm-1.min-1. The present studies assessed the change in early PCT acidification kinetics in response to an increase in microperfusion rate to 45 nl/min. First, bicarbonate permeability in the early PCT was measured and was found to be flow dependent. Proton secretion was then calculated using perfusate bicarbonate concentrations from 8 to 100 mM. Saturation of early proximal acidification (Vmax) still occurred at approximately 500-600 peq.mm-1.min-1, but the bicarbonate concentration effecting half-maximal acidification (apparent Km) decreased (from approximately 11 mM at 30 nl/min perfusion rate to less than 6 mM at 45 nl/min). By increasing luminal perfusion rate further to 60 nl/min at constant luminal bicarbonate concentration (25 mM), we confirmed that luminal flow rate did not affect the maximal level of acidification. Similar flow-dependent changes in acidification kinetics in the late PCT were also found, as has been previously shown. In conclusion, although an increase in luminal flow increased bicarbonate permeability and apparent affinity for substrate transport, there was no effect on maximal acidification rate in the early PCT.

Animals↗
PubMed1990

Role of protein kinase C in proximal bicarbonate absorption and angiotensin signaling.

Using in vivo microperfusion in the proximal convoluted tubule (PCT) of the Munich-Wistar rat, we investigated the impact of varying protein kinase C (PKC) activity on the rate of bicarbonate reabsorption and on its regulation by angiotensin II. Activation of PKC with luminal perfusion of phorbol 12-myristate 13-acetate (PMA, 5 x 10(-7) M) caused bicarbonate absorption in the S1 PCT to increase by 25%, from 346 +/- 7 to 432 +/- 4 peq.mm-1.min-1 (P less than 0.001), without affecting intracellular cAMP level. Another PKC stimulator, dioctanoylglycerol, had the same effect. Inhibition of PKC activity with luminal perfusion of 5 x 10(-6) M sphingosine had the opposite effect, decreasing bicarbonate absorption by 45% to 190 +/- 2 peq.mm-1.min-1 (P less than 0.001). Pretreatment with PMA or with sphingosine each attenuated by approximately one-third the bicarbonate absorptive response usually observed following angiotensin II administration. Similar results for the action of PKC, but of smaller magnitude, were found in the S2 PCT. In conclusion, activation of PKC increases bicarbonate and water absorption in the S1 and S2 PCT in vivo, and PKC may participate in as much as one-third of the transport stimulation induced by angiotensin II.

Absorption↗
PubMed1994

Bicarbonate dependency of betaine synthesis in cultured LLC-PK1 cells.

Betaine, one of the major renal organic osmolytes, is synthesized from choline by choline dehydrogenase (EC 1.1.99.1) and betaine-aldehyde dehydrogenase (EC 1.2.1.8) in the kidney. A recent in vitro study has shown that betaine synthesis by renal cortical homogenate is dependent on millimolar amounts of bicarbonate. The present study was aimed to investigate the bicarbonate dependency of betaine formation in cultured LLC-PK1 cells. The data show that betaine formation increases in accordance with a rise in extracellular bicarbonate levels. The measured quantities of [14C]betaine synthesis ranged from 13.4 +/- 1.5 (4.6 mM HCO3-) to 38.0 +/- 1.4 pmol.micrograms protein-1.h-1 (24 mM HCO3-). The carbonic anhydrase inhibitor acetazolamide, added to the incubation medium to block bicarbonate transport, reduced betaine synthesis from choline by 41-49%. We conclude that betaine synthesis in LLC-PK1 cells is dependent on extracellular bicarbonate levels and is reduced by the inhibition of carbonic anhydrase. Because betaine accumulates in renal medulla during antidiuresis, our observations suggest a possible link between acid-base homeostasis and concentration mechanisms in the kidney.

Acetazolamide↗
PubMed1997

Effect of luminal angiotensin II on rabbit proximal convoluted tubule bicarbonate absorption.

The present in vitro microperfusion study examined the effect of luminal angiotensin II on proximal convoluted tubule (PCT) volume absorption and bicarbonate transport. Neither 10(-11) M, 10(-10) M, nor 2 x 10(-8) M luminal angiotensin II significantly affected PCT transport. When tubules were first perfused with enalaprilat to inhibit endogenous angiotensin II production, addition of 10(-10) M luminal angiotensin II increased volume absorption (0.72 +/- 0.08 vs. 0.86 +/- 0.07 nl x mm(-1) xmin(-1), P < 0.01) and bicarbonate transport (52.3 +/- 3.7 vs. 67.9 +/- 4.2 pmol x mm(-1) min(-1), P < 0.01). Addition of 10(-6) M losartan, an AT1 inhibitor, to the luminal perfusate inhibited volume absorption (0.95 +/- 0.14 vs. 0.72 +/- 0.11 nl x mm(-1) x min(-1), P < 0.05) and bicarbonate transport (65.0 +/- 7.3 vs. 54.7 +/- 9.2 pmol x mm(-1) x min(-1), P < 0.05). Addition of 10(-4) M luminal PD-123319, an AT2 inhibitor, was without effect. In tubules perfused with 10(-4) M luminal enalaprilat and 10(-4) M luminal PD-123319, addition of 10(-10) M luminal angiotensin II in the experimental period resulted in a stimulation in volume absorption (0.61 +/- 0.08 vs. 0.81 +/- 0.10 nl x mm(-1) x min(-1), P < 0.01) and bicarbonate transport (49.9 +/- 6.3 vs. 77.4 +/- 14.3 pmol x mm(-1) x min(-1), P < 0.01). In tubules perfused with 10(-6) M losartan and 10(-4) M enalaprilat, addition of luminal 10(-10) M angiotensin II resulted in no change in transport. These data are consistent with endogenous angiotensin II affecting PCT bicarbonate transport in vitro via luminal AT1 receptors.

Absorption↗
PubMed2003

Effect of vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide on pancreatic, hepatic and duodenal mucosal bicarbonate secretion in the pig.

BACKGROUND AND METHOD: The potency of pituitary adenylate cyclase-activating polypeptide (PACAP) and the related vasoactive intestinal peptide (VIP) on pancreaticobiliary and duodenal mucosal bicarbonate secretion (DMBS) was studied in anaesthetized pigs. VIP, PACAP27 and PACAP38 were infused at doses of 250, 500, 1,000, 2,000 and 6,000 pmol/kg x h. RESULTS: Infusion of VIP in these concentrations increased the portal plasma concentrations of VIP from 9 to 102, 220, 600, 850 and 3,795 pM, respectively. At doses of 1,000 and 6,000 pmol/kg.h all three peptides significantly stimulated pancreatic bicarbonate secretion, VIP from 0.0 to 0.3 and 7.6 mmol/h, PACAP27 from 0.0 to 2.3 and 8.2 mmol/h, and PACAP38 from 0.0 to 0.2 and 7.4 mmol/h, respectively. Only during infusion of 6,000 pmol/kg.h did the three peptides elicit a significant increase in hepatic bicarbonate output. At this dose VIP increased hepatic bicarbonate output from 0.4 to 3.8 mmol/h, PACAP27 from 0.3 to 3.6 mmol/h, and PACAP38 from 0.1 to 1.4 mmol/h, respectively. Infusion of VIP (500, 1,000, 2,000 and 6,000 pmol/kg.h) dose-dependently and significantly enlarged DMBS from 0.09 to 0.19, 0.41, 0.54 and 0.53 mmol/h, respectively. A significant effect of PACAP27 and PACAP38 on DMBS was only obtained at a dose of 6,000 pmol/kg.h, and at this dose VIP-induced DMBS was 4- and 8-fold higher than that induced by PACAP27 and PACAP38, respectively. CONCLUSIONS: VIP, PACAP27 and PACAP38 all have a pharmacological effect on both DMBS and pancreaticobiliary bicarbonate secretion. When comparing these results with the distribution of VIP/PACAP neurons and relevant receptors, it seems likely that VIP and PACAP have a physiological importance as neurotransmitters in the pancreas and duodenum, but not in the liver. The differences in the effect of VIP and PACAP on DMBS observed in this study indicate that there are variations between pancreatic and duodenal PACAP/VIP receptor subtypes, or that the duodenal inactivation of the peptides is different from the inactivation in the pancreas.

Animals↗
PubMed1981

Hypotension during acetate and bicarbonate dialysis in patients with acute renal failure.

Bicarbonate dialysate is claimed to be superior to acetate for both chronic and acute hemodialysis. We compared acetate and bicarbonate dialysates in 30 acute renal failure patients during 120 dialyses. 4 patients were diabetic and 2 had liver failure. Patients were dialyzed alternating acetate and bicarbonate dialysate in a double-blind cross-over manner; each patient was his own control. BUN, creatinine, Na+, K+, osmolality, delta osmolality, % ultrafiltration, arterial blood gases, pre, post and lowest dialysis mean arterial blood pressure, dialysis with hypotensive episodes and symptoms of hypotension were recorded. The measurements obtained for each patient during dialyses with acetate and bicarbonate were compared. There was no difference in predialysis chemistries, osmolality or osmolality fall, no change in mean arterial blood pressure or hypotensive episodes and symptoms and ultrafiltration. PCO2 and pH were slightly lower for the acetate group at the 2nd h but not at the end of dialysis. 4 patients had serum acetate determinations, all metabolized acetate normally. These findings contradict recent suggestions that severely ill patients should not be dialyzed against acetate. Since acetate is technically much easier to use and has no clinical drawbacks, it does not need to be replaced with bicarbonate in acute patients. Other factors must be more important than acetate in generating hypotension during acute dialysis.

Acetates↗